Spiritual practices for the adaptation of cold and heat. Methodical development. Topic: “Physiologically, the basis of adaptation of an athlete's body to new climatic conditions. If clothing and exercise-related metabolism are sufficient to support those
Content
I. Introduction
II. Main part
1. Optium and pessium. The sum of the efficiency of the temperatures
2. Poikilothermic organisms
2.1 Passive resistance
2.2 Metabolic rate
2.3 Temperature adaptations
3. Homeothermal organisms
3.1 Body temperature
3.2 Mechanism of thermoregulation
Bibliography
I. Introduction
Organisms are real carriers of life, discrete units of metabolism. In the process of metabolism, the body consumes the necessary substances from the environment and releases metabolic products into it, which can be used by other organisms; dying, the body also becomes a source of nutrition for certain types of living beings. Thus, the activity of individual organisms underlies the manifestation of life at all levels of its organization.
The study of fundamental metabolic processes in a living organism is a subject of physiology. However, these processes take place in a complex, dynamic environment of the natural habitat, are under the constant influence of a complex of its factors. Maintaining a stable metabolism in fluctuating environmental conditions is impossible without special adaptations. The study of these adaptations is a task for ecology.
Adaptations to environmental factors can be based on the structural features of the organism - morphaological adaptations - or on specific forms of functional response to external influences - physiological adaptations. In higher animals, higher nervous activity plays an important role in adaptation, on the basis of which adaptive forms of behavior - ecological adaptations - are formed.
In the field of studying adaptations at the level of the organism, the ecologist comes into the closest interaction with physiology and applies many physiological methods. However, applying physiological methods, ecologists use them to solve their specific problems: the ecologist is primarily interested not in the fine structure of the physiological process, but in its final result and the dependence of the process on the influence of external factors. In other words, in ecology, physiological indicators serve as criteria for the body's response to external conditions, and physiological processes are considered primarily as a mechanism that ensures the uninterrupted implementation of fundamental physiological functions in a complex and dynamic environment.
II. MAIN PART
1. Optimum and pessimum. Sum of effective temperatures
Any organism is capable of living within a certain temperature range. The temperature range on the planets of the solar system is thousands of degrees, and the limits are. In which the life we know can exist are very narrow - from -200 to + 100 ° C. Most species live in an even narrower temperature range.
Some organisms. Especially in the resting stage, they can exist at very low temperatures, and certain types of microorganisms are able to live and multiply in urban springs at temperatures close to the boiling point. The range of temperature fluctuations in water is usually less than on land. The range of tolerance changes accordingly. Zoning and stratification are often associated with temperature in both water and terrestrial habitats. The degree of temperature variability and its fluctuations are also important, that is, if the temperature changes in the range from 10 to 20 C and the average value is 15 C, this does not mean that the fluctuating temperature has the same effect as the constant one. Many organisms thrive in varying temperatures.
The optimal conditions are those under which all physiological processes in the body or ecosystems run with maximum efficiency. For most species, the temperature optimum is in the range of 20-25 ° C, slightly shifting in one direction or another: in the dry tropics it is higher - 25-28 ° C, in temperate and cold zones below - 10-20 ° C. In the course of evolution, adapting not only to periodic changes in temperature, but also to regions of different heat supply, plants and animals have developed different needs for heat in different periods of life. Each species has its own optimal temperature range, and for different processes (growth, flowering, fruiting, etc.) there are also “own” optimum values.
It is known that physiological processes in plant tissues begin at a temperature of + 5 ° C and are activated at + 10 ° C and above. In coastal forests, the development of spring species is especially clearly associated with average daily temperatures from -5 ° C to + 5 ° C. A day or two before the temperature passes through -5 ° С under the forest litter, the development of the star spring and Amur adonis begins, and during the transition through 0 ° С, the first flowering individuals appear. And even at an average daily temperature of + 5 ° C, both species bloom. Due to the lack of heat, neither adonis nor the spring plant form a continuous cover, they grow singly, less often - several individuals together. A little later than them - with a difference of 1-3 days, anemones start to grow and bloom.
Temperatures "lying" between lethal and optimal are considered pessimal. In the pessimum zone, all life processes are very weak and very slow.
The temperatures at which active physiological processes take place are called effective, their values do not go beyond the lethal temperatures. The sum of effective temperatures (ET), or the sum of heat, is a constant value for each type. It is calculated by the formula:
ET = (t - t1) × n,
Where t is the ambient temperature (actual), t1 is the temperature of the lower developmental threshold, often 10 ° C, n is the duration of development in days (hours).
It was revealed that each phase of the development of plants and ectothermic animals begins at a certain value of this indicator, provided that other factors are at the optimum. So, coltsfoot bloom occurs at a sum of temperatures of 77 ° C, strawberries - at 500 ° C. The sum of effective temperatures (ET) for the entire life cycle allows to identify the potential geographic range of any species, as well as to make a retrospective analysis of the distribution of species in the past. For example, the northern limit of woody vegetation, in particular of Cajander larch, coincides with the July isotherm of + 12 ° С and the total ET above 10 ° С - 600 °. For early crops, the total ET is 750 °, which is quite enough for growing early varieties of potatoes even in the Magadan region. And for Korean cedar, the total ET is 2200 °, for whole-leaved fir - about 2600 °, therefore both species grow in Primorye, and fir (Abies holophylla) - only in the south of the region.
2. POYKILOTHERM ORGANISMS
All taxa of the organic world are classified as poikilothermic (from the Greek poikilos - changeable, changing) organisms, except for two classes of vertebrates - birds and mammals. The name emphasizes one of the most noticeable properties of the representatives of this group: instability, their body temperature, varying widely depending on changes in ambient temperature.
Body temperature . The principal feature of heat exchange in poikilothermic organisms is that, due to their relatively low metabolic rate, external heat is their main source of energy. This explains the direct dependence of the body temperature of poikilotherms on the temperature of the environment, more precisely on the influx of heat from the outside, since terrestrial poikilothermic forms also use radiation heating.
However, full correspondence between body and environmental temperatures is rarely observed and is characteristic mainly of organisms of very small sizes. In most cases, there is some discrepancy between these indicators. In the range of low and moderate ambient temperatures, the body temperature of organisms that are not in a state of numbness turns out to be higher, and in very hot conditions, it is lower. The reason for the excess body temperature over the environment is that even with a low level of metabolism, endogenous heat is produced - it causes an increase in body temperature. This is manifested, in particular, in a significant increase in temperature in actively moving animals. For example, in insects at rest, the excess of body temperature over the environment is expressed in tenths of a degree, while in actively flying butterflies, bumblebees and other species, the temperature is maintained at 36 - 40 "C even when the air temperature is below 10" C.
The temperature lowered in comparison with the environment during heat is characteristic of terrestrial organisms and is explained primarily by the loss of heat with evaporation, which increases significantly at high temperature and low humidity.
The rate of changes in body temperature of poikilotherms is inversely related to their size. This is primarily determined by the ratio of mass and surface: in larger forms, the relative surface of the body decreases, which leads to a decrease in the rate of heat loss. This is of great ecological importance, determining for different species the possibility of settling in geographic areas or biotopes with certain temperature regimes. It has been shown, for example, that in large leatherback turtles caught in cold waters the temperature in the depth of the body was - 18 "C higher than the temperature of the water; it is the large size that allows these turtles to penetrate into the colder regions of the ocean, which is not characteristic of smaller species.
2.1 Passive resistance
The considered patterns cover the range of temperature changes, within which active vital activity is maintained. Outside this range, which vary widely in different species and even geographic populations of the same species, active forms of activity of poikilothermic organisms cease, and they pass into a state of numbness, characterized by a sharp decrease in the level of metabolic processes, up to a complete loss of visible manifestations of life. In such a passive state, poikilothermic organisms can tolerate a sufficiently strong increase and an even more pronounced decrease in temperature without pathological consequences. The basis of such temperature tolerance lies in a high degree of tissue stability, inherent in all poikilothermic species and often supported by severe dehydration (seeds, spores, some small animals).
The transition to a state of numbness should be considered as an adaptive reaction: an almost non-functioning organism is not exposed to many damaging influences, and also does not consume energy, which allows it to survive under adverse temperature conditions for a long time. Moreover, the very process of transition to a state of torpor can be a form of active rearrangement, such as a reaction to temperature. "Hardening" of frost-resistant plants is an active seasonal process that goes in stages and is associated with rather complex physiological and biochemical changes in the body. In animals, falling into torpor in natural conditions is often also expressed seasonally and is preceded by a complex of physiological rearrangements in the body. There is evidence that the process of transition to stupor can be regulated by some hormonal factors; objective material on this matter is not yet sufficient for broad conclusions.
When the temperature of the environment goes beyond the limits of tolerance, the death of the organism occurs from the reasons discussed at the beginning of this chapter.
2.2 Metabolic rate
Temperature variability entails corresponding changes in the rate of metabolic reactions. Since the dynamics of the body temperature of poikilothermic organisms is determined by changes in the temperature of the environment, the intensity of metabolism is also directly dependent on the external temperature. The rate of oxygen consumption, in particular, with rapid changes in temperature, follows these changes, increasing with an increase and decreasing with a decrease. The same applies to other physiological functions: heart rate, intensity of digestion, etc. In plants, depending on temperature, the rate of water and nutrient intake through the roots changes: an increase in temperature to a certain limit increases the permeability of protoplasm to water. It has been shown that with a decrease in temperature from 20 to 0 "C, water absorption by roots decreases by 60 - 70%. As in animals, an increase in temperature causes increased respiration in plants.
The last example shows that the influence of temperature is not straightforward: upon reaching a certain threshold, the stimulation of the process is replaced by its suppression. This is a general rule due to the approach to the threshold of normal life.
In animals, the dependence on temperature is very noticeably expressed in changes in activity, which reflects the total reaction of the organism, and in poikilothermic forms it depends in the most significant way on temperature conditions. It is well known that insects, lizards and many other animals are most mobile during the warm time of the day and on warm days, while in cool weather they become lethargic and inactive. The onset of their vigorous activity is determined by the rate of warming up of the body, which depends on the temperature of the environment and on direct solar irradiation. The level of mobility of active animals is, in principle, also related to the ambient temperature, although in the most active forms this relationship can be “masked” by endogenous heat production associated with the work of the muscles.
2.3 Temperature adaptations
Poikilothermic living organisms are widespread in all environments, occupying habitats of different temperature conditions, up to the most extreme: they practically inhabit the entire temperature range recorded in the biosphere. Retaining in all cases the general principles of temperature reactions (discussed above), different species and even populations of the same species exhibit these reactions in accordance with the characteristics of the climate, adapting the body's responses to a certain range of temperature effects. This is manifested, in particular, in the forms of resistance to heat and cold: species living in colder climates are more resistant to low temperatures and less to high; inhabitants of hot regions show opposite reactions.It is known that tropical forest plants are damaged and die at temperatures of + 5 ... + 8 ° C, while the inhabitants of the Siberian taiga can withstand complete freezing in a state of numbness.
Various species of kart-toothed fish showed a clear correlation of the upper lethality threshold with water temperature in the species-specific water bodies.
Arctic and Antarctic fish, on the other hand, show high resistance to low temperatures and are very sensitive to its rise. So, Antarctic fish die when the temperature rises to 6 "C. Similar data have been obtained for many species of poikilothermic animals. For example, observations on the island of Hokkaido (Japan) showed a clear connection between the cold resistance of several species of beetles and their larvae with their winter ecology: the most resistant In the experiments with amoeba it was found that their heat resistance directly depends on the temperature of cultivation.
3. HOMOYOTHERMAL ORGANISMS
This group does not include two classes of higher vertebrates - birds and mammals. The fundamental difference between the heat exchange of homeothermal animals and poikilothermic animals is that their adaptation to changing temperature conditions of the environment is based on the functioning of a complex of active regulatory mechanisms for maintaining thermal homeostasis of the internal environment of the body. Due to this, biochemical and physiological processes always proceed under optimal temperature conditions.
The homeothermal type of heat exchange is based on the high metabolic rate inherent in birds and mammals. The metabolic rate of these animals is one to two orders of magnitude higher than that of all other living organisms at the optimum ambient temperature. So, in small mammals, oxygen consumption at an ambient temperature of 15 - 0 "C is about 4 - thousand cm 3 kg -1 h -1, and in invertebrates at the same temperature - 10 - 0 cm 3 kg -1 h -1 .With the same body weight (2.5 kg), the daily metabolism of a rattlesnake is 32.3 J / kg (382 J / m 2), in a marmot - 120.5 J / kg (1755 J / m 2), in a rabbit - 188.2 J / kg (2600 J / m 2).
A high metabolic rate leads to the fact that in homeothermal animals, the basis of the heat balance is the use of their own heat production, the value of external heating is relatively small. Therefore, birds and mammals are referred to as endothermic "organisms. Endothermy is an important property, due to which the dependence of the body's vital activity on the temperature of the external environment is significantly reduced.
3.1 Body temperature
Homeothermal animals are not only provided with heat due to their own heat production, but are also able to actively regulate its production and consumption. Due to this, they are characterized by a high and fairly stable body temperature. In birds, the deep body temperature is normally about 41 "C with fluctuations in different species from 38 to 43.5" C (data for 400 species). Under conditions of complete rest (basal metabolism), these differences are somewhat smoothed out, ranging from 39.5 to 43.0 "C. At the level of an individual organism, the body temperature shows a high degree of stability: the range of its daily changes usually does not exceed 2 - ~ 4" C, moreover, these fluctuations are not associated with air temperature, but reflect the rhythm of metabolism. Even in Arctic and Antarctic species, at ambient temperatures up to 20 - 50 "C frost, the body temperature fluctuates within the same 2 - 4" C.
An increase in ambient temperature is sometimes accompanied by a slight increase in body temperature. If pathological conditions are excluded, it turns out that in conditions of living in a hot climate, a certain degree of hyperthermia can be adaptive: in this case, the difference in body and environmental temperatures decreases and water consumption for evaporative thermoregulation decreases. A similar phenomenon has been noted in some mammals: in a camel, for example, with a water shortage, the body temperature can rise from 34 to 40 "C. In all such cases, an increased tissue resistance to hyperthermia is noted.
In mammals, body temperature is slightly lower than in birds, and in many species it is subject to greater fluctuations. Different taxa also differ in this indicator. In monotremes, rectal temperature is 30 - 3 "C (at an ambient temperature of 20" C), in marsupials it is slightly higher - about 34 "C at the same external temperature. In representatives of both these groups, as well as in non-edentulous, fluctuations in body temperature are quite noticeable in connection with the external temperature: with a decrease in air temperature from 20 - 5 to 14 - 15 "C, a drop in body temperature was recorded by more than two degrees, and in some cases even by 5" C. In rodents, the average body temperature in an active state fluctuates within 35 - 9.5 "С, in most cases being 36 - 37" С. external temperature from 0 to 35 "C.
In ungulates and carnivores, body temperature is maintained very steadily at the level characteristic of the species; interspecies differences usually fall within the range from 35.2 to 39 "C. Many mammals are characterized by a decrease in temperature during sleep; the magnitude of this decrease varies in different species from tenths of a degree to 4 -" C.
All of the above refers to the so-called deep body temperature, which characterizes the thermal state of the thermostated "core" of the body. In all homeothermic animals, the outer layers of the body (integument, part of the musculature, etc.) form a more or less pronounced "shell", the temperature of which varies within wide limits. Thus, the stable temperature characterizes only the area of localization of important internal organs and processes. Surface tissues can withstand more pronounced temperature fluctuations. This can be beneficial for the organism, since in such a situation the temperature gradient at the border of the organism and the environment decreases, which makes it possible to maintain the thermal homeostasis of the “core” of the organism with less energy expenditure.
3.2 Mechanisms of thermoregulation
Physiological mechanisms providing thermal homeostasis of the body (its "nucleus") are subdivided into two functional groups: mechanisms of chemical and physical thermoregulation. Chemical thermoregulation is the regulation of the body's heat production. Heat is constantly generated in the body during the redox reactions of metabolism. At the same time, part of it is given to the external environment, the more, the greater the difference between the temperature of the body and the environment. Therefore, maintaining a stable body temperature with a decrease in the temperature of the environment requires a corresponding increase in metabolic processes and the accompanying heat generation, which compensates for heat loss and leads to the preservation of the overall heat balance of the body and maintaining the constancy of the internal temperature. The process of reflex enhancement of heat production in response to a decrease in ambient temperature is called chemical thermoregulation. The release of energy in the form of heat accompanies the functional load of all organs and tissues and is characteristic of all living organisms. The specificity of homeothermic animals is that a change in heat production as a reaction to a changing temperature represents a special reaction of the organism in them, which does not affect the level of functioning of the main physiological systems.
Specific thermoregulatory heat production is concentrated mainly in skeletal muscles and is associated with special forms of muscle functioning that do not affect their direct motor activity. An increase in heat generation during cooling can also occur in a resting muscle, as well as when the contractile function is artificially turned off by the action of specific poisons.
One of the most common mechanisms of specific thermoregulatory heat production in muscles is the so-called thermoregulatory tone. It is expressed by microcontractions of fibrils, recorded as an increase in the electrical activity of an externally immobile muscle when it is cooled. Thermoregulatory tone increases the oxygen consumption of the muscle, sometimes by more than 150%. With stronger cooling, along with a sharp increase in thermoregulatory tone, visible muscle contractions in the form of cold shivering are included. In this case, gas exchange increases to 300 - 400%. It is characteristic that muscles are unequal in terms of the share of participation in thermoregulatory heat generation. In mammals, the most important role is played by the chewing muscles and muscles that support the animal's posture, that is, they function mainly as tonic muscles. A similar phenomenon is observed in birds.
With prolonged exposure to cold, the contractile type of thermogenesis can be replaced (or supplemented) to one degree or another by switching tissue respiration in the muscle to the so-called free (non-phosphorylating) pathway, in which the phase of formation and subsequent breakdown of ATP falls out. This mechanism is not associated with muscle contractile activity. The total mass of heat released during free breathing is practically the same as in yeast thermogenesis, but most of the thermal energy is consumed immediately, and oxidative processes cannot be inhibited by a lack of ADP or inorganic phosphate.
The latter circumstance makes it possible to freely maintain a high level of heat generation for a long time.
In mammals, there is another form of non-yeast thermogenesis associated with the oxidation of a special brown adipose tissue deposited under the skin in the interscapular space, neck and thoracic spine. Brown fat contains a large number of mitochondria and is permeated with numerous blood vessels. Under the influence of cold, the blood supply to brown fat increases, its respiration intensifies, and the release of heat increases. It is important that in this case the organs located nearby are directly heated: the heart, large vessels, lymph nodes, as well as the central nervous system. Brown fat is used mainly as a source of emergency heat generation, in particular when warming up the body of animals coming out of hibernation. The role of brown fat in birds is not clear. For a long time it was believed that they did not have it at all; Recently, there have been reports of the discovery of this type of adipose tissue in birds, but no precise identification or functional assessment has been carried out.
Changes in the intensity of metabolism caused by the influence of ambient temperature on the organism of homeothermal animals are natural. In a certain range of external temperatures, heat production corresponding to the exchange of a resting organism is completely compensated by its "normal" (without active intensification) heat transfer. The heat exchange between the body and the environment is balanced. This temperature range is called the thermoneutral zone. The exchange rate in this zone is minimal. They often speak of a critical point, implying a specific temperature value at which a heat balance with the environment is achieved. Theoretically, this is true, but it is practically impossible to establish such a point experimentally due to constant irregular fluctuations in metabolism and instability of the heat-insulating properties of the covers.
A decrease in the temperature of the environment outside the thermoneutral zone causes a reflex increase in the level of metabolism and heat production until the heat balance of the body is balanced under new conditions. Because of this, the body temperature remains unchanged.
An increase in the temperature of the environment outside the thermoneutral zone also causes an increase in the level of metabolism, which is caused by the activation of mechanisms for activating the release of heat, which require additional energy consumption for their work. Thus, a zone of physical thermoregulation is formed, during which the temperature of the takyre remains stable. Upon reaching a certain threshold, the mechanisms for enhancing heat transfer turn out to be ineffective, overheating begins and, ultimately, the death of the organism.
Species differences in chemical thermoregulation are expressed in the difference in the level of the main (in the zone of thermoneutrality) metabolism, the position and width of the thermoneutral zone, the intensity of chemical thermoregulation (an increase in metabolism with a decrease in the temperature of the medium by 1 "C), as well as in the range of effective action of thermoregulation. All these parameters reflect ecological specificity of individual species and adaptively change depending on the geographic location of the region, season of the year, altitude and a number of other environmental factors.
Physical thermoregulation combines a complex of morphophysiological mechanisms associated with the regulation of heat transfer from the body as one of the constituent parts of its overall heat balance. The main device that determines the general level of heat transfer from the body of a homeothermic animal is the structure of the heat-insulating covers. Thermal insulating structures (feathers, hair) do not cause homeothermia, as is sometimes thought. It is based on high and that, by reducing heat loss, it contributes to the maintenance of homeothermy with lower energy costs. This is especially important when living in conditions of persistently low temperatures; therefore, heat-insulating integumentary structures and layers of subcutaneous fat are most pronounced in animals from regions of cold climates.
The mechanism of the heat-insulating action of feathers and hairs is that groups of hair or feathers, located in a certain way, different in structure, hold a layer of air around the body, which acts as a heat insulator. Adaptive changes in the heat-insulating function of integuments are reduced to a restructuring of their structure, including the ratio of different types of hair or feathers, their length and density. It is by these parameters that the inhabitants of different climatic zones differ, they also determine the seasonal changes in thermal insulation. It has been shown, for example, that in tropical mammals the thermal insulation properties of the coat are almost an order of magnitude lower than in the inhabitants of the Arctic. The same adaptive direction is followed by seasonal changes in the heat-insulating properties of the mantles during molting.
The considered features characterize the stable properties of heat-insulating covers, which determine the overall level of heat losses, and, in essence, do not represent active thermoregulation reactions. The possibility of labile regulation of heat transfer is determined by the mobility of feathers and hair, due to which, against the background of a constant structure of the cover, rapid changes in the thickness of the heat-insulating air layer, and, accordingly, in the intensity of heat transfer are possible. The degree of looseness of hair or feathers can change rapidly depending on the temperature of the air and on the activity of the animal itself. This form of physical thermoregulation is referred to as the pilomotor reaction. This form of regulation of heat transfer acts mainly at low ambient temperatures and provides no less quick and effective response to thermal imbalance than chemical thermoregulation, while requiring less energy.
Regulatory reactions aimed at maintaining a constant body temperature during overheating are represented by various mechanisms for enhancing heat transfer to the external environment. Among them, heat transfer is widespread and highly efficient by intensifying the evaporation of moisture from the surface of the body and / or upper respiratory tract. When moisture evaporates, heat is consumed, which can help maintain heat balance. The reaction turns on when there are signs of starting overheating of the body. So, adaptive changes in heat exchange in homeothermal animals can be aimed not only at maintaining a high level of metabolism, as in most birds and mammals, but also at setting a low level in conditions that threaten the depletion of energy reserves.
Bibliography
1. Fundamentals of ecology: Textbook VV Mavrishchev. Minsk: Vysh. Shk., 2003 .-- 416 p.
2.http: \\ Abiotic factors of the environment.htm
3.http: \\ Abiotic environmental factors and organisms.htm
- Specialty VAK RF03.00.16
- Number of pages 101
CHAPTER 1. MODERN CONCEPTS ABOUT THE MECHANISM OF ADAPTATION OF THE BODY TO COLD AND TOCOPHEROL DEFICIENCY.
1.1 New ideas about the biological functions of reactive oxygen species during adaptive metabolic transformations.
1.2 Mechanisms of adaptation of the body to cold and the role of oxidative stress in this process.
1.3 Mechanisms of adaptation of the body to tocopherol deficiency and the role of oxidative stress in this process.
CHAPTER 2. MATERIAL AND RESEARCH METHODS.
2.1 Organization of research.
2.1.1 Organization of experiments on the influence of cold.
2.1.2 Organization of experiments on the influence of tocopherol deficiency.
2.2 Research methods
2.2.1 Hematological parameters
2.2.2 Research on energy metabolism.
2.2.3 Study of oxidative metabolism.
2.3 Statistical processing of results.
CHAPTER 3. RESEARCH OF OXIDATIVE HOMEOSTASIS, BASIC MORPHOFUNCTIONAL PARAMETERS OF RAT'S ORGANISM AND Erythrocytes under LONG EXPOSURE TO COLD.
CHAPTER 4. STUDY OF OXIDATIVE HOMEOSTASIS, BASIC MORPHOFUNCTIONAL PARAMETERS OF RAT'S BODY AND ERYTHROCYTES IN LONG TOCOPHEROL DEFICIENCY.
Recommended list of dissertations
Physiological aspects of cellular and molecular patterns of adaptation of animal organisms to extreme situations 2013, Doctor of Biological Sciences Cherkesova, Dilara Ulubievna
Mechanisms of the participation of tocopherol in adaptive transformations in the cold 2000, Doctor of Biological Sciences Kolosova, Natalia Gorislavovna
Features of the functioning of the hypothalamic-pituitary-reproductive system at the stages of ontogenesis and under conditions of using geroprotectors 2010, Doctor of Biological Sciences Kozak, Mikhail Vladimirovich
Ecological and physiological aspects of the formation of adaptive mechanisms of mammals to hypothermia under experimental conditions 2005, candidate of biological sciences Solodovnikova, Olga Grigorievna
Biochemical mechanisms of the antistress effect of α-tocopherol 1999, doctor of biological sciences Saburova, Anna Mukhammadievna
Dissertation introduction (part of the abstract) on the topic "Experimental study of enzyme antioxidant systems during adaptation to prolonged exposure to cold and tocopherol deficiency"
Relevance of the topic. Recent studies have shown that the so-called reactive oxygen species - superoxide and hydroxyl radicals, hydrogen peroxide, and others - play an important role in the mechanisms of adaptation of the organism to environmental factors (Finkel, 1998; Kausalya, Nath, 1998). It has been established that these free-radical oxygen metabolites, which until recently were considered only as damaging agents, are signaling molecules and regulate adaptive transformations of the nervous system, arterial hemodynamics and morphogenesis. (Luscher, Noll, Vanhoute, 1996; Groves, 1999; Wilder, 1998; Drexler, Homig, 1999). The main source of reactive oxygen species is a number of enzymatic systems of the epithelium and endothelium (NADP oxidase, cyclooxygenase, lipoxygenase, xanthine oxidase), which are activated upon stimulation of the chemo and mechanoreceptors located on the luminal membrane of the cells of these tissues.
At the same time, it is known that with an increase in the production and accumulation of reactive oxygen species in the body, that is, under the so-called oxidative stress, their physiological function can be transformed into a pathological one with the development of biopolymer peroxidation and damage to cells and tissues as a result. (Kausalua, Nath, 1998; Smith, Guilbelrt, Yui et al. 1999). Obviously, the possibility of such a transformation is primarily determined by the rate of ROS inactivation by antioxidant systems. In this regard, of particular interest is the study of changes in reactive oxygen species inactivators - enzymatic antioxidant systems of the body, with prolonged exposure to the body of such extreme factors as cold and a deficiency of the vitamin antioxidant - tocopherol, which are currently considered as endo- and exogenous inducers of oxidative stress.
The purpose and objectives of the study. The aim of this work was to study the changes in the main enzyme antioxidant systems during adaptation of rats to prolonged exposure to cold and tocopherol deficiency.
Research objectives:
1. To compare changes in indicators of oxidative homeostasis with changes in the main morphological and functional parameters of the organism of rats and erythrocytes under prolonged exposure to cold.
2. To compare the changes in the indicators of oxidative homeostasis with the changes in the main morphological and functional parameters of the organism of rats and erythrocytes in the presence of tocopherol deficiency.
3. To carry out a comparative analysis of the changes in oxidative metabolism and the nature of the adaptive reaction of the rat organism under prolonged exposure to cold and tocopherol deficiency.
Scientific novelty. It was established for the first time that long-term intermittent exposure to cold (+ 5 ° C for 8 hours a day for 6 months) causes a number of morphological and functional changes in the adaptive orientation in the rat body: acceleration of body weight gain, an increase in the content of spectrin and actin in erythrocyte membranes. , an increase in the activity of key glycolysis enzymes, the concentration of ATP and ADP, as well as the activity of ATP-ases.
It was shown for the first time that oxidative stress plays an important role in the mechanism of development of adaptation to cold, a feature of which is an increase in the activity of the components of the antioxidant system - enzymes of the NADPH-generating pentose phosphate pathway of glucose decomposition, superoxidismutase, catalase and glutathione pyroxidase.
It was shown for the first time that the development of pathological morpho-functional changes in the presence of tocopherol deficiency is associated with pronounced oxidative stress occurring against the background of decreased activity of the main antioxidant enzymes and enzymes of the pentose phosphate pathway of glucose breakdown.
It was established for the first time that the result of metabolic transformations when the body is exposed to environmental factors depends on an adaptive increase in the activity of antioxidant enzymes and the associated severity of oxidative stress.
Scientific and practical significance of the work. The new facts obtained in the work expand the understanding of the mechanisms of adaptation of the organism to the factors of the external environment. The dependence of the result of adaptive metabolic transformations on the degree of activation of the main enzymatic antioxidants was revealed, which indicates the need for a directed development of the adaptive potential of this nonspecific stress-resistance system of the organism when environmental conditions change.
The main provisions for the defense:
1. Prolonged exposure to cold causes a complex of changes in the adaptive orientation in the rats' organism: an increase in resistance to the action of cold, which was expressed in a weakening of hypothermia; acceleration of body weight gain; an increase in the content of spectrin and actin in the membranes of erythrocytes; an increase in the rate of glycolysis, an increase in the concentration of ATP and ADP; an increase in the activity of ATP-ase. The mechanism of these changes is associated with the development of oxidative stress in combination with an adaptive increase in the activity of the components of the antioxidant defense system - the enzymes of the pentose-phosphate shunt, as well as the main intracellular antioxidant enzymes, primarily superoxide dismutase.
2. Long-term deficiency of tocopherol in rats causes a persistent hypotrophic effect, damage to erythrocyte membranes, inhibition of glycolysis, a decrease in the concentration of ATP and ADP, and the activity of cellular ATP-ases. In the mechanism of the development of these changes, insufficient activation of antioxidant systems - NADPH-generating pentose-phosphate pathway and antioxidant enzymes, which creates conditions for the damaging action of reactive oxygen species, is essential.
Approbation of work. The research results were reported at a joint meeting of the Department of Biochemistry and the Department of Normal Physiology of the Altai State Medical Institute (Barnaul, 1998, 2000), at a scientific conference dedicated to the 40th anniversary of the Department of Pharmacology of the Altai State Medical University (Barnaul, 1997), at a scientific and practical conference " Modern problems of balneology and therapy "dedicated to the 55th anniversary of the Barnaulsky sanatorium (Barnaul, 2000), at the II International Conference of Young Scientists of Russia (Moscow, 2001).
Similar dissertations in the specialty "Ecology", 03.00.16 code VAK
Investigation of the role of the glutathione system in natural aging of erythrocytes produced under conditions of normal and intense erythropoiesis 2002, candidate of biological sciences Kudryashov, Alexander Mikhailovich
Indicators of the antioxidant system of erythrocytes in burn injury 1999, candidate of biological sciences Eremina, Tatyana Vladimirovna
Biochemical changes in mammalian membranes during hibernation and hypothermia 2005, Doctor of Biological Sciences Klichkhanov, Nisred Kadirovich
Study of the effect of thioctic acid on free radical homeostasis in rat tissues with pathologies associated with oxidative stress 2007, candidate of biological sciences Makeeva, Anna Vitalievna
Correlation between prooxidant and antioxidant systems in erythrocytes under immobilization stress in rats 2009, candidate of biological sciences Lapteva, Irina Azatovna
Conclusion of the thesis on the topic "Ecology", Skuryatina, Yulia Vladimirovna
1. Prolonged intermittent exposure to cold (+ 5 ° C for 8 hours a day for 6 months) causes a complex of adaptive changes in the rat body: dissipation of the hypothermic reaction to cold, acceleration of body weight gain, increase in the content of spectrin and actin in erythrocyte membranes, glycolysis, an increase in the total concentration of ATP and ADP and the activity of ATP-ases.
2. The state of adaptation of rats to long-term intermittent exposure to cold corresponds to oxidative stress, which is characterized by increased activity of the components of enzyme antioxidant systems - glucose-6-phosphate dehydrogenase, superoxide dismutase, catalase and glutathione peroxidase.
3. Long-term (6 months) nutritional deficiency of tocopherol in rats causes a persistent hypotrophic effect, anemia, damage to erythrocyte membranes, inhibition of glycolysis in erythrocytes, a decrease in the total concentration of ATP and ADP, as well as the activity of Na +, K + - ATP-ase.
4. Dysadaptive changes in rats with tocopherol deficiency are associated with the development of pronounced oxidative stress, which is characterized by a decrease in catalase and glutathione peroxidase activity in combination with a moderate increase in glucose-6-phosphate dehydrogenase and superoxide dismutase activity.
5. The result of metabolic adaptive transformations in response to prolonged exposure to cold and alimentary tocopherol deficiency depends on the severity of oxidative stress, which is largely determined by an increase in the activity of antioxidant enzymes.
CONCLUSION
By now, there is a fairly clear idea that the adaptation of the human and animal organism is determined by the interaction of the genotype with external factors (Meerson, Malyshev, 1981; Panin, 1983; Goldstein, Brown, 1993; Ado, Bochkov, 1994). It should be borne in mind that a genetically determined inadequacy of the inclusion of adaptive mechanisms under the influence of extreme factors can lead to the transformation of the stress state into an acute or chronic pathological process (Kaznacheev, 1980).
The adaptation of the organism to the new conditions of the internal and external environment is based on the mechanisms of urgent and long-term adaptation (Meerson, Malyshev, 1981). At the same time, the process of urgent adaptation, considered as a temporary measure that the body resorts to in critical situations, has been studied in sufficient detail (Davis, 1960, 1963; Isahakyan, 1972; Tkachenko, 1975; Rohlfs, Daniel, Premont et al., 1995; Beattie, Black, Wood et al. 1996; Marmonier, Duchamp, Cohen-Adad et al., 1997). During this period, the increased production of various signaling factors, including hormonal ones, induces a significant local and systemic rearrangement of metabolism in various organs and tissues, which ultimately determines a true, long-term adaptation (Hochachka and Somero, 1988). The activation of biosynthesis processes at the level of replication and transcription causes the developing structural changes, which are manifested by hypertrophy and hyperplasia of cells and organs (Meerson, 1986). Therefore, the study of the biochemical foundations of adaptation to long-term exposure to disturbing factors is not only of scientific but also of great practical interest, especially from the point of view of the prevalence of dysadaptive diseases (Lopez-Torres et al., 1993; Pipkin, 1995; Wallace, Bell, 1995; Sun et al., 1996).
There is no doubt that the development of long-term adaptation of the organism is a very complex process, which is realized with the participation of the entire complex of hierarchically organized metabolic regulation system, and many aspects of the mechanism of this regulation remain unknown. According to the latest literature data, the adaptation of an organism to long-term disturbing factors begins with local and systemic activation of the phylogenetically most ancient process of free radical oxidation, leading to the formation of physiologically important signaling molecules in the form of reactive oxygen and nitrogen species - nitric oxide, superoxide and hydroxyl radical, hydrogen peroxide, etc. These metabolites play a leading mediator role in the adaptive local and systemic regulation of metabolism by autocrine and paracrine mechanisms (Sundaresan, Yu, Ferrans et. al., 1995; Finkel, 1998; Givertz, Colucci, 1998).
In this regard, in the study of the physiological and pathophysiological aspects of adaptive and dysadaptive reactions, the issues of regulation by free-radical metabolites are occupied, and the issues of biochemical mechanisms of adaptation during long-term exposure to the body of inducers of oxidative stress are of particular relevance (Cowan, Langille, 1996; Kemeny, Peakman, 1998; Farrace, Cenni, Tuozzi et al., 1999).
Undoubtedly, the greatest information in this regard can be obtained in experimental studies on the appropriate "models" of common types of oxidative stress. As such, the most well-known models of exogenous oxidative stress caused by cold exposure and endogenous oxidative stress arising from a deficiency of vitamin E, one of the most important membrane antioxidants. These models were used in this work to elucidate the biochemical basis of the body's adaptation to prolonged oxidative stress.
In accordance with numerous literature data (Spirichev, Matusis, Bronstein, 1979; Aloia, Raison, 1989; Glofcheski, Borrelli, Stafford, Kruuv, 1993; Beattie, Black, Wood, Trayhurn, 1996), we have established that the daily 8-hour Cold exposure for 24 weeks led to a pronounced increase in the concentration of malonyldialdehyde in erythrocytes. This indicates the development of chronic oxidative stress under the influence of cold. Similar changes took place in the body of rats kept for the same period on a diet devoid of vitamin E. This fact also corresponds to the observations of other researchers (Masugi,
Nakamura, 1976; Tamai., Miki, Mino, 1986; Archipenko, Konovalova, Japaridze et al., 1988; Matsuo, Gomi, Dooley, 1992; Cai, Chen, Zhu et al., 1994). However, the causes of oxidative stress during prolonged intermittent exposure to cold and oxidative stress during prolonged tocopherol deficiency are different. If in the first case, the cause of the stress state is the effect of an external factor - cold, which causes an increase in the production of oxiradicals due to the induction of the synthesis of uncoupling protein in mitochondria (Nohl, 1994; Bhaumik, Srivastava, Selvamurthy et al., 1995; Rohlfs, Daniel, Premont et al. ., 1995; Beattie, Black, Wood et. Al., 1996; Femandez-Checa, Kaplowitz, Garcia-Ruiz et al., 1997; Marmonier, Duchamp, Cohen-Adad et al., 1997; Rauen, de Groot, 1998 ), then with a deficiency of the membrane antioxidant tocopherol, oxidative stress was caused by a decrease in the rate of neutralization of oxyradical mediators (Lawler, Cline, Ni, Coast, 1997; Richter, 1997; Polyak, Xia, Zweier et al., 1997; Sen, Atalay, Agren et al., 1997; Higashi, Sasaki, Sasaki et al., 1999). Considering the fact that prolonged exposure to cold and vitamin deficiency E cause the accumulation of reactive oxygen species, one could expect the transformation of the physiological regulatory role of the latter into a pathological one, with cell damage due to peroxidation of biopolymers. In connection with the generally accepted until recently concept of the damaging effect of reactive oxygen species, cold and tocopherol deficiency are considered as factors provoking the development of many chronic diseases (Cadenas, Rojas, Perez-Campo et al., 1995; de Gritz, 1995; Jain, Wise , 1995; Luoma, Nayha, Sikkila, Hassi., 1995; Barja, Cadenas, Rojas et al., 1996; Dutta-Roy, 1996; Jacob, Burri, 1996; Snircova, Kucharska, Herichova et al., 1996; Va- Squezvivar, Santos, Junqueira, 1996; Cooke, Dzau, 1997; Lauren, Chaudhuri, 1997; Davidge, Ojimba, Mc Laughlin, 1998; Kemeny, Peakman, 1998; Peng, Kimura, Fregly, Phillips, 1998; Nath, Grande, Croatt et al., 1998; Newaz, Nawal, 1998; Taylor, 1998). Obviously, in the light of the concept of the mediator role of reactive oxygen species, the realization of the possibility of transforming physiological oxidative stress into pathological one largely depends on the adaptive increase in the activity of antioxidant enzymes. In accordance with the concept of the enzyme antioxidant complex as a functionally dynamic system, there is a recently revealed phenomenon of substrate induction of gene expression of all three main antioxidant enzymes - superoxide dismutase, catalase, and glutathione peroxidase (Peskin, 1997; Tate, Miceli, Newsome, 1995; Pinkus, Weiner Daniel, 1996; Watson, Palmer. , Jauniaux et al., 1997; Sugino, Hirosawa-Takamori, Zhong, 1998). It is important to note that the effect of such induction has a rather long lag period, measured in tens of hours and even days (Beattie, Black, Wood, Trayhurn, 1996; Battersby, Moyes, 1998; Lin, Coughlin, Pilch, 1998). Therefore, this phenomenon is capable of accelerating the inactivation of reactive oxygen species only with prolonged exposure to stress factors.
The studies carried out in the work showed that long-term intermittent exposure to cold caused a harmonious activation of all studied antioxidant enzymes. This is consistent with the opinion of Bhaumik G. et al (1995) about the protective role of these enzymes in limiting complications during prolonged cold stress.
At the same time, in the erythrocytes of rats with a deficiency of vitamin E, at the end of the 24-week observation period, only superoxidismutase was activated. It should be noted that such an effect was not observed in previous similar studies (Xu, Diplock, 1983; Chow, 1992; Matsuo, Gomi, Dooley, 1992; Walsh, Kennedy, Goodall, Kennedy, 1993; Cai, Chen, Zhu et al. , 1994; Tiidus, Houston, 1994; Ashour, Salem, El Gadban et al., 1999). However, it should be noted that the increase in the activity of superoxide dismutase was not accompanied by an adequate increase in the activity of catalase and glutathione peroxidase and did not prevent the development of the damaging effect of reactive oxygen species. The latter was evidenced by a significant accumulation in erythrocytes of the product of lipid peroxidation - malonidialdehyde. It should be noted that peroxidation of biopolymers is currently considered the main cause of pathological changes in vitamin E deficiency (Chow, Ibrahim, Wei and Chan, 1999).
The effectiveness of antioxidant protection in experiments on the study of cold exposure was evidenced by the absence of pronounced changes in hematological parameters and the preservation of the resistance of erythrocytes to the action of various hemolytics. Similar results were previously reported by other researchers (Marachev, 1979; Rapoport, 1979; Sun, Cade, Katovich, Fregly, 1999). On the contrary, in animals with E-avitaminosis, a complex of changes was observed that indicated the damaging effect of reactive oxygen species: anemia with symptoms of intravascular hemolysis, the appearance of erythrocytes with reduced resistance to hemolytics. The latter is considered a very characteristic manifestation of oxidative stress in E-avitamnosis (Brin, Horn, Barker, 1974; Gross, Landaw, Oski, 1977; Machlin, Filipski, Nelson et al., 1977; Siddons, Mills, 1981; Wang, Huang, Chow, 1996). The foregoing convinces of the body's significant capabilities to neutralize the effects of oxidative stress of external genesis, in particular, caused by cold, and the inadequacy of adaptation to endogenous oxidative stress in the case of E-avitaminosis.
The system for generating NADPH, which is a cofactor of heme oxygenase, glutathione reductase and thioredoxin reductase, which reduce iron, glutathione and other thio compounds, also belongs to the group of antioxidant factors in erythrocytes. In our experiments, a very significant increase in the activity of glucose-6-phosphate dehydrogenase in rat erythrocytes was observed both under the action of cold and with a deficiency of tocopherol, which was previously observed by other researchers (Kaznacheev, 1977; Ulasevich, Grozina, 1978;
Gonpern, 1979; Kulikov, Lyakhovich, 1980; Landyshev, 1980; Fudge, Stevens, Ballantyne, 1997). This indicates the activation in experimental animals of the pentose phosphate shunt, in which NADPH is synthesized.
The mechanism of development of the observed effect becomes much clearer when analyzing changes in the parameters of carbohydrate metabolism. An increase in the absorption of glucose by the erythrocytes of animals was observed both against the background of oxidative stress caused by cold and during oxidative stress induced by tocopherol deficiency. This was accompanied by a significant activation of membrane hexokinase, the first enzyme for the intracellular utilization of carbohydrates, which is in good agreement with the data of other researchers (Lyakh, 1974, 1975; Panin, 1978; Ulasevich and Grozina, 1978; Nakamura, Moriya, Murakoshi. Et al., 1997; Rodnick , Sidell, 1997). However, further transformations of glucose-6-phosphate, which is intensively formed in these cases, differed significantly. Upon adaptation to cold, the metabolism of this intermediate increased both in glycolysis (as evidenced by an increase in the activity of hexophosphate isomerase and aldolase) and in the pentose phosphate pathway. The latter was confirmed by an increase in the activity of glucose-6-phosphate dehydrogenase. At the same time, in E-avitaminosis animals, the rearrangement of carbohydrate metabolism was associated with an increase in the activity of only glucose-6-phosphate dehydrogenase, while the activity of key glycolysis enzymes did not change or even decreased. Consequently, in any case, oxidative stress causes an increase in the rate of glucose metabolism in the pentose phosphate shunt, which provides the synthesis of NADPH. This seems to be very expedient in conditions of an increase in the demand of cells for redox equivalents, in particular, NADPH. It can be assumed that in E-avitaminosis animals this phenomenon develops to the detriment of glycolytic energy-producing processes.
The noted difference in the effects of exogenous and endogenous oxidative stress on glycolytic energy production also affected the energy status of cells, as well as energy consumption systems. Under cold exposure, a significant increase in the concentration of ATP + ADP was observed with a decrease in the concentration of inorganic phosphate, an increase in the activity of total ATP-ase, Mg ^ -ATP-ase and Na +, K + -ATP-ase. On the contrary, in the erythrocytes of rats with E-avitaminosis, a decrease in the content of macroergs and the activity of ATPases was observed. At the same time, the calculated ATP + ADP / Fn index confirmed the available information that for cold, but not for E-avitaminous oxidative stress, the prevalence of energy production over energy consumption is characteristic (Marachev, Sorokovoy, Korchev et al., 1983; Rodnick, Sidell, 1997; Hardewig, Van Dijk, Portner, 1998).
Thus, with prolonged intermittent exposure to cold, the restructuring of the processes of energy production and energy consumption in the body of animals had a clear anabolic character. This is evidenced by the observed acceleration of the increase in body weight of animals. The disappearance of the hypothermic reaction to cold in rats by the 8th week of the experiment indicates a stable adaptation of their body to cold and, consequently, the adequacy of adaptive metabolic transformations. At the same time, judging by the main morphofunctional, hematological and biochemical parameters, changes in energy metabolism in E-avitaminosis rats did not lead to an adaptively expedient result. It seems that the main reason for such an organism's response to tocopherol deficiency is the outflow of glucose from energy-producing processes into the formation of the endogenous antioxidant NADPH. Probably, the severity of adaptive oxidative stress is a kind of regulator of glucose metabolism in the body: this factor is able to turn on and enhance the production of antioxidants during glucose metabolism, which is more significant for the body's survival under the powerful damaging effect of reactive oxygen species than the production of macroergs.
It should be noted that, according to modern data, oxygen radicals are inducers of the synthesis of individual replication and transcription factors that stimulate adaptive proliferation and differentiation of cells of various organs and tissues (Agani, Semenza, 1998). In this case, one of the most important targets for free radical mediators are transcription factors of the NFkB type, which induce the expression of genes for antioxidant enzymes and other adaptive proteins (Sundaresan, Yu, Ferrans et. Al, 1995; Finkel, 1998; Givertz, Colucci, 1998). Thus, one can think that it is this mechanism that is triggered by cold-induced oxidative stress and provides an increase in the activity of not only specific enzymes of antioxidant protection (superoxide dismutase, catalase, and glutathione peroxidase), but also an increase in the activity of enzymes of the pentose phosphate pathway. With more pronounced oxidative stress caused by a deficiency of the membrane antioxidant - tocopherol, the adaptive substrate inducibility of these components of the antioxidant defense is realized only partially and, most likely, insufficiently effective. It should be noted that the low efficiency of this system ultimately led to the transformation of physiological oxidative stress into pathological one.
The data obtained in this work allow us to conclude that the result of adaptive metabolic transformations in response to disturbing environmental factors, in the development of which reactive oxygen species are involved, is largely determined by the adequacy of the associated increase in the activity of the main antioxidant enzymes, as well as enzymes of the NADPH-generating pentose phosphate pathway. breakdown of glucose. In this regard, when the conditions for the existence of a macroorganism change, especially in so-called environmental disasters, the severity of oxidative stress and the activity of enzymatic antioxidants should become not only an object of observation, but also one of the criteria for the effectiveness of adaptation of the organism.
List of dissertation research literature candidate of biological sciences Skuryatina, Yulia Vladimirovna, 2001
1. Abrarov A.A. The effect of fat and fat-soluble vitamins A, D, E on the biological properties of erythrocytes: Diss. doct. honey. sciences. M., 1971.- S. 379.
2. Ado AD, Ado NA, Bochkov GV Pathological physiology.- Tomsk: Publishing house of TSU, 1994.- P. 19.
3. Asatiani VS Enzymatic methods of analysis. Moscow: Nauka, 1969 .-- 740 p.
4. Benisovich VI, Idelson LI The formation of peroxides and the composition of fatty acids in the lipids of erythrocytes in patients with Markiafava Mikeli's disease // Probl. hematol. and blood transfusion. - 1973. - No. 11. - S. 3-11.
5. Bobyrev VN, Voskresenskiy ON Changes in the activity of antioxidant enzymes in lipid peroxidation syndrome in rabbits // Vopr. honey. chemistry. 1982. - vol. 28 (2). - S. 75-78.
6. Viru A. A. Hormonal mechanisms of adaptation and training. Moscow: Nauka, 1981, pp. 155.
7. Goldstein DL, Brown MS Genetic aspects of diseases // Internal diseases / Under. ed. E. Braunwald, K. D. Isselbacher, R. G. Petersdorf and others - M .: Medicine, 1993. - T. 2. - S. 135.
8. Datsenko 3. M., Donchenko G. V., Shakhman O. V., Gubchenko K. M., Khmel T. O. The role of phospholipids in the functioning of various cell membranes in conditions of violation of the antioxidant system // Ukr. biochem. J.- 1996.- t. 68 (1) .- S. 49-54.
9. Yu. Degtyarev VM, Grigoriev GP Automatic recording of acidic erythrograms on the EFA-1 densitometer // Lab. case.- 1965.- No. 9.- S. 530-533.
10. P. Derviz GV, Byalko NK Refinement of the method for determining hemoglobin dissolved in blood plasma // Lab. case.- 1966.- No. 8.- S. 461-464.
11. Deryapa NR, Ryabinin IF Human adaptation in the polar regions of the Earth.- L .: Medicine, 1977.- P. 296.
12. Dzhumaniyazova KR Influence of vitamins A, D, E on erythrocytes of peripheral blood: Diss. Cand. honey. Sciences. - Tashkent, 1970. - P. 134.
13. Donchenko GV, Metalnikova NP, Palivoda OM et al. Regulation of a-tocopherol and actinomycin D biosynthesis of ubiquinone and protein in rat liver with E-hypovitaminosis // Ukr. biochem. J.- 1981.- T. 53 (5) .- S. 69-72.
14. Dubinina EE, Salnikova LA, Efimova LF Activity and isoenzyme spectrum of erythrocyte and blood plasma superoxide dismutase // Lab. delo.- 1983.-№10.-p. 30-33.
15. Isahakyan JI. A. Metabolic structure of temperature adaptations D .: Nauka, 1972.-S. 136.
16. Kaznacheev VP Biosystem and adaptation // Report at the II session of the Scientific Council of the Academy of Sciences of the USSR on the problem of applied human physiology. Novosibirsk, 1973, p. 74.
17. Kaznacheev VP Problems of human adaptation (results and prospects) // 2 All-Union. conf. to adapt a person to different. geographic, climatic, and production conditions: Abstracts. report - Novosibirsk, 1977. - t. 1 - S. 3-11.
18. Kaznacheev VP Modern aspects of adaptation.- Novosibirsk: Science, 1980.-P. 191.
19. Kalashnikov Yu. K., Geisler BV On the method of determining blood hemoglobin using acetone cyanohydrin // Lab. case.- 1975.- No. 6.- SG373-374.
20. Kandror IS Essays on human physiology and hygiene in the Far North.- M .: Medicine, 1968.- P. 288.
21. Kashevnik L. D. Metabolism in vitamin deficiency S. - Tomsk., 1955. - P. 76.
22. Korovkin B. F. Enzymes in the diagnosis of myocardial infarction.- L: Nauka, 1965.- P. 33.
23. Kulikov V. Yu., Lyakhovich VV Reactions of free radical oxidation of lipids and some indicators of oxygen metabolism // Mechanisms of human adaptation in conditions of high latitudes / Ed. V.P. Kaznacheeva.- L .: Medicine, 1980.- S. 60-86.
24. Landyshev SS Adaptation of erythrocyte metabolism to the action of low temperatures and respiratory failure // Adaptation of humans and animals in different climatic zones / Ed. M. 3. Zhits.- Chita, 1980.- S. 51-53.
25. Lankin V. 3., Gurevich S. M., Koshelevtseva N. P. The role of lipid peroxides in the pathogenesis of atherosclerosis. Detoxification of lipoperoxides by the glutathione peroxidase system in the aorta // Vopr. honey. chemistry. - 1976. - No. 3, - S. 392-395.
26. Lyakh LA On the stages of adaptation to cold formation // Theoretical and practical problems of the effect of low temperatures on the body: Abstracts. IV All-Union. Conf. - 1975. - S. 117-118.
27. Marachev A. G., Sorokova V. I., Korchev A. V. et al. Bioenergetics of erythrocytes in the inhabitants of the North // Human Physiology. 1983. No. 3. P. 407-415.
28. Marachev A.G. The structure and function of human erythron in the North // Biological problems of the North. VII symposium. Human adaptation to the conditions of the North / Ed. V.F. Burkhanova, N.R. Deryapy.- Kirovsk, 1979.- S. 7173.
29. Matus I. I. Functional relationship of vitamins E and K in the metabolism of animals // Vitamins.- Kiev: Naukova Dumka, 1975.- t. 8.-S. 71-79.
30. Meerson F. 3., Malyshev Yu. I. The phenomenon of adaptation and stabilization of structures and protection of the heart.- M: Medicine, 1981.- P. 158.
31. Meerson F. 3. Basic laws of individual adaptation // Physiology of adaptation processes. Moscow: Nauka, 1986, pp. 10-76.
32. Panin JI. E. Some biochemical problems of adaptation // Medical and biological aspects of adaptation processes / Ed. JI. P. Nepomnyashikh.-Novosibirsk: Nauka.-1975a.-S. 34-45.
33. Panin LE The role of hormones of the pituitary adrenal system and pancreas in the violation of cholesterol metabolism in some extreme conditions: Diss. doct. honey. Sciences. - M., 19756. - P. 368.
34. Panin L. E. Energy aspects of adaptation.- Leningrad: Medicine, 1978.- 192 p. 43. Panin L. E. Features of energy metabolism // Mechanisms of human adaptation to conditions of high latitudes / Ed. V.P. Kaznacheeva.- L .: Medicine, 1980.- S. 98-108.
35. Peskin A. V. Interaction of active oxygen with DNA (Review) // Biochemistry. 1997. T. 62. No. 12. S. 1571-1578.
36. Poberezkina NB, Khmelevsky Yu. V. Disruption of the structure and function of erythrocyte membranes E in avitaminosis rats and its correction with antioxidants // Ukr. biochem. J.- 1990.- t. 62 (6) .- S. 105-108.
37. Pokrovsky A. A., Orlova T. A., Pozdnyakov A. JL Influence of tocopherol deficiency on the activity of some enzymes and their isoenzymes in the testes of rats // Vitamins and reactivity of the organism: Proceedings of MOIP.- M., 1978.-T. 54.- S. 102-111.
38. Rapoport J. J. Adaptation of a child in the North.- L .: Medicine, 1979.- P. 191.
39. Rossomakhin Yu. I. Features of thermoregulation and resistance of the body to the contrasting effects of heat and cold in different modes of temperature adaptations: Author's abstract. diss. Cand. biol. Sciences. - Donetsk, 1974. - S. 28.
40. Seitz IF On the quantitative determination of adenosine and adenosine diphosphates // Byull. exp. biol. and medical - 1957. - No. 2. - S. 119-122.
41. Sen, IP Development of E-vitamin deficiency in white rats when fed with qualitatively different fats: Diss. Cand. honey. Sciences. - M., 1966. - S. 244.
42. Slonim AD About physiological mechanisms of natural adaptations of animals and humans // Dokl. for the year. meeting Academic Council dedicated. in memory of acad. K.M.Bykova.- JL, 1964.
43. Slonim AD Physiological adaptations and the peripheral structure of the body's reflex responses // Physiological adaptations to heat and cold / Ed. A. D. Slonim.- JL: Nauka, 1969.- S. 5-19.
44. Spirichev VB, Matusis II, Bronstein JL M. Vitamin E. // In the book: Experimental vitaminology / Ed. Yu.M. Ostrovsky.- Minsk: Science and technology, 1979.- S. 18-57.
45. Stabrovsky EM Energy metabolism of carbohydrates and its endocrine regulation under the influence of low environmental temperature on the body: Avto-ref. diss. doct. biol. Sciences.- JL, 1975.- P. 44.
46. Warm D. JL, Ibragimov F. Kh. Changes in the permeability of erythrocyte membranes in rodents under the influence of fish oil, vitamin E and fatty acids // J. Evolution. Biochemistry and Physiology, 1975, vol. 11 (1), pp. 58-64.
47. Terskov I. A., Gitelzon I. I. Erythrograms as a method of clinical blood research.- Krasnoyarsk, 1959.- P. 247.
48. Terskov I. A., Gitelzon I. I. The value of dispersion methods for the analysis of erythrocytes in health and disease // Issues of biophysics, biochemistry and pathology of erythrocytes.- Moscow: Nauka, 1967.- pp. 41-48.
49. Tkachenko E. Ya. About the ratio of contractile and non-contractile thermogenesis in the body during adaptation to cold // Physiological adaptations to cold, mountain and subarctic conditions / Ed. K. P. Ivanova, A. D. Slonim.-Novosibirsk: Nauka, 1975.- pp. 6-9.
50. Uzbekov GA, Uzbekov MG Highly sensitive micromethod of photometric determination of phosphorus // Lab. case.- 1964.- No. 6.- S. 349-352.
51. Hochachka P., Somero J. Biochemical adaptation: trans. from English M .: Mir, 1988.-576 p.
52. Shcheglova AI Adaptive changes in gas exchange in rodents with different ecological specialization // Physiological adaptations to heat and cold / Ed. A.D. Slonim.- Leningrad: Nauka, 1969.- pp. 57-69.
53. Yakusheva I. Ya., Orlova LI Method for the determination of adenosine triphosphatases in hemolysates of blood erythrocytes // Lab. delo.- 1970.- No. 8.- S. 497-501.
54. Agani F., Semenza G. L. Mersalyl is a novel inducer of vascular endothelial growth factor gene expression and hypoxia-inducible factor 1 activity // Mol. Pharmacol. 1998. Vol. 54 (5) .- P. 749-754.
55. Ahuja B. S., Nath R. A kinetik study of superoxide dismutase in normal human erytrocytes and its possible role in anemia and radiation damage // Simpos. on control mechanisms in cell, processes, Bombey, 1973, P. 531-544.
56. Aloia R. C., Raison J. K. Membrane function in mammalian hibernation // Bio-chim. Biophys. Acta. 1989. Vol. 988.- P. 123-146.
57. Asfour R. Y., Firzli S. Hematologic stadies in undernowrished children with low serum vitamin E levels // Amer. J. Clin. Nutr. 1965. Vol. 17 (3) .- P. 158-163.
58. Ashour M. N., Salem S. I., El Gadban H. M., Elwan N. M., Basu T. K. Antioxidant status in children with protein-energy malnutrition (PEM) living in Cairo, Egypt // Eur. J. Clin. Nutr.- 1999.- Vol. 53 (8) .- P. 669-673.
59. Bang H. O., Dierberg J., Nielsen A. B. Plasma lipid and lipoprotein pattern in Greenlandic west coast Eskimos // Lancet. 1971. Vol. 7710 (1). - P. 1143-1145.
60. Barja G., Cadenas S., Rojas C., et al. Effect of dietary vitamin E levels on fatty acid profiles and nonenzymatic lipid peroxidation in the guinea pig liver // Lipids.-1996.- Vol. 31 (9) .- P. 963-970.
61. Barker M. O., Brin M. Mechanisms of lipid peroxidation in erithrocytes of vitamin E deficients rats and in phospholipid model sistems // Arch. Biochem. and Biophys. 1975. Vol. 166 (1) .- P. 32-40.
62. Battersby B. J., Moyes C. D. Influence of acclimation temperature on mitochondrial dna, rna and enzymes in skeletal muscle // APStracts. 1998 Vol. 5.- P. 195.
63. Beattie J. H., Black D. J., Wood A. M., Trayhurn P. Cold-induced expression of the metallothionein-1 gene in brown adipose tissue of rats // Am. J. Physiol. 1996. Vol. 270 (5) .- Pt 2.- P. 971-977.
64. Bhaumik G., Srivastava K. K., Selvamurthy W., Purkayastha S. S. The role of free radicals in cold injuries // Int. J. Biometeorol. 1995. Vol. 38 (4) .- P. 171-175.
65. Brin M., Horn L. R., Barker M. O. Relationship between fatty acid composition oferithrocytes and susceptibility to vitamin E deficiency // Amer. J. Clin. Nutr. -% 1974. - Vol. 27 (9) .- P. 945-950.
66. Caasi P. I., Hauswirt J. W., Nair P. P. Biosynthesis of heme in vitamin E deficiency // Ann. N. Y. Acad. Sci. 1972. Vol. 203.- P. 93-100.
67. Cadenas S., Rojas C., Perez-Campo R., Lopez-Torres M., Barja G. Vitamin E protects guinea pig liver from lipid peroxidation without depressing levels of antioxidants // Int. J. Biochem. Cell. Biol. 1995. Vol. 27 (11) .- P. 1175-1181.
68. Cai Q. Y., Chen X. S., Zhu L. Z., et al. Biochemical and morphological changes in the lenses of selenium and / or vitamin E deficient rats // Biomed. Environ. Sci. 1994. Vol. 7 (2) .- P. 109-115.
69. Cannon R. O. Role of nitric oxide in cardiovascular disease: focus on the endothelium // Clin. Chem. 1998 Vol. 44.- P. 1809-1819.
70. Chaudiere J., Clement M., Gerard D., Bourre J. M. Brain alterations induced by vitamin E deficiency and intoxication with methyl ethyl ketone peroxide // Neuro-toxicology. 1988. Vol. 9 (2) .- P. 173-179.
71. Chow C. K. Distribution of tocopherols in human plasma and red blood cells // Amer. J. Clin. Nutr. 1975. Vol. 28 (7) .- P. 756-760.
72. Chow S. K. Oxidative damage in the red cells of vitamin E-deficient rats // Free. Radic. Res. Commun. 1992 vol. 16 (4) .- P. 247-258.
73. Chow C. K., Ibrahim W., Wei Z., Chan A. C. Vitamin E regulates mitochondrial hydrogen peroxide generation // Free Radic. Biol. Med. 1999. Vol. 27 (5-6) .- P. 580-587.
74. Combs G. F. Influences of dietary vitamin E and selenium on the oxidant defense system of the chick // Poult. Sci. 1981. Vol. 60 (9) .- P. 2098-2105.
75. Cooke J. P., Dzau V. J. Nitric oxide synthase: Role in the Genesis of Vascular Disease // Ann. Rev. Med. 1997. Vol. 48.- P. 489-509.
76. Cowan D. B., Langille B. L. Cellular and molecular biology of vascular remodeling // Current Opinion in Lipidology. 1996 Vol. 7.- P. 94-100.
77. Das KC, Lewis-Molock Y., White C W. Elevation of manganese superoxide dismutase gene expression by thioredoxin // Am. J. Respir. Cell Mol. Biol. 1997 Vol. 17 (6) .- P. 12713-12726.
78. Davidge S. T., Ojimba J., McLaughlin M. K. Vascular Function in the Vitamin E Deprived Rat. An Interaction Between Nitric Oxide and Superoxide Anions // Hypertension. 1998 Vol. 31.- P. 830-835.
79. Davis T. R. A. Shivering and nonshivering heat production in animals and man // Cold Injury: Ed. S. H. Horvath. N. Y. I960 P. 223-269.
80. Davis, T. R. A. Nonshivering thermogenesis, Feder. Proc.- 1963.- Vol. 22 (3) .- P. 777-782.
81. Depocas F. Calorigenesis from various organ systems in the whole animal // Feder. Proc.- I960.-Vol. 19 (2) .- P. 19-24.
82. Desaultes M., Zaror-Behrens G., Hims-Hagen J. Increased purine nucleotide binding, altered polipeptide composition and thermogenesis in brown adipose tissue mitochondria of cold-acclimated rats // Can. J. Biochem. - 1978. - Vol. 78 (6) .- P. 378-383.
83. Drexler H., Hornig B. Endothelial dysfunction in human disease // J. Mol. Cell. Cardiol. 1999 Vol. 31 (1) .- P. 51-60.
84. Dutta-Roy A. K. Therapy and clinical trials // Current Opinion in Lipidology.-1996.-Vol. 7.-P. 34-37.
85. Elmadfa I., Both-Bedenbender N., Sierakowski B., Steinhagen-Thiessen E. Significance of vitamin E in aging // Z. Gerontol. - 1986. - Vol. 19 (3) .- P. 206-214.
86. Farrace S., Cenni P., Tuozzi G., et al. Endocrine and psychophysiological aspects of human adaptation to the extreme // Physiol. Behav. - 1999. - Vol. 66 (4). - P. 613-620.
87. Fernandez-Checa, J. C., Kaplowitz N., Garcia-Ruiz C., et al. Importance and characteristics of glutahione transport in mitochondria: defense against TNF-induced oxidative stress and defect induced by alcohol // APStracts.- 1997.-Vol.4.- P. 0073G.
88. Finkel T. Oxygen radicals and signaling // Current Opinion in Cell Biology. 1998. Vol. 10.-P. 248-253.
89. Photobiol. 1993. Vol. 58 (2) .- P. 304-312.
90. Fudge D. S., Stevens E. D., Ballantyne J. S. Enzyme adaptation along a hetero-thermic tissue the visceral retia mirabilia of the bluefin tuna // APStracts. 1997 Vol. 4, - P. 0059R.
91. Givertz M. M., Colucci W. S. New targets for heart-failure therapy: endothelin, inflammatory cytokines, and oxidative stress // Lancet. - 1998. - Vol. 352- Suppl 1.-P. 34-38.
92. Glofcheski D. J., Borrelli M. J., Stafford D. M., Kruuv J. Induction of tolerance to hypothermia and hyperthermia by a common mechanism in mammalian cells // J. Cell. Physiol. 1993 Vol. 156.- P. 104-111.
93. Chemical Biology. 1999. Vol. 3.- P. 226-235.1 ll. Guarnieri C., Flamigni F., Caldarera R. C :, Ferrari R. Myocardial mitochondrial functions in alpha-tocopherol-deficient and -refed rabbits // Adv. Myocardiol. 1982. Vol. 3 P. 621-627.
94. Hardewig I., Van Dijk P. L. M., Portner H. O. High energy turnover at low temperatures: recovery from exhaustive exercise in antarctic and temperate eelpouts (zoarcidae) // APStracts. 1998 Vol. 5.- P. 0083R.
95. Hassan H., Hashins A., van Italie T. B., Sebrell W. H. Syndrom in premature infants anemia associated with low plasma vitamin E level and high poliunsaturated fatty acid diet // Amer. J. Clin. Nutr.-1966.-Vol. 19 (3) .- P. 147-153.
96. Hauswirth G. W., Nair P. P. Some aspects of vitamine E in expression of biological information // Ann. N. Y. Acad. Sci. 1972. Vol. 203.- P. 111-122.
97. Henle E. S., Linn S. Formation, prevention, and repair of DNA damage by iron / hydrogen peroxide // J. Biol, chem. 1997. Vol. 272 (31). - P. 19095-19098.
98. Higashi Y., Sasaki S., Sasaki N., et al. Daily aerobic exercise improves reactive hyperemia in patients with essential hypertension // Hypertension. 1999 Vol. 33 (1) .- Pt 2.-P. 591-597.
99. Howarth P. H Pathogenic mechanisms: a rational basis for treatment // B. M. J.-1998.-Vol. 316.-P. 758-761.
100. Hubbell R. B., Mendel L. B., Wakeman A. J. A new salt mixture for use in experimental diets // J. Nutr. 1937 Vol. 14.- P. 273-285.
101. Jacob R. A., Burri B. J. Oxidative damage and defense // Am. J. Clin. Nutr.-1996.-Vol. 63.- P. 985S-990S.
102. Jain S. K., Wise R. Relationship between elevated lipid peroxides, vitamin E deficiency and hypertension in preeclampsia // Mol. Cell. Biochem. 1995 Vol. 151 (1) .- P. 33-38.
103. Karel P., Palkovits M., Yadid G., et al. Heterogeneous neurochemical responses to different stressors: a test of selye "s doctrine of nonspecificity // APStracts.-1998.-Vol. 5.-P. 0221R.
104. Kausalya S., Nath J. Interactive role of nitric oxide and superoxide anion in neu-trophil-mediated endothelial cell in injury // J. Leukoc. Biol. 1998. Vol. 64 (2) .- P. 185-191.
105. Kemeny M., Peakman M. Immunology // B. M. J. - 1998. - Vol. 316.- P. 600-603.
106. Kozyreva T. V., Tkachenko E. Y., Kozaruk V. P., Latysheva T. V., Gilinsky M. A. The effects of slow and rapid cooling on catecholamine concentration in arterial plasma and the skin // APStracts. 1999. Vol. 6.- P. 0081R.
107. Lauren N., Chaudhuri G. Estrogens and atherosclerosis // Ann. Rev. Pharmacol. Toxicol. 1997 Vol. 37.- P. 477-515.
108. Lawler J. M., Cline C. C., Hu Z., Coast J. R. Effect of oxidative stress and acidosis on diaphragm contractile function // Am. J. Physiol. 1997 Vol. 273 (2) .- Pt 2.-P. 630-636.
109. Lin B., Coughlin S., Pilch P. F. Bi-directional regulation of uncoupling protein-3 and glut4 mrna in skeletal muscle by cold // APStracts. 1998 Vol. 5.- P. 0115E.
110. Lindquist J. M., Rehnmark S. Ambient temperature regulation of apoptosis in brown adipose tissue // J. Biol. Chem. 1998 Vol. 273 (46) .- P. 30147-30156.
111. Lowry O. H., Rosenbrough N. G., Farr A. L., Randell R. I. Protein measurement with the Folin phenol reagent // J. Biol. Chem. -195L-Vol. 193.- P. 265-275.
112. Luoma P. V., Nayha S., Sikkila K., Hassi J. High serum alpha-tocopherol, albumin, selenium and cholesterol, and low mortality from coronary heart disease in northern Finland // J. Intern. Med. 1995.-Vol. 237 (1) .- P. 49-54.
113. Luscher T. F., Noll G., Vanhoutte P. M. Endothelial dysfunction in hypertension // J. Hypertens. - 1996. - Vol. 14 (5) .- P. 383-393.
114. Machlin L. J., Filipski R., Nelson J., Horn L. R., Brin M. Effect of prolonged vitamin E deficiency in the rat // J. Nutr. 1977. Vol. 107 (7) .- P. 1200-1208.
115. Marmonier F., Duchamp C., Cohen-Adad F., Eldershaw T. P. D., Barra H. Hormonal control of thermogenesis in perfused muscle of muscovy ducklings // AP-Stracts. 1997. Vol. 4.- P. 0286R.
116. Marvin H. N. Erithrocyte survival of rat deficient in vitamin E or vitamin B6 // J. Nutr. - 1963.-Vol. 80 (2) .- P. 185-190.
117. Masugi F., Nakamura T. Effect of vitamin E deficiency on the level of superoxide dismutase, glutathione peroxidase, catalase and lipid peroxide in rat liver // Int. J. Vitam. Nutr. Res. - 1976. - Vol. 46 (2) .- P. 187-191.
118. Matsuo M., Gomi F., Dooley M. M. Age-related alterations in antioxidant capacity and lipid peroxidation in brain, liver, and lung homogenates of normal and vitamin E-deficient rats // Mech. Ageing Dev. 1992 Vol. 64 (3) .- P. 273-292.
119. Mazor D., Brill G., Shorer Z., Moses S., Meyerstein N. Oxidative damage in red blood cells of vitamin E deficient patients // Clin. Chim. Acta. 1997. Vol. 265 (l) .- P. 131-137.
120. Mircevova L. The role of Mg ++ - ATPase (actomyosine-like protein) in maintaining the biconcave shape of erythrocytes // Blut. 1977 vol 35 (4) P. 323-327.
121. Mircevova L., Victora L., Kodicek M., Rehackova H., Simonova A. The role of spectrin dependent ATPase in erytrocyte shape maintenance // Biomed. Biochim. Acta. 1983 Vol. 42 (11/12) .- P. 67-71.
122. Nair P. P. Vitamine E and metabolic regulation // Ann. N. Y. Acad. Sci. 1972a.-Vol. 203.- P. 53-61.
123. Nair P. P. Vitamine E regulation of the biosintesis of porphirins and heme // J. Agr. and Food Chem. 1972b. Vol. 20 (3) .- P. 476-480.
124. Nakamura T., Moriya M., Murakoshi N., Shimizu Y., Nishimura M. Effects of phenylalanine and tyrosine on cold acclimation in mice // Nippon Yakurigaku Zasshi. 1997 Vol. 110 (1) .- P. 177-182.
125. Nath K. A., Grande J., Croatt A., et al. Redox regulation of renal DNA synthesis, transforming growth factor-betal and collagen gene expression // Kidney Int.-1998.- Vol. 53 (2) .- P. 367-381.
126. Nathan C. Perspectives Series: Nitric Oxide and Nitric Oxide Synthases Inducible Nitric Oxide Synthase: What Difference Does It Make? // J. Clin. Invest. 1997.- Vol. 100 (10) .- P. 2417-2423.
127. Newaz M. A., Nawal N. N. Effect of alpha-tocopherol on lipid peroxidation and total antioxidant status in spontaneously hypertensive rats // Am J Hypertens. 1998.-Vol. 11 (12) .- P. 1480-1485.
128. Nishiyama H., Itoh K., Kaneko Y., et al. Glycine-rich RNA-binding Protein Mediating Cold-inducible Suppression of Mammalian Cell Growth // J. Cell. Biol. 1997 Vol. 137 (4) .- P. 899-908.
129. Nohl H. Generation of superoxide radicals as byproduct of cellular respiration // Ann. Biol. Clin. (Paris) 1994 Vol. 52 (3) .- P. 199-204.
130. Pendergast D. R., Krasney J. A., De Roberts D. Effects of immersio in cool water on lung-exhaled nitric oxide at rest and during exercise // Respir. Physiol. 1999. Vol. 115 (1) .- P. 73-81.
131. Peng J. F., Kimura B., Fregly M., Phillips M. I. Reduction of cold-induced hypertension by antisense oligodeoxynucleotides to angiotensinogen mRNA and ATi receptor mRNA in brain and blood // Hypertension. 1998 Vol. 31.- P. 13171323.
132. Pinkus R., Weiner L. M., Daniel V. Role of oxidants and antioxidants in the induction of AP-1, NF-kappa B and glutathione S ~ transferase gene expression // J. Biol. Client. 1996. Vol. 271 (23) .- P. 13422-13429.
133. Pipkin F. B. Fortnightly Review: The hypertensive disorders of pregnancy // BMJ. 1995. Vol. 311.-P. 609-613.
134. Reis S. E., Blumenthal R. S., Gloth S. T., Gerstenblith R. G., Brinken J. A. Estrogen acutely abolishes cold-induced coronary vasoconstriction in postmenopausal women // Circulation. 1994. Vol. 90.- P. 457.
135. Salminen A., Kainulainen H., Arstila A. U., Vihko V. Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles // Acta Physiol. Scand. 1984. Vol. 122 (4) .- P. 565-570.
136. Sampson G. M. A., Muller D. P. Studies on the neurobiology of vitamin E (al-pha-tocopherol) and some other antioxidant systems in the rat // Neuropathol. Appl. Neurobiol. 1987. Vol. 13 (4) .- P. 289-296.
137. Sen S. K., Atalay M., Agren J., Laaksonen DE, Roy S., Hanninen O. Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise // APStracts.- 1997.- Vol ... 4.- P. 0101 A.
138. Shapiro S. S., Mott D. D., Machlin L. J. Altered binding of glyceraldehyde 3 -phosphate dehidrogenase to its binding site in vitamine E - deficient red blood cells // Nutr. Rept. Int. - 1982. - Vol. 25 (3) .- P. 507-517.
139. Sharmanov A. T., Aidarkhanov V. V., Kurmangalinov S. M. Effect of vitamin E deficiency on oxidative metabolism and antioxidant enzyme activity of macrophages // Ann. Nutr. Metab. 1990 Vol. 34 (3) .- P. 143-146.
140. Siddons R. C., Mills C. F. Glutatione peroxidase activity and erythrocyte stability in calves differing in selenium and vitamin E status // Brit. J. Nutr. 1981. Vol. 46 (2) .- P. 345-355.
141. Simonoff M., Sergeant C., Gamier N., et al. Antioxidant status (selenium, vitamins A and E) and aging // EXS. 1992. Vol. 62.- P. 368-397.
142. Sklan D., Rabinowitch H. D., Donaghue S. Superoxide dismutase: effect of vitamins A and E // Nutr. Rept. Int. - 1981. - Vol. 24 (3) .- P. 551-555.
143. Smith S. C., Guilbert L. J., Yui J., Baker P. N., Davidge S. T. The role of reactive nitrogen / oxygen intermediates in cytokine-induced trophoblast apoptosis // Placenta. 1999. Vol. 20 (4) .- P. 309-315.
144. Snircova M., Kucharska J., Herichova I., Bada V., Gvozdjakova A. The effect of an alpha-tocopherol analog, MDL 73404, on myocardial bioenergetics // Bratisl Lek Listy. 1996. Vol. 97. P. 355-359.
145 Soliman M. K. Uber die Blutveranderungen bei Ratten nach verfuttem einer Tocopherol und Ubichinon Mangeldiat. 1. Zytologische und biochemische Ve-randerungen im Blut von vitamin E Mangelratten // Zbl. Veterinarmed. 1973. Vol. 20 (8) .- P. 624-630.
146. Stampfer M. J., Hennekens C. H., Manson J. E., et al. Vitamin E consumption and the risk of coronary disease in women // N. Engl. J. Med. 1993. Vol. 328.- P. 1444-1449.
147. Sun J. Z., Tang X. L., Park S. W., et al. Evidence for an Essential Role of Reactive Oxygen Species in the Genesis of Late Preconditioning Against Myocardial Stunning in Conscious Pigs // J. Clin. Invest. 1996, - Vol. 97 (2) .- P. 562-576.
148. Sun Z., Cade J. R., Fregly M. J. Cold-induced hypertension. A model of miner-alocorticoid-induced hypertension // Ann. N. Y. Acad. Sci. 1997. Vol. 813 P.682-688.
149. Sun Z., Cade R, Katovich M. J., Fregly M. J. Body fluid distribution in rats with cold-induced hypertension // Physiol. Behav. 1999 Vol. 65 (4-5) .- P. 879-884.
150. Sundaresan M., Yu Z.-X., Ferrans VJ, Irani K., Finkel T. Requirement for generation of H202 for platelet-derived growth factor signal transduction // Science (Wash. DC). 1995. Vol ... 270.- P. 296-299.
151. Suzuki J., Gao M., Ohinata H., Kuroshima A., Koyama T. Chronic cold exposure stimulates microvascular remodeling preferentially in oxidative muscles in rats // Jpn. J. Physiol. 1997 Vol. 47 (6) .- P. 513-520.
152. Tamai H., Miki M., Mino M. Hemolysis and membrane lipid changes induced by xanthine oxidase in vitamin E deficient red cells // J. Free Radic. Biol. Med.-1986.-Vol. 2 (1) .- P. 49-56.
153. Tanaka M., Sotomatsu A., Hirai S. Aging of the brain and vitamin E // J. Nutr. Sci. Vitaminol. (Tokyo). - 1992. - Spec. No.- P. 240-243.
154. Tappel A. L. Free radical lipid peroxidation damage and its inhibition by vita-mine E and selenium // Fed. Proc.- 1965.- Vol. 24 (1) .- P. 73-78.
155. Tappel A. L. Lipid peroxidation damage to cell components // Fed. Proc.- 1973.-Vol. 32 (8) .- P. 1870-1874.
156. Taylor A.J. N. Asthma and allergy // B. M. J. - 1998. - Vol. 316.- P. 997-999.
157. Tate D. J., Miceli M. V., Newsome D. A. Phagocytosis and H2C> 2 induce catalase and metaliothionein irene expression in human retinal pigment epithelial cells // Invest. Onithalmol. Vis. Sci. 1995. Vol. 36.- P. 1271-1279.
158. Tensuo N. Effect of daily infusion of noradrenaline on metabolism and skin temperature in rabbits // J. Appl. Physiol. 1972. Vol. 32 (2) .- P. 199-202.
159. Tiidus P. M., Houston M. E. Antioxidant and oxidative enzyme adaptations to vitamin E deprivation and training // Med. Sci. Sports. Exerc.- 1994.- Vol. 26 (3) .- P. 354-359.
160. Tsen C. C., Collier H. B. The protective action of tocopherol against hemolisis of rat eritrocites by dialuric acid // Canad. J. Biochem. Physiol. - I960. - Vol. 38 (9) .- P. 957-964.
161. Tudhope G. R., Hopkins J. Lipid peroxidation in human erythrocytes in tocopherol deficiency // Acta Haematol. 1975. Vol. 53 (2) .- P. 98-104.
162. Valentine J. S., Wertz D. L., Lyons T. J., Liou L.-L., Goto J. J., Gralla E. B. The dark side of dioxygen biochemistry // Current Opinion in Chemical Biology. 1998. Vol. 2.-P. 253-262.
163. Vransky V. K. Red blood cell membrane resistanse // Biophys. Membrane Transport Wroclaw 1976 Part 2 P. 185-213
164. Vuillanine R. Role biologiqe et mode d "action des vitamines E // Rec. Med vet. 1974. Vol. 150 (7) P 587-592.
165. Wang J., Huang C. J., Chow C. K. Red cell vitamin E and oxidative damage: a dual role of reducing agents // Free Radic. Res. - 1996 Vol. 24 (4) .- P. 291-298.
166. Wagner B. A., Buettner G. R., Burns C. P. Vitamin E slows the rate of free radical-mediated lipid peroxidation in cells // Arch. Biochem. Biophys. 1996 Vol. 334.-P. 261-267.
167. Wallace J. L., Bell C. J. Gastroduodenal mucosal defense // Current Opinion in Gastroenterology 1994.-Vol. 10.-P. 589-594.
168. Walsh D. M., Kennedy D. G., Goodall E. A., Kennedy S. Antioxidant enzyme activity in the muscles of calves depleted of vitamin E or selenium or both // Br. J. Nutr. 1993 Vol. 70 (2) .- P. 621-630.
169. Watson A. L., Palmer M. E., Jauniaux E., Burton G. J. Variations in expression of copper / zinc superoxide dismutase in villous trophoblast of the human placenta with gestational age // Placenta. 1997. Vol. 18 (4) .- P. 295-299.
170. Young J. B., Shimano Y. Effects of rearing temperature on body weight and abdominal fat in male and female rats // APStracts. 1991. Vol. 4.- P. 041 OR.
171. Zeiher A. M., Drexler H., Wollschlager H., Just H. Endothelial dysfunction of the coronary microvasculature is associated with coronary blood flow regulation in patients with early atherosclerosis // Circulation. 1991. Vol. 84.- P. 19841992.
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I'll tell you about one of the most incredible, from the point of view of everyday ideas, practices - the practice of free adaptation to the cold.
According to generally accepted ideas, a person cannot be in the cold without warm clothes. The cold is absolutely destructive, and as fate willed to go out into the street without a jacket, the unfortunate person is waiting for a painful freezing, and an inevitable bouquet of illnesses upon his return.
In other words, generally accepted concepts completely deny a person the ability to adapt to the cold. The comfort range is considered to be located exclusively above room temperature.
It seems that you can not argue. You can't spend the whole winter in Russia in shorts and a T-shirt ...
The fact of the matter is that you can !!
No, without clenching your teeth, overgrown with icicles to set a ridiculous record. And free. Feeling, on average, even more comfortable than those around her. This is a real hands-on experience that breaks conventional wisdom in a crushing way.
It would seem, why own such practices? Everything is very simple. New horizons always make life more interesting. Removing the instilled fears, you become freer.
The comfort range is expanding enormously. When the rest is hot, sometimes cold, you feel good everywhere. Phobias disappear completely. Instead of fear of getting sick, if you don't dress warmly enough, you get complete freedom and confidence in your abilities. Running in the cold is really nice. If you go beyond your powers, then this does not entail any consequences.
How is this even possible? Everything is very simple. We are much better organized than is commonly believed. And we have mechanisms that allow us to be free in the cold.
First, when the temperature fluctuates within certain limits, the metabolic rate, the properties of the skin, etc. change. In order not to dissipate heat, the outer contour of the body lowers the temperature greatly, while the core temperature remains very stable. (Yes, cold paws are normal !! No matter how we were convinced in childhood, this is not a sign of freezing!)
With an even greater cold load, specific mechanisms of thermogenesis are activated. We know about contractile thermogenesis, in other words, tremors. The mechanism is, in fact, an emergency. The shiver warms, but it turns on not from a good life, but when you really freeze.
But there is also non-contractile thermogenesis, which produces heat through the direct oxidation of nutrients in the mitochondria directly into heat. In the circle of people practicing cold practices, this mechanism was simply called the "stove". When the "stove" is turned on, heat is regularly produced in the background in an amount sufficient for a long stay in the cold without clothes.
Subjectively, this feels rather unusual. In Russian, the word “cold” is used to describe two fundamentally different sensations: “cold outside” and “cold for you”. They can be present independently. You can get cold in a warm enough room. And you can feel a burning cold outside on your skin, but do not freeze at all and not experience discomfort. Moreover, it is pleasant.
How does one learn to use these mechanisms? I will emphatically say that I consider "learning by article" risky. The technology must be handed over personally.
Non-contractile thermogenesis starts in a fairly severe frost. And its inclusion is quite inertial. The “stove” does not start working earlier than in a few minutes. Therefore, paradoxically, learning to walk freely in the cold is much easier in severe frost than on a cool autumn day.
As soon as you go out into the cold, you begin to feel the cold. At the same time, an inexperienced person is seized with panic horror. It seems to him that if it is already cold now, then in ten minutes a full paragraph will come. Many simply do not wait for the "reactor" to reach operating mode.
When the “stove” is still started, it becomes clear that, contrary to expectations, it is quite comfortable to be in the cold. This experience is useful in that it immediately breaks the patterns inspired from childhood about the impossibility of such a thing, and helps to look differently at reality as a whole.
For the first time, you need to go out into the cold under the guidance of a person who already knows how to do this, or where you can return to the warmth at any time!
And you need to go out extremely naked. Shorts, even better without a T-shirt and nothing else. The body needs to be scared properly so that it turns on forgotten adaptation systems. If you get scared and put on a sweater, trowel, or something similar, then the heat loss will be enough to freeze very much, but the "reactor" will not start!
For the same reason, gradual "hardening" is dangerous. A decrease in the temperature of the air or bath "by one degree in ten days" leads to the fact that sooner or later the moment comes when it is already cold enough to get sick, but not enough to trigger thermogenesis. Truly, only iron people can withstand such hardening. But almost everyone can go straight out into the cold or dive into an ice-hole.
After what has been said, one can already guess that adapting not to frost, but to low above-zero temperatures is a more difficult task than jogging in frost, and it requires higher preparation. The "stove" at +10 does not turn on at all, and only nonspecific mechanisms work.
It should be remembered that severe discomfort cannot be tolerated. When everything works out correctly, no hypothermia develops. If you start to get very cold, then you need to interrupt the practice. Periodic going beyond the limits of comfort is inevitable (otherwise it will not be possible to push these limits), but the extreme should not be allowed to grow into a kick-ass.
The heating system gets tired of working under load over time. The limits of endurance are very far. But they are. You can walk freely at -10 all day, and at -20 a couple of hours. But you won't be able to go on a ski trip in one T-shirt. (Field conditions are a separate topic altogether. weather. But, with experience)
For greater comfort, it is better to walk like this in more or less clean air, away from the sources of smoke and from smog - the sensitivity to what we breathe in this state increases significantly. It is clear that practice is generally incompatible with smoking and booze.
Being in the cold can cause cold euphoria. The feeling is pleasant, but requires extreme self-control in order to avoid loss of adequacy. This is one of the reasons why it is highly undesirable to start the practice without a teacher.
Another important nuance is a prolonged reboot of the heating system after significant loads. Having picked up the cold properly, you can feel pretty good, but when you enter a warm room, the "stove" turns off, and the body begins to warm up with tremors. If at the same time go out into the cold again, the "stove" will not turn on, and you can get very cold.
Finally, you need to understand that mastery of practice does not guarantee that you will not freeze anywhere and never. The condition changes and many factors affect. But, the likelihood of getting into trouble from the weather is still reduced. Just as the likelihood of being physically deflated for an athlete is differently lower than that of a squishy.
Alas, it was not possible to create a complete article. I only outlined this practice in general terms (more precisely, a complex of practices, because diving into an ice hole, jogging in a T-shirt in the cold and wandering through the woods in the Mowgli style are different). Let me summarize where I started. Owning your own resources allows you to get rid of fears and feel much more comfortable. And this is interesting.
Dmitry Kulikov
Like any creature, the horse is able to adapt to some extent to the cold. The question is: how harmless will such an adaptation be for the horse's health? What is the critical temperature? Do we have confidence that all horses react the same to cold?
Even if we talk about a healthy horse, which is practically unrealistic after its participation in sports or riding of any kind, is it so good for it in the cold, rain and snow, as horse owners of all faiths, from athletes to naturists, believe in it?
Thanks to "sports" veterinarians, we have a huge amount of research on the effect of heat and overheating on a horse - it is understandable: runs, races ... And there are too few serious works on the effect of cold on the body. Such studies can be counted on one hand.
The trotters found out that at temperatures below -23 ° C trotters die on the tracks ... from the cold air.
And when training in the cold at -22 ° C they stay alive! From which it is concluded that at -22 ° C it is necessary to go out on the track, but in a blanket ...
For several years, the Finns have found out in detail how the Finnish horses are freezing, measured the thickness of subcutaneous fat, the length of the hair - and found out that they are very cold. Conclusion: you need to wear blankets.
That, perhaps, is all the research ...
Of course, any attempts to study the question of the effect of cold on the body will be inadequate until we know what the horse itself thinks about this.
In the meantime, we are not sure what the horse actually feels in winter, we are forced to be guided by strictly scientific data of anatomy and physiology and, of course, our own guesses and common sense. After all, our task is to make any weather of our not the most gentle climate as comfortable as possible for horses.
A comfortable temperature for a horse is considered to be from +24 to + 5 ° C (in the absence of other irritating factors, of course). With this temperature regime, the horse does not need to expend additional energy for heating, provided that it is healthy and in good condition and in decent housing conditions.
Obviously, in any case, at temperatures below -GC, the horse will need additional sources of heat, and often, given the humidity, windiness, etc., such a need may arise even in the “comfortable” temperature range.
What is the body's physiological response to cold?
Immediate response. It occurs in response to a sudden sharp change in air temperature. The horse freezes noticeably, its coat stands on end (piloerection), blood from the limbs flows to the internal organs - the legs, ears, nose become cold. The horse stands with its tail between its legs and does not move in order to save energy.
Adaptation. This is the next reaction of the horse when exposed to further constant exposure to cold. It usually takes a horse 10 to 21 days to get some cold adaptation. For example, a horse kept at a temperature of + 20 ° C suddenly falls into an environment with a temperature of + 5 ° C. She adapts to the new environment in 21 days. With a further decrease in temperature from +5 to -5 ° C, the horse will need up to 21 days to adapt. And so on until the temperature reaches the lower critical mark (LOC) of -15 ° C for an adult horse or 0 ° C for a growing horse. Upon reaching a critical temperature, the horse's body will begin to work in "emergency mode", not to live, but to survive, which will lead to a serious and, at times, irreversible, depletion of its resources.
As soon as NCO is reached, stressful physiological changes begin, and the horse needs human intervention to cope with the cold: heating, additional nutrition.
It is clear that all data are arbitrary and differ for each particular horse. However, science today does not have accurate data.
Physiological changes consist in "concentrating" the blood supply on the internal organs, the circulatory system begins to work as if in a "small circle". There is a decrease in respiratory and heart rhythms to keep warm, resulting in the horse's inactivity in winter. The most visible external sign of physiological changes is the growth of long, thick hair.
Fouling varies greatly in intensity from horse to horse under the same conditions. Breed, health, fatness, gender, type are of great importance. The more "thick-skinned" the horse, the heavier its type, the more it grows overgrown. As noted by ND Alekseev (1992), Yakut horses have the thickest skin in comparison with horses of other breeds (4.4 + 0.05 mm in winter in the area of the last rib). Compare: in the European warm-blooded horse, the thickness of the skin in the same place is approximately 3-3.6 mm. There are exceptions associated with the individual characteristics of the metabolism. Temperament plays a role: active "thin-skinned" stallions of warm-blooded breeds overgrow little or not overgrow at all. For example, Kao lives in the same conditions as our other horses, but does not overgrow at all - he walks in summer wool in winter. Ponies, draft horses, trotters grow, as a rule, more strongly, they have pronounced "brushes", hair growth from the wrist to the corolla significantly increases, and a not very attractive, downright priest's beard appears. The same applies to sick and hungry horses - the body is trying to compensate for the lack of heat-insulating fat layer and malnutrition, spending its last reserves on growing hair, although here everything is strictly individual. By the length of a horse's coat, you can always accurately judge its health, maintenance and care.
In general, fouling seems to be a familiar thing for everyone ... But what is it worth to a horse? I can’t say better than my spouse, therefore I am citing a direct quote: “A substantial part of physiological forces is spent on the fouling process. Just try to calculate how much it costs a horse to raise, keep, salted, etc. long hair. It was not her husband who bought her a fur coat, she had to withdraw a very large "sum" from her own biological and physiological system and spend it on wool, moreover, the horse's biological resource is not so great. Nature has established a certain "insulation standard" for a given strip (north, west, center of Russia). It is easy to calculate this standard by analyzing the norms of warming of wild animals that fundamentally live in the natural environment of a given region, by counting and analyzing the length of the coat, the depth and density of the undercoat, and the body temperature (normally) of these animals. This is a normal "natural" program to suit the climate and season. The man did not interfere with it.
By natural selection, this thermal standard and the thermal insulation standard have been developed for tens of thousands of years. It is precisely this amount of protective wool, just such a density and depth of the undercoat, just such a body temperature as presented by the wild natural inhabitants of the region - that is the norm that ensures survival, and possibly some comfort.
The horse is not suitable here as a "trendsetter", being an introduced creature alien to the given strip - no matter in what generation. A kind of "lost exotic dog".
But it takes millennia for adaptive evolutionary changes!
All that a horse can "present" to the Russian cold is 2.5 - 3 cm of wool. No undercoat.
Having found out the discrepancy between the quality of horse warming and local natural standards, we can confidently talk about the physiological suffering of the horse, about the infliction of both physiological and functional harm by the cold on the horse. And this, and only this, will be a strictly scientific point of view. The argument based on the analysis of what is "worn in a given band" for survival is irrefutable and very serious. Even a two-hour winter walk under the influence of the natural climatic conditions of the North-West on the body, unfortunately, is either very uncomfortable for the horse, or frankly dangerous. "
- 2036I'll tell you about one of the most incredible, from the point of view of everyday ideas, practices - the practice of free adaptation to the cold.
According to generally accepted ideas, a person cannot be in the cold without warm clothes. The cold is absolutely destructive, and as fate willed to go out into the street without a jacket, the unfortunate person is waiting for a painful freezing, and an inevitable bouquet of illnesses upon his return.
In other words, generally accepted concepts completely deny a person the ability to adapt to the cold. The comfort range is considered to be located exclusively above room temperature.
It seems that you can not argue. You can't spend the whole winter in Russia in shorts and a T-shirt ...
The fact of the matter is that you can !!
No, without clenching your teeth, overgrown with icicles to set a ridiculous record. And free. Feeling, on average, even more comfortable than those around her. This is a real hands-on experience that breaks conventional wisdom in a crushing way.
It would seem, why own such practices? Everything is very simple. New horizons always make life more interesting. Removing the instilled fears, you become freer.
The comfort range is expanding enormously. When the rest is hot, sometimes cold, you feel good everywhere. Phobias disappear completely. Instead of fear of getting sick, if you don't dress warmly enough, you get complete freedom and confidence in your abilities. Running in the cold is really nice. If you go beyond your powers, then this does not entail any consequences.
How is this even possible? Everything is very simple. We are much better organized than is commonly believed. And we have mechanisms that allow us to be free in the cold.
First, when the temperature fluctuates within certain limits, the metabolic rate, the properties of the skin, etc. change. In order not to dissipate heat, the outer contour of the body lowers the temperature greatly, while the core temperature remains very stable. (Yes, cold paws are normal !! No matter how we were convinced in childhood, this is not a sign of freezing!)
With an even greater cold load, specific mechanisms of thermogenesis are activated. We know about contractile thermogenesis, in other words, tremors. The mechanism is, in fact, an emergency. The shiver warms, but it turns on not from a good life, but when you really freeze.
But there is also non-contractile thermogenesis, which produces heat through the direct oxidation of nutrients in the mitochondria directly into heat. In the circle of people practicing cold practices, this mechanism was simply called the "stove". When the "stove" is turned on, heat is regularly produced in the background in an amount sufficient for a long stay in the cold without clothes.
Subjectively, this feels rather unusual. In Russian, the word “cold” is used to describe two fundamentally different sensations: “cold outside” and “cold for you”. They can be present independently. You can get cold in a warm enough room. And you can feel a burning cold outside on your skin, but do not freeze at all and not experience discomfort. Moreover, it is pleasant.
How does one learn to use these mechanisms? I will emphatically say that I consider "learning by article" risky. The technology must be handed over personally.
Non-contractile thermogenesis starts in a fairly severe frost. And its inclusion is quite inertial. The “stove” does not start working earlier than in a few minutes. Therefore, paradoxically, learning to walk freely in the cold is much easier in severe frost than on a cool autumn day.
As soon as you go out into the cold, you begin to feel the cold. At the same time, an inexperienced person is seized with panic horror. It seems to him that if it is already cold now, then in ten minutes a full paragraph will come. Many simply do not wait for the "reactor" to reach operating mode.
When the “stove” is still started, it becomes clear that, contrary to expectations, it is quite comfortable to be in the cold. This experience is useful in that it immediately breaks the patterns inspired from childhood about the impossibility of such a thing, and helps to look differently at reality as a whole.
For the first time, you need to go out into the cold under the guidance of a person who already knows how to do this, or where you can return to the warmth at any time!
And you need to go out extremely naked. Shorts, even better without a T-shirt and nothing else. The body needs to be scared properly so that it turns on forgotten adaptation systems. If you get scared and put on a sweater, trowel, or something similar, then the heat loss will be enough to freeze very much, but the "reactor" will not start!
For the same reason, gradual "hardening" is dangerous. A decrease in the temperature of the air or bath "by one degree in ten days" leads to the fact that sooner or later the moment comes when it is already cold enough to get sick, but not enough to trigger thermogenesis. Truly, only iron people can withstand such hardening. But almost everyone can go straight out into the cold or dive into an ice-hole.
After what has been said, one can already guess that adapting not to frost, but to low above-zero temperatures is a more difficult task than jogging in frost, and it requires higher preparation. The "stove" at +10 does not turn on at all, and only non-specific mechanisms work.
It should be remembered that severe discomfort cannot be tolerated. When everything works out correctly, no hypothermia develops. If you start to get very cold, then you need to interrupt the practice. Periodic going beyond the limits of comfort is inevitable (otherwise it will not be possible to push these limits), but the extreme should not be allowed to grow into a kick-ass.
The heating system gets tired of working under load over time. The limits of endurance are very far. But they are. You can walk freely at -10 all day, and at -20 a couple of hours. But you won't be able to go on a ski trip in one T-shirt. (Field conditions are a separate topic altogether. weather. But, with experience)
For greater comfort, it is better to walk like this in more or less clean air, away from sources of smoke and from smog - the sensitivity to what we breathe in this state increases significantly. It is clear that practice is generally incompatible with smoking and booze.
Being in the cold can cause cold euphoria. The feeling is pleasant, but requires extreme self-control in order to avoid loss of adequacy. This is one of the reasons why it is highly undesirable to start the practice without a teacher.
Another important nuance is a prolonged reboot of the heating system after significant loads. Having picked up the cold properly, you can feel pretty good, but when you enter a warm room, the "stove" turns off, and the body begins to warm up with tremors. If at the same time go out into the cold again, the "stove" will not turn on, and you can get very cold.
Finally, you need to understand that mastery of practice does not guarantee that you will not freeze anywhere and never. The condition changes and many factors affect. But, the likelihood of getting into trouble from the weather is still reduced. Just as the likelihood of being physically deflated for an athlete is differently lower than that of a squishy.
Alas, it was not possible to create a complete article. I only outlined this practice in general terms (more precisely, a complex of practices, because diving into an ice hole, jogging in a T-shirt in the cold and wandering through the woods in the Mowgli style are different). Let me summarize where I started. Owning your own resources allows you to get rid of fears and feel much more comfortable. And this is interesting.
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