Thermoregulation: Physiological Responses and Adaptations to Exercise in Hot and Cold Environments
By: Joe “Yu Yevon” King
King J. Thermoregulation: Physiological Responses and Adaptations to Exercise in Hot and Cold Environments. J. Hyperplasia Research. 4(3), 2004.
Various body systems must coordinate their activities to allow our bodies to perform physical activity. This process is known as synergy. Likewise, these systems have the God-given capacity to adapt when exposed to the stresses of specific training. This article attempts to discuss how the body responds and adapts when challenged to exercise under abnormal or extreme environmental conditions. The mechanisms by which the body can regulate its internal temperature both at rest and during exercise will be discussed, as well as exercising in both hot and cold environments, along with health risks that are associated with physical activity in the aforementioned environments.
Recommended reading in conjunction with this article for full comprehension of topics discussed:
Physical exertion is very taxing to our bodies, and this effect is multiplied exponentially when under extreme environmental conditions. Performing in hot and cold environments places a heavy burden on the mechanisms that are designed to regulate body temperature. These mechanisms are incredibly effective in maintaining homeostasis in vivo; however, they can be severely taxed or strained when the external conditions change.
Body temperature is kept constant by balancing both heat gain and heat loss. Humans need to maintain a constant body temperature of about 37°C. To maintain this temperature at a constant point throughout the body’s internal systems, mechanisms must be in place to accurately measure present body temperature, and to regulate as needed. This system is known as the thermoregulatory system. The metabolic heat generated by oxidation of food in the visceral organs and tissues (body core) is a constant source of heat. Core body temperature can also be dramatically increased with muscular activity, nervous and hormonal factors (such as sympathetic nervous activity), catecholamines, and thyroid hormones.
Body temperature can vary in different regions. The tissues of the extremities and the skin are far from the core (the core consists of the brain and visceral organs and tissues in the trunk), and they are in direct contact with the external environment. These tissues tend to have slightly lower temperatures.
For example: In a room temperature of 21°C, hand, foot and skin temperatures are about 28 °C and 21 °C respectively.
Even core temperature is not a constant 37°C at all times. A circadian (diurnal) cycle exists, core temperature being the lowest in morning (36.7 °C) and highest in the evening (37.2°C).
Mechanisms by Which Our Body Regulates Temperature
Transfer of Body Heat
In temperature regulation, it is imperative that your body can transfer internal heat out away from the body and into the external environment. To do this, heat from the interior of the body needs to be moved to the skin via the blood. Once the heat reaches the skin, it can be transferred to the external environment in one of four ways: conduction, convection, radiation or evaporation.
Heat conduction involves the transfer of heat from one material to another through direct molecular contact. Heat from the body’s interior can transfer itself from one tissue to an adjacent tissue until it reaches the outer surface of the skin, where it is released into the atmosphere. This mechanism can work both ways. If a hot object is pressed against the skin (such as a heating pad), the heat from the object will transfer to the skin, heating the general area.
Convection involves moving heat from one place to another by the motion of a gas or liquid across the heated surface. The air around us is in constant motion. As it circulates over the skin of an individual, it displaces the air molecules that have been warmed by their contact with the skin. The greater the movement of air (or liquid, such as water), the greater the amount of heat removal by convection. When convection is combined with conduction, convection can cause the body to gain heat in an already hot environment when the surroundings are hotter than the skin.
Although both of the aforementioned mechanisms of body heat transfer remove body heat when the air temperature is lower than skin temperature, their contribution to the body’s total heat loss is relatively small – only about 10% to 20%. If, however, an individual is submerged in cold water, the amount of heat dissipated from the body to the water is nearly 26 times greater than when the body is exposed to a similar air temperature. When air or water temperature is greater than the skin temperature, the body will gain heat through both conduction and convection. Therefore it can be concluded that both conduction and convection can either contribute to heat loss or heat gain, depending on whether or not the external temperature of the environment exceeds that of the internal temperature of the individual. The gradient works in both directions.
When the body is in its resting state, the primary method the body utilizes for discharging extra internal heat is radiation. At normal room temperature (21-25°C), the body loses about 60% of its heat via radiation. In this method of thermoregulation, the heat is given off in the form of infrared rays, which are a type of electromagnetic wave. The skin is constantly radiating heat in all directions to the objects adjacent to it, such as clothing or furniture. The body can also receive heat from objects around it via radiation from objects that are warmer. If the temperature of the surrounding objects is greater than that of the skin, the body will experience a net heat gain through radiation. A tremendous amount of radiational heat is received from exposure to the sun.
Evaporation is the primary avenue for heat dissipation. As fluid evaporates, heat is lost into the external environment. Evaporation accounts for about 80% of the total heat loss during activity, but only about 20% at rest. Whenever body fluid is brought into contact with the external environment, such as in the lungs, at the mucosa and at the skin insensible water loss takes place. Insensible water loss is simply water that is lost from the body without the individual’s conscious recognition. Insensible water loss removes about 10% of the total metabolic heat produced by the body, but this mechanism for heat loss is relatively constant, even during activity. Therefore, when the body needs to lose more heat quickly, insensible water loss is vastly inefficient. Instead, as internal body temperature increases, sweat production also increases. As sweat reaches the skin, it is converted from a liquid to a vapor by heat from the surface of the skin. Evaporation of 1 L of sweat results in the loss of 580 kcal.
BONUS: Yet another way the body can affect heat loss is by the use of body hair. Although this mechanism is of little value in humans, as was preordained, the use of body hair (and fur) is of great value to animals, especially those living in cold environments. In cold weather, skin hairs in both humans and animals stand up (called piloerection), which causes entrapment of the air in the hair web. The trapped air forms an insulating layer due to the blood exchanging heat with the warmer microclimate created by the hair web, rather than the colder environment of the air outside of the web.
Table 1: Estimated Caloric Heat Loss at Rest and During Prolonged Exercise (70% of VO2max)
Adapted from C.V. Gisolfi and C.B. Wegner, 1984.
Table 1 represents the estimated caloric heat loss both at rest and during prolonged bouts of exercise at 70% of VO2max. At 70% VO2max, heat production is ten times higher than at rest. The values presented in Table 1 are averages, because individual metabolic heat production varies with body size, composition, and temperature. Environmental conditions, such as air velocity, humidity, and sun exposure will also affect these values.
Humidity and Heat Loss
Humidity (water vapor content of air) plays a significant role in heat loss, especially by evaporation. In high humidity climates, the air already contains many water molecules, which decreases the air’s capacity to accept more water. This is due to the concentration gradient, which is decreased in cases of high humidity. The high humidity limits sweat evaporation, and hence, heat loss. On the other hand, low humidity promotes heat loss through evaporation, especially during exercise. Nonetheless, low humidity environments are not without their problems to the athlete. If water from the skin evaporates faster than sweat production, severe dryness of the skin may occur.
Humidity plays a deeper role than most athletes realize. Humidity affects an individual’s perception of thermal stress. Consider the two following scenarios:
Exposure to dry desert air (90°F) with 10% relative humidity (low) compared with the exposure to air at the same temperature (90°F) with 90% relative humidity (high). An individual will sweat profusely in the desert air (due to the concentration gradient being low in the dryer air). Evaporation in the dry air will occur so quickly that the individual may not even be aware of the presence of sweat. In the air that is 90% saturated with water, very little sweat is allowed to evaporate. The result is a continuous bath of sweat dripping from the skin. As a result, there is little heat removal, and the comfort level of the individual decreases.
Even at moderate environmental temperatures, humidity is of primary concern during activity due to the fact that evaporation is the primary method of internal heat removal. Fortunately, God designed our mechanisms of heat removal to be very effective, even when environmental conditions are less than ideal.
Control of Heat Exchange
Normally, internal body temperature is kept at a steady 98.6°F. During activity, the body is often unable to dissipate heat as rapidly as it is being produced (heat is one of the byproducts of the ATP producing metabolic pathways). As a result, an athlete can develop a heightened internal temperature sometimes exceeding 104°F with temperatures above 107.6°F in active muscles! The metabolic pathways in skeletal muscles can become more efficient with a slight increase in local temperature, but core temperature above 104°F can display adverse affects upon the nervous system and can even further inhibit the mechanisms designed to release internal heat into the external environment. In order to keep the body working efficiently; it must be designed with an internal mechanism that regulates internal temperature. Enter the hypothalamus gland.
This author discussed the hypothalamus gland in-depth in Endocrine Insanity Part I:
The hypothalamus is the controller of the endocrine system. It's the king of the crop. The hypothalamus is the connection from the endocrine system to the brain. Parts of the hypothalamus that are visible in basal and mid-sagittal views of the gross brain include the mammillary body and the infundibulum (tuber cinereum).
The hypothalamus is a region of the brain located just above the pituitary gland. In fact, it’s intimately related to the pituitary and connected via the hypophyseal stalk. The hypothalamus releases six hormones, which regulate function of the pituitary gland.
Thyrotropin-Releasing Hormone (TRH) is a tripeptide hormone released by special hypothalamic secretory cells. TRH moves down the hypophyseal stalk via the hypothalamal-hypophyseal tract and into the anterior pituitary gland. Here, TRH stimulates the release of thyroid-stimulating hormone (TSH) and prolactin.
Gonadotropin-releasing hormone (GnRH) is a peptide hormone consisting of ten amino acids. GnRH stimulates the release of LH and FSH from the anterior pituitary; thus indirectly increasing increased testosterone levels in males and increased estrogen and progesterone levels in females.
Growth hormone-releasing hormone (GHRH) is a very large, powerful and complex hormone. GHRH consists of two peptides, one containing 40 amino acids, and the other containing 44. As the name indicates, GHRH stimulates the anterior pituitary to release GH. GHRH is secreted in pulses preceding the GH release pulse.
Corticotropin-releasing hormone (CRH) is a peptide consisting of 41 amino acids. The hypothalamus secretes CRH into the hypophysial portal blood. CRH then stimulates the release of ACTH (adrenocorticotropin hormone) in the anterior pituitary.
Somatostatin is a mixture of two peptides. One containing 14 amino acids and the other, 28 aminos. Somatostatin can also be called growth hormone-inhibiting hormone (GHIH) due to its effects on the release of GH. Somatostatin inhibits the release of both GH and TSH by the anterior pituitary.
Dopamine derives from the amino acid tyrosine and acts as an inhibiting hormone, much like somatostatin. But rather than inhibiting GH and TSH, dopamine inhibits prolactin production by the anterior pituitary.
Dopamine also effects breathing, as stated here by Doctors T. Nishino and S. Lahiri:
The steady-state relationship between
chemoreceptor activity and ventilation shows that the ventilatory
equivalent for carotid chemoreceptor activity is increased during
because of its greater inhibitory effect on carotid chemoreceptor
activity than on ventilation with the decrease of arterial O2
As you can see, the hypothalamus strictly regulates the anterior pituitary. This regulation, or control, is called homeostatic control. The hypothalamus’ neuroendocrine role in conjunction with the pituitary gland and the autonomic nervous system (ANS) control the hormone levels all throughout the body. I discuss how in Part 2 of this series .
Not mentioned in the above excerpt is the role of the hypothalamus in thermoregulation. Sensory receptors, called thermoreceptors, are fine-tuned sensory machines that can detect changes in body temperature and instantly relay said messages to the hypothalamus gland. In response to the thermoreceptor’s incoming messages, the hypothalamus activates mechanisms that regulate internal body temperature. The hypothalamus has a type of internal memory bank where the optimal body temperature is stored. If this temperature has not been reached, the hypothalamus will act to see that it is. The smallest deviation from the optimal body temperature will trigger the thermoregulatory center of the hypothalamus to initiate these mechanisms.
Any changes in body temperature will be picked up by two different sets of thermoreceptors: central receptors and peripheral receptors. Central thermoreceptors are located within the hypothalamus, and are thus “central” to the thermoregulatory system. Central thermoreceptors monitor the temperature of the blood as it circulates throughout the brain. The central receptors are sensitive to temperature changes as little as .018°F. Peripheral receptors are located in the skin. These receptors provide the hypothalamus and cerebral cortex with information about external temperature, thus allowing the individual to consciously perceive temperature so that the individual can voluntarily control exposure to heat and cold environments. During massive sweat evaporation, however, the skin can feel cold while the interior of the body is hyperthermic (overheated). In this case, the peripheral receptors would incorrectly notify the hypothalamus and cerebral cortex that the individual is cold, when in fact the body may be nearing a critically high temperature.
When body temperature fluctuates, it can be restored to normal levels via the actions of four effector mechanisms.
Sweat glands: When either the skin or the blood is heated above normal equilibrium levels, the hypothalamus will initiate impulses to the sweat glands, instructing them to actively secrete sweat that moistens the skin. The hotter the internal temperature, the more sweat is produced. Evaporation will take over once the sweat reaches the surface, as discussed earlier in this journal entry.
Smooth muscle around arterioles: When the skin or the blood is heated, the hypothalamus will not only send impulses to sweat glands, but also to smooth muscle tissue in the walls of the arterioles that supply the skin with blood, causing them to vasodilate (increase in diameter). This reaction will subsequently increase local blood flow to the skin. The blood carries heat from the deep interior of the body, and is more able to release that heat if blood flow to the surface of the skin is increased.
Endocrine glands: The effects of several hormones can cause groups of cells to increase their metabolic rates. Increased metabolism affects heat balance because it also increases heat production. Cooling the body stimulates the release of thyroxine from the thyroid gland. Thyroxine can elevate the metabolic rate throughout the body by more than 100%. Catecholamines (such as epinephrine and norepinephrine) have the capacity to mimic and enhance the activity of the sympathetic nervous system. Thus, they can directly affect the metabolic rate of virtually all of the body’s cells.
Special Insert – Hormone Profile – Thyroxine (T4):
Thyroxine is a hormone produced in the thyroid gland (see Endocrine Insanity Part I for more about this gland). The follicle cells within the thyroid gland secrete thyroxine and triiodothyronine. The thyroxine molecule contains four atoms of iodine (hence the nickname T4). T4 accounts for over 90% of the thyroid’s hormonal secretions. Thyroxine’s primary function is to accelerate cellular reactions within most body cells. T4 also increases body metabolism by increasing the rate at which cells use organic molecules and oxygen to produce heat and ATP. Another function of T4 is to make the body more sensitive to the actions of the sympathetic hormones (the effect if which is to increase cardiac output). T4 also helps to control homeostasis, modulating the skeletal and central nervous systems, stimulating protein synthesis, and helping the body maintain a proper water balance.
The entire process of thyroxine secretion is controlled by endocrine biofeedback and involves two hormones: thyroid-stimulating hormone (TSH) and thyrotroponin-releasing hormone (TRH). TSH is released when thyroxine levels in the blood fall. Other factors that influence the release of thyroxine include stress, cold temperature (as measured by the thermoreceptors) or pregnancy. When blood concentrations of thyroxine rise, TSH production is reduced. TRH is inhibited as long as thyroxine levels are high in the blood. Once they fall, TRH output is increased, which in turn increases the secretion of TSH (by the anterior pituitary gland)—the end result is a greater thyroid gland activity.
T4’s use in bodybuilding: Bodybuilders have long since taken advantage of this hormone to increase metabolism, especially during pre-contest preparation. One side-effect of a pre-contest diet is a slowdown of activity of the thyroid gland, which decreases the total metabolic output of the body (lowering resting metabolic rate). Another side-effect of a pre-contest diet is a slowdown in thermogenesis—the process by which excess calories are converted to heat rather than stored as fat.
During a pre-contest diet, it may be useful for the athlete to ingest an iodine supplement, which will promote the synthesis of T4 [18,34].
Physiological Responses to Exercise in Heated Environments
In cold environments, your body will see great benefit from producing heat during activity because it helps maintain normal core body temperature. Metabolic heat load places a considerable burden on the mechanisms that control internal body temperature in any environment, however. In this section, the effects of heat on cardiovascular function, energy production, and bodily fluid homeostasis will be analyzed.
It is well established that exercise places considerable demand on the cardiovascular system. During activity, when the demand of body temperature regulation is highest, the cardiovascular system can become burdened during exercise in a heated environment. The circulatory system, as mentioned briefly earlier, transports heat generated by the ATP-producing metabolic pathways to the surface of the body, where the heat can then be transferred to the external environment. To accomplish this task during exercise in the heat, a large portion of cardiac output must be taken up by the skin and the exercising muscles. Because the volume of blood in circulation is limited, exercise poses a complex problem: An increase in blood flow to one of these areas automatically decreases blood flow to the others. This can lead to potentially problematic situations.
Side Note: Stroke volume (SV) is the amount of blood ejected from the left ventricle during contraction, the difference between the end-diastolic volume and the end-systolic volume (Heart Rate x Stroke Volume = Cardiac Output).
With the slow decline of end-diastolic volume, coupled with the gradual increase in heart rate throughout the early stages of activity, cardiac output can remain reasonably constant, even with the decrease of stroke volume. This phenomenon is known as cardiovascular drift.
Eventually, the body is unable to compensate for the increased metabolic and heat removal demands of exercise in the heat. As a result, neither the muscles nor the skin are able to receive adequate blood supply to continue their metabolic processes. This leads to a decrease in performance, and can make the athlete susceptible to overheating. Above 80% of maximal cardiac output, blood flow to the skin will decrease due to the blood being diverted to the muscles. As a result, adequate heat will not be able to dissipate into the external environment. Performance will be adversely affected.
In addition to increasing body temperature and heart rate, exercise in heated environments also increases total oxygen uptake, which causes the working muscles to utilize more glycogen and to produce more lactate compared with exercise in cold environments . Repeated bouts (15 minutes) of exercise in the heat (104°F) increases heart rate and oxygen uptake significantly compared with exercise in a cool environment (48°F). As described earlier, a warmer environment places greater stress on the cardiovascular system, which in turn increases heart rate. Further, increased sweat production and respiration requires more energy, thus requiring a higher oxygen uptake.
Exercise in the heat hastens glycogen depletion and increases muscle lactate levels, both of which are antecedents of sensations of fatigue and exhaustion. Increased muscle temperature may impair skeletal muscle function and metabolism, which can also lead to fatigue . Moreover, increased carbohydrate utilization appears to be directly linked to the increased secretion of epinephrine with elevated body temperature (hyperthermia).
Bodily Fluid Homeostasis
In heated environments, it is not uncommon for the external temperature to exceed that of the temperature of the skin and the internal temperature of the body. These conditions, as discussed earlier, make heat dissipation by way of evaporation all that more important, since heat dissipation via radiation, convection and conduction are rendered less effective. In fact, radiation, convection and conduction can lead to heat gain in a heated environment, further inhibiting the body’s ability to dissipate excess heat from its core. An increased reliability on evaporation leads to increased sweating.
The sweat glands are controlled by the hypothalamus, which is activated by stimulation from the thermoreceptors. Once the thermoregulatory portion of the hypothalamus is alerted of a higher blood temperature, impulses are transmitted from the hypothalamus through the sympathetic nerve fibers to the millions of sweat glands distributed over the body’s surface. Sweat glands are tubular structures that extend through the dermis and the epidermis, and open onto the surface of the skin.
The sweat substance is formed by the secretory portion of the sweat gland. As the filtrate sweat passes through the duct of the gland, sodium and chloride are gradually reabsorbed back into the surrounding tissues, and then into the blood. During light sweating, the filtrate sweat travels slowly through the tubules, which gives the sodium and chloride more time to reabsorb. The sweat that is formed during light sweating therefore contains very little sodium and chloride by the time it reaches the surface of the skin. When sweating is heavy, however, the filtrate moves more quickly through the tubules; therefore the sweat that reaches the surface is high in sodium and chloride content.
Table 2: Sodium, Chloride, and Potassium Concentrations in the Sweat of Trained and Untrained Subjects during Exercise.
Adapted from the Human Performance Laboratory, Ball State University
Table 2 illustrates the mineral content of both trained and untrained male and female subjects. It is apparent that the values are significantly different. The reason being, with training and repeated exposure to heat, the hormone aldosterone can strongly stimulate the sweat glands, causing them to reabsorb more sodium and chloride. Potassium, calcium and magnesium are not reabsorbed by the sweat glands; therefore their concentrations in the sweat remain constant.
Special Insert – Hormone Profile – Aldosterone and Anti-Diuretic Hormone
Aldosterone is a naturally occurring steroid hormone, which is produced and secreted by the adrenal cortex. The stimulation and release of this hormone is initiated by the Na+/K+ ratio of the body and also by the hormone angiotensin (an octapeptide produced in the blood from an inactive precursor—angiotensinogen—by the enzyme renin secreted by the kidney).
Anti-Diuretic Hormone (ADH) is a peptide based hormone composed of nine different amino acids. ADH is produced by the posterior pituitary and is released in the bloodstream to act on the kidneys. Its main mechanism of action is to increase the permeability of the kidney tubules, thereby allowing water to be reabsorbed into the body rather than excreted with urine. ADH secretion can even be influenced by blood hemorrhaging or anything causing a drop in blood pressure. The body responds by conserving water to maintain fluid balance. Increased water loss due to evaporation from the skin will also cause ADH to be released. The opposite may also be true. If excess water is consumed, ADH secretion will be inhibited.
Alcohol poses an additional problem, especially in relation to ADH. The increased fluid present when consuming an alcoholic beverage, and alcohol’s diuretic effects, lead to increased fluid removal from the body. Alcohol also acts as an ADH blocker, however. Thus, the mechanism by which the kidneys reabsorb water is shut down. This poses some potentially serious problems to the athlete .
When performing activities in hot environments, the body can lose more than 1L of sweat per hour per square meter of body surface. This is an astronomical amount. The average sized individual (110-165 lb.) might lose 1.6 to 2.0 L of sweat (or about 2.5% to 3.2% of total body weight) each hour! A high rate of sweating reduces blood volume, which in turn limits the volume of blood available to supply the needs of the working muscles and to prevent heat buildup, which reduces performance potential. This is more prominent in endurance athletes. Marathon runners have been known to lose as much as 10% of their bodyweight during a marathon in a heated environment (that is an excess of 3 to 4 L of sweat an hour). Such severe dehydration can limit subsequent sweating and make the athlete easily susceptible to heat related illnesses.
The loss of minerals and water via sweating triggers the release of aldosterone and antidiuretic hormone (ADH). ADH maintains fluid balance, while aldosterone (as discussed above) maintains appropriate sodium levels. During acute exercise in the heat and during repeated bouts of exercise in a heated environment, aldosterone limits sodium excretion from the kidneys, thus causing more sodium to be retained throughout the body, which promotes water retention. This effect allows the body to retain water and sodium in preparation for additional exposure to heat and the subsequent sweat loss.
Further, exercise and body water loss stimulates the posterior pituitary gland to release ADH. This hormone stimulates water reabsorption from the kidneys, which will further promote fluid retention. God fashioned in humans this mechanism to compensate for loss of minerals and water during periods of heat stress and heavy sweating. It is by this mechanism, this author believes, that Jesus Christ was able to sustain in the desert in Matthew 4:
1Then was Jesus led up of the Spirit into the wilderness to be tempted of the devil
This time of testing showed that Jesus really was the Son of God, able to overcome the devil and his temptations. A person has not shown true obedience if he or she has never had the opportunity to disobey. We read in Deuteronomy 8:2 that God led Israel into the desert to humble and test them. God wanted to see whether or not his people would really obey him.
The devil, also called Satan, tempted Eve in the Garden of Eden, and he tempted Jesus in the desert. This temptation by the devil shows that Jesus was human, and it gave Jesus the opportunity to reaffirm God’s plan for his ministry. Jesus’ temptation was an important demonstration of his sinlessness. He would face temptation and not give in. Notice that Jesus wasn’t tempted in the temple or at his baptism, but in the desert (wilderness) when he was tired, alone, and hungry (he fasted for 40 days and nights, therefore he would be completely dehydrated, causing ADH and aldosterone to be in full effect), and thus more vulnerable.
2And when he had fasted forty days and forty nights, he was afterward an hungered. 3And when the tempter came to him, he said, If thou be the Son of God, command that these stones be made bread. 4But he answered and said, It is written, Man shall not live by bread alone, but by every word that proceedeth out of the mouth of God. 5Then the devil taketh him up into the holy city, and setteth him on a pinnacle of the temple, 6And saith unto him, If thou be the Son of God, cast thyself down: for it is written, He shall give his angels charge concerning thee: and in their hands they shall bear thee up, lest at any time thou dash thy foot against a stone. 7Jesus said unto him, It is written again, Thou shalt not tempt the Lord thy God. 8Again, the devil taketh him up into an exceeding high mountain, and showeth him all the kingdoms of the world, and the glory of them; 9And saith unto him, All these things will I give thee, if thou wilt fall down and worship me. 10Then saith Jesus unto him, Get thee hence, Satan: for it is written, Thou shalt worship the Lord thy God, and him only shalt thou serve.
The devil’s temptation focused on three crucial areas: physical needs and desires, possessions and power and pride. But Jesus did not give in! Jesus was hungry, dehydrated and weak after fasting for 40 days, but he chose not to use his divine power to satisfy his natural desire for food. Food, hunger and eating are all good, but the timing was wrong. Jesus was in the desert to fast, not to eat. Because Jesus had given up the unlimited, independent use of his divine power in order to experience humanity fully, he wouldn’t use his power to change the stones to bread. Jesus was able to resist all of the devil’s temptations because he not only knew Scripture, but he also obeyed it. Ephesians 6:17 says that God’s Word is a sword to use in spiritual combat. Knowing Bible verses is an important step in helping to resist the devil’s attacks, but the Bible must also be obeyed. Note that Satan has memorized Scripture, but he failed to obey it.
During the 40 day fast, there is no doubt that the mechanisms to help prevent water loss were in effect and operating as God had designed them to.
Health Risks during Exercise in Heated Environments
Despite the body’s aforementioned defenses against overheating, excessive heat production by the active muscles, heat gained from the environment and conditions that prevent the dissipation of excess body heat may elevate the internal body temperature to levels that impair normal cellular functions. In these conditions, excessive heat gains pose serious risk to health. Air temperature alone is not an accurate index of the total physiological stress imposed on the body in a hot environment. Four total variables need to be taken into account:
· Air temperature
· Air velocity
· Amount of thermal radiation
All of these factors influence the degree of heat stress that an individual experiences.
Measuring Heat Stress
Over the past few decades, major efforts have been brought fourth to effectively quantify atmospheric variables. In the 1970s, the wet bulb globe temperature (WBGT) was devised to simultaneously account for conduction, convection, evaporation and radiation. This instrument is able to provide a single temperature reading in order to estimate the cooling capacity of the surrounding environment. The dry bulb measures the actual air temperature (TDB). The wet bulb is kept moist. As water evaporates from the wet bulb, its temperature (TWB) will be lower than that of the dry bulb, which effectively simulates the effect of sweat evaporating from the skin. The difference in temperature between the two bulbs indicates the environment’s capacity for cooling via evaporation. Therefore, in still air with 100% humidity, the temperatures of both bulbs will be equal, since evaporation under these conditions is impossible. Lower humidity and moving air will promote evaporation, which will increase the difference in temperature between the two bulbs. On the machine there is also a black globe which is designed to reabsorb radiated heat. Therefore, its temperature (TG) is an accurate indicator of the environment’s capacity for transmitting radiated heat.
The temperatures from these three bulbs can be combined by using the following equation to estimate the overall atmospheric challenge to body temperature in a given environment:
WBGT = 0.1 TDB + 0.7 TWB + 0.2 TG
The result is a measurement of thermal stress, which can be used by educators, athletes and coaches to assess and anticipate the health risks associated with exercising under certain atmospheric conditions. Table 3 represents the Universal WBGT Index.
Table 3: The Universal WBGT Index.
* Rest means minimal physical activity and is measured in the shade.
Unfortunately, heat related injuries occur more often than necessary and can have severe and lasting effects. It is imperative that recognition and prevention of these injuries be understood in order to decrease the frequency of their occurrence.
Heat Rash: Heat rash, also called prickly heat, is a benign condition associated with a red, raised rash accompanied by sensations of prickling and tingling during sweating. Heat rashes usually occur when the skin is continuously wet with unevaporated sweat. The rash is generally localized to areas of the body that are covered with clothing. Continually drying the body with a towel can help prevent the formation of a rash .
Heat Syncope: Also known as heat collapse, heat syncope is associated with rapid physical fatigue during overexposure to heat. This injury is not to be confused with heat exhaustion. Heat collapse usually occurs from standing (not necessarily exercising) in the heat for long periods of time. This causes peripheral vasodilation of the superficial blood vessels in the skin, causing hyoptension, or a pooling of the blood in the extremities, which will result in dizziness, fainting and nausea. Heat syncope can be quickly relieved by laying in a cool environment and ingestion of fluids .
Heat Cramps: Heat cramps are characterized by severe cramping of the skeletal muscles, particularly the muscles involved in movement during the activity in which the athlete is participating. This injury is brought on by mineral loss and dehydration that accompanies high rates of sweating; however, a complete understanding of the cause-effect relationship has not been fully established. To treat heat cramps, the athlete must move to a cooler location and ingest fluids or a saline solution. The intake of fluids to treat heat injuries has been well known for thousands of years. Luke wrote about it in Luke 16:24, quoting Jesus:
And he cried and said, Father Abraham, have mercy on me, and send Lazarus, that he may dip the tip of his finger in water, and cool my tongue; for I am tormented in this flame.
The Jews used to call Abraham their father, and were proud of their descent from him (Matthew 3:9, John 8:33, 39). The quote, “that he may dip the tip of his finger in water,” is in allusion to the washings and purifications of the Jews, and the sprinkling of blood by the finger of the high priest; which were typical of cleansing, pardon, comfort, and refreshment, by the grace and blood of Christ. So the water in this sense was not only refreshing to the body, which was in dire need of internal cooling, but to also wash away sin.
“And cool my tongue” is in reference to cleansing the tongue which has spoken so many blasphemous things of Christ; saying that he was a sinner, a glutton, and a winebibber, a Samaritan, and had a devil: that he cast out devils by Beelzebub, the prince of devils; and that he was a seditious person, and guilty of blasphemy.
This man could not so much as get a drop of water to cool his tongue, not the least refreshment nor mitigation of the anguish of his conscience, for the sins of his tongue.
Heat Exhaustion: This injury is commonly accompanied by such symptoms as extreme fatigue, breathlessness, dizziness, vomiting, fainting, cold and clammy skin, or hot and dry skin, hypotension (low blood pressure), and a weak, rapid pulse. Heat exhaustion is caused by the cardiovascular system’s inability to adequately meet the body’s needs. Recall that during activity in a heated environment, the active muscles and the skin, through which heat is lost, compete for blood volume. Heat exhaustion results when these simultaneous demands cannot be met. Heat exhaustion will occur when blood volume decreases via either excessive fluid loss or mineral loss from excessive sweating. During heat exhaustion, the thermoregulatory mechanisms of heat dissipation are working optimally, but cannot dissipate the heat quickly enough due to the insufficient blood volume. Heat exhaustion is not always associated with a high internal temperature, which can be misleading to some. It is apparent that individuals who are poorly conditioned or are not accustomed to exercising in the heat are more susceptible to heat exhaustion. Treatment for this injury includes rest in a cooler environment with the feet in an elevated position (above the heart) to avoid shock. If the athlete is conscious, salt water should be ingested. If the athlete is unconscious, intravenous administration of a saline solution is recommended. If left untreated, heat exhaustion can easily lead to heat stroke.
Heat Stroke: Heat stroke is a life-threatening heat disorder that requires immediate medical attention. Heat stroke is characterized by:
· Increased internal body temperature to a value exceeding 104°F
· Cessation of sweating
· Hot and dry skin
· Rapid pulse and respiration
· Hypertension (high blood pressure)
· Eventually unconsciousness
If left untreated (especially if the athlete is exercising alone), heat stroke will progress to a coma, and death quickly follows. Treatment of heat stroke involves a rapid cooling of the body in a bath of ice water or wrapping the athlete in cold, wet sheets and fanning the body. Heat stroke is caused by a complete collapse of the thermoregulatory mechanisms. Body heat production during exercise depends directly on both exercise intensity and body weight; therefore, heavier athletes such as bodybuilders run a higher risk of overheating. Heat stroke does not just occur under excessively hot external temperatures, but can occur in moderate environmental temperatures (70°F with a humidity of 30%) as well [15, 77]. Without proper medical attention, heat stroke survivors can sustain permanent central nervous system damage.
Environmental conditions are largely beyond human control. Therefore, in excessively heated conditions, the athlete must be aware enough to control his or her intensity in effort to decrease heat production and the risk of developing hyperthermia. Hyperthermia is simply a high internal body temperature. It is imperative that athletes and coaches alike are able to recognize the signs of the early stages of hyperthermia, before it is able to reach the advanced, life-threatening stages. Table 4 illustrates these symptoms.
Table 4: Subjective Symptoms Associated with Hyperthermia
Heat disorders can and must be prevented. Competition and practice should not be held outdoors when the WBGT is more than 82.4°F. Scheduling practices and events either in the early morning or in the evening avoids the severe heat stress of the midday. Fluids should be readily available, and athletes must be required to drink as much as they can every 10 to 20 minutes. It is well established that drinking fluid both before and during exercise can greatly reduce the negative effects of exercising in a heated environment. Adequate fluid intake will attenuate the increase in core body temperature and heart rate normally observed during exercise in the heat. Clothing must also be considered. The foolish practice of exercising in a rubberized suit to promote weight loss is an excellent example of how a dangerous microenvironment (the isolated environment inside the suit) can be created in which temperature and humidity can reach a sufficiently high level to block all heat loss from the body. This can rapidly lead to heat exhaustion and heat stroke. Athletes should wear as little clothing as possible when heat stress is a potential limitation to thermoregulation. The clothing worn should also be loose around the skin to allow the unloading of as much heat as possible. Light colored clothing will reflect heat back into the environment, while darker clothing will absorb it. Therefore, when exercising in a heated environment, it is recommended that the clothing not only be loose, but also light in color.
Hyponatremia: Hyponatremia is a condition that results in an abnormally low concentration of sodium in the blood. This can be caused by the ingestion of too little sodium or by the ingestion of so much water that the concentration of sodium is decreased. An athlete who experiences a low rate of sweating that continues to ingest large quantities of water over a several hour period of exercise is vulnerable to this injury. A very low concentration of sodium can compromise the central nervous system, thus creating a potentially life-threatening condition. Hyponatremia can be completely avoided with adequate ingestion of sodium.
Prevention of Heat-Related Illnesses
All heat-related illnesses are completely preventable if the athlete uses caution when exercising in a heated environment. An athlete can only perform at an optimal level when dehydration and hyperthermia are minimized by the ingestion of ample volumes of fluid during exercise and by commonsense precautions in keeping cool . In a heated environment, it is essential that the athlete continually replaces lost fluids by drinking large quantities of water . Even low level dehydration can impair cardiovascular and thermoregulatory function and can reduce the capacity to exercise [35, 50]. The average adult performing minimal physical activity requires a minimum of 2.5 liters of water a day. A normal sweat loss rate for a person during an hour of exercise ranges between 0.8 and 3 liters of water.
Most athletes who drink only when thirsty can only replace about 50% of the water lost through sweating and evaporation, which is not enough to maintain homeostasis. There is absolutely no reason for an athlete to become hypohydrated (lacking water intake) . There are a number of physiological and potentially pathological effects resulting from a lack of water intake along with dehydration. These effects include reduced muscular strength and endurance, decreased blood and plasma volume, altered cardiac function, impaired thermoregulation, decreased kidney function, reduced glycogen stores, and a loss of electrolytes . It has been shown that replacing lost fluids with a sports drink is more effective than using water alone . Sports drinks are able to replace fluids and electrolytes that are lost through the sweat during activity and can provide energy to the working muscles. The small amount of sodium found in most sports drinks will allow the body to hold onto the fluid consumed rather than losing it through the urine . Not all sports drinks are the same, however, and many are not optimal for adequate replenishment. The optimal level of carbohydrates is 14 grams per 8 ounces of water. This results in the quickest fluid absorption. Therefore, sports drinks should not be diluted with extra water. Further, sports drinks which contain excessive carbohydrates are absorbed more slowly, which will negate its effects.
Prevention of heat-related illnesses also depends on heat acclimatization, which is discussed in-depth below.
Athletes with certain body characteristics can be more prone to heat-related illnesses. Athletes with a large amount of muscle mass, such as bodybuilders, are particularly prone to heat-related illnesses . Overweight individuals are also susceptible. The reason being metabolic heat is produced proportionately to surface area. Women are less susceptible to heat-related illnesses, as they are more physiologically efficient in body temperature regulation than men, even though women possess as many heat-activated sweat glands as men do. Women in general sweat less and manifest a higher heart rate when working in the heat .
Acclimatization to Exercise in the Heat
Effects of Heat Acclimatization
Repeated, prolonged exercise bouts in a heated environment can cause adaptations to the heat stress placed upon the body. The thermoregulatory system can be stressed so that it adapts to the heat demand by enabling the body to eliminate excess body heat more effectively. This process is known as heat acclimatization. With this adaptation, many adjustments are made in both blood flow and sweating. The rate of sweating during activity in the heat increases with heat acclimatization, and the amount of sweat produced often increases in the most exposed areas that are most effective at dissipating body heat. At the onset of exercise sweating will occur earlier in an acclimatized person, which will improve overall heat tolerance, resulting in a lower skin temperature. A lower skin temperature will increase the temperature gradient between the internal temperature to the skin temperature and the external temperature. Because heat loss is facilitated by blood, less blood needs to flow to the skin for body heat transfer; therefore more blood will be available to continue muscular function. In addition, the sweat produced is more diluted following training in the heat in an acclimatized individual, which will conserve the body’s mineral stores.
It can therefore be concluded that an individual’s heat loss capacity at a given workload can be enhanced by training; body temperatures during exercise increase less after training in the heat than in before training . Moreover, in an acclimatized individual, heart rate will increase more slowly after training in the heat. This particular adaptation is a result of the increased blood volume, and reduced blood flow to the skin. Both of these changes increase stroke volume. It is also important to note that these adaptations are not permanent; blood volume usually returns to its normal levels after 10 days. This is most likely due to the body’s efforts to retain sodium by expanding plasma volume.
In addition to the aforementioned adaptations to exercise in the heat, the workload of the individual can be positively affected as well. More work can be done before the onset of fatigue or exhaustion. Heat acclimatization reduces the rate of muscle glycogen use by as much as 50% to 60% (note that heat acclimatization is not related to exercising in the heat during repeated days of training as mentioned earlier, which quickly depletes muscle glycogen stores).
Achieving Heat Acclimatization
Heat acclimatization requires much more than merely exercising frequently in the heat. Rather, it depends on several factors:
· The environmental conditions during each exercise session
· The duration of exposure to heat
· The rate of internal heat production (as related to exercise intensity)
At this point in time, the research literature is not in total agreement, thereby making this section of this journal entry subject to reproof. The current research suggests that an athlete must exercise in a heated environment to attain heat acclimatization that carries over to exercise in the heat. Simply sitting in a hot environment (such as a sauna or out in the hot sun) will not provide these adaptations. Other studies suggest that at least partial heat acclimatization can be obtained simply through training, even in cooler environments. Scientists observed that when an athlete becomes acclimatized to heat stress, they are able to increase their performance in not only heated environments, but in cooled ones as well.
If an athlete must compete in hot weather, at least part of their training should be conducted in the heat of the day. Workouts in the heat over a five to ten day period will be enough to gain nearly complete heat acclimatization; however, during this training, workout intensity should be limited to 60% of max to help prevent excessive heat stress. Also during this training, proper precautions should be taken to avoid heat injury.
Physiological Responses to Exercise in Cooled Environments
Thus far, this author has established the physiological mechanisms for heat dissipation and bodily reactions to heated environments; however, it is obvious that the external environment is not always warmer than internal temperatures. In these instances, whole new adaptations and reactions take place to maintain normal body temperature and optimal physiological function.
For the purpose of this journal entry, cold stress will be referred to as any environmental condition that causes a loss of body heat that threatens homeostasis. The two major cold stressors are air and water.
To review briefly, the hypothalamus gland has a temperature set point of about 98.6°F, but can fluctuate slightly throughout the day without cause for concern. A decrease in either skin temperature or blood temperature stimulates the thermoreceptors to provide feedback to the thermoregulatory center within the hypothalamus to activate the mechanisms that will conserve body heat and increase heat production. The primary mechanisms utilized by the body to increase internal temperatures in cold environments are shivering, non-shivering thermogenesis, and peripheral vasoconstriction. Because these effectors (or mechanisms) of heat production and conservation are often less than adequate, individuals must rely on clothing and subcutaneous fat to aid in the insulation of the deep body tissues from the cold external environment.
Shivering: Shivering is a rapid, involuntary cycle of contraction and relaxation of skeletal muscles. This response can increase the body’s resting rate of heat production by four or five times that of normal.
Non-Shivering Thermogenesis: This mechanism involves the stimulation of the sympathetic nervous system to stimulate an increase in metabolic processes. Increasing the metabolic rate of tissues in turn increases the amount of internal heat production.
Peripheral Vasodilation: This method is also stimulated by the sympathetic nervous system. The SNS signals the smooth muscle surrounding the arterioles in the skin to contract, causing vasoconstriction. This effectively reduces the blood flow to the shell of the skin and prevents unnecessary heat loss. The metabolic rate for the skin (although seemingly counter to the non-shivering thermogenesis mechanism) will decrease, so the skin requires less oxygen.
Factors Affecting Loss of Bodily Heat
In cold environments, the body’s ability to meet the demands of thermoregulation is limited. Too much heat loss can occur. The mechanisms of conduction, convection, radiation, and evaporation are extremely efficient in heat dissipation; therefore, these mechanisms work counter to the body’s efforts to conserve heat in a cold environment and can dissipate heat faster than it is being produced by the body. Thermal balance depends on a wide range of factors that affect the gradient of body heat production and heat loss. The larger the difference in temperature of the skin to the external environment, the more internal heat is lost; however, there are a number of environmental and anatomical factors that can work to control the rate of heat loss.
Body Size and Composition: Insulating the body against cold is the most effective method of protection against hypothermia. Subcutaneous fat provides such insulation . The thermal conductivity of fat (its ability for heat transfer) is relatively low; therefore fat impedes heat transfer from the deep tissues to the skin. To simplify, individuals who have more fat mass conserve heat more efficiently in cold environments.
The relation of body surface area to body mass also influences the rate at which heat is dissipated into the external environment. Individuals who are tall and heavy have a small surface area to body mass ratio, making them less susceptible to hypothermia. Children and adolescents have a large area to mass ratio, making it more difficult for children to maintain normal body temperature in cold environments. There is little observable difference in heat dissipation based on body size and composition between males and females, although some evidence suggests that in cold water submersion, females may have an advantage due to a higher body fat percentage .
The body’s insulating shell consists of two main layers: the superficial skin together with subcutaneous fat, and the underlying muscle. When skin temperature drops, vasoconstriction in the skin coupled with the involuntary contraction of the skeletal muscles increase the shell’s total insulating capacity. It is estimated that vasoconstricted inactive muscle can provide as much as 85% of the body’s total insulation during exposure to extreme cold. This represents a resistance to heat loss that is two to three times higher than that of the overlying fat and skin tissues [58, 61].
Windchill: As with heat, air temperature alone is not a valid index of the amount of thermal stress from cold experienced by the individual. Wind creates a chill factor known as windchill. Windchill created the rate of heat loss via convection and conduction. Moreover, the more humid the external air, the greater the physiological stress, as outlined above. A dry, still day at 50°F in direct sunlight can be rather comfortable; however, if the temperature (50°F) is exactly the same, but the conditions are a higher humidity, cloud cover, and a light wind, the air will be very uncomfortable.
Heat Loss in Cold Water
In water, conduction is the greatest contributing factor to heat transfer. Water has a thermal conductivity about 26 times greater than that of air. This means that heat loss via conduction is 26 times faster in water than in air. With all variables considered, the body transfers heat about four times faster in water than it does in air of the same temperature. Humans can maintain a normal internal temperature when submerged in water when they remain inactive in temperatures down to about 89.6°F. When the water temperature is lower than this, the body becomes hypothermic at a rate directly proportional to the duration of their exposure of the thermal gradient [46, 53]. It is obvious that prolonged exposure to cold water can lead to extreme hypothermia and death. When submerged in water at 59°F, the body will experience a decrease in internal temperature of about 3.8°F per hour. If the water temperature was lowered to 39.2°F, internal temperature will decrease at a rate of 5.8°F per hour . The rate of heat loss will be further accelerated if the water is moving, since this promotes the increase in convection. Survival time in cold water under these conditions is quite brief. Victims can become weak and lose consciousness within minutes.
If the metabolic rate of the individual is low, such as when at rest, even moderately cool water can induce severe hypothermia. Exercise in cold water increases metabolic rate, and can offset some of this heat loss. For example, heat loss increases in a swimmer moving at high speeds through cold water (due to convection); however, the swimmer’s accelerated rate of metabolic heat production easily compensates for the greater heat transfer into the external environment. When exercise ceases, the skin will cool rapidly, as well as the internal temperature.
Cooling a muscle causes it to become weaker and lose flexibility. In response to muscle cooling, the nervous system will alter the normal muscle fiber recruitment patterns . There are some scientists that argue this adaptation will cause the muscle to decrease in efficiency, but this has yet to be definitively established. It is well established, however, that both muscle shortening velocity and power can decrease significantly when the temperature of the muscle is lowered. When an athlete attempts to work at a high level of performance when the muscle is cool (77°F or less) rather than when it is warm (95°F), they can experience fatigue earlier. If both the clothing the athlete is wearing and the exercise metabolism are sufficient in maintaining internal body temperature while exercising in a cold environment, exercise performance may be completely unimpaired. Once fatigue does set in, however, muscle activity will slow and body heat production will decrease. These effects of fatigue will occur more rapidly once fatigue is reached in a cold environment, as opposed to a warmer environment.
It is well-established that prolonged bouts of aerobic activity increase the mobilization and oxidation of free fatty acids (FFA), much more so than that of short duration, high-intensity training such as HIIT. The primary stimulus for this increased lipid metabolism is the release of catecholamines, specifically epinephrine and norepinephrine, into the vascular system. Cold environments increase the secretion of these two hormones, but FFA levels increase much less than during prolonged aerobic exercise in warmer conditions. As noted earlier, cold exposure initiates vasoconstriction of the vessels in the skin and subcutaneous tissues, yet it is in the subcutaneous tissue that is the major storage site for lipids (in the form of adipose tissue). Therefore, the vasoconstriction reduces blood flow to the area from which the FFA would be mobilized. It can be concluded that FFA levels do not increase as much as the elevated levels of catecholamines would indicate.
Blood glucose levels also play a major role in tolerance to cold temperatures and also to exercise endurance. Hypoglycemia (low blood sugar) suppresses the shivering response to cold and significantly reduces internal temperature, both of which are detrimental to performance and overall health in a cold environment. Blood glucose levels are maintained reasonably well with a diet with a proper balance of proteins, carbohydrates and fats. Low-carbohydrate diets, such as Atkins and CKD diets will significantly reduce the body’s ability to maintain constant body temperature when exposed to cold environments, which in turn will severely inhibit performance. Muscle glycogen, on the other hand, is used at a higher rate in cold temperatures (especially cold water) than in warmer conditions .
Brown fat can aid in increasing internal temperature, as it produces a large amount of heat during ß-oxidation. In brown fat, mitochondria density is high and oxidizes the fat in such a way as to produce a great deal more heat than ATP. Brown fat is predominantly found in younger animals and humans, but some adults may keep brown fat after adolescence.
Health Risks during Exercise in Cooled Environments
Individuals who are immersed in near-freezing water will die within mere minutes when the internal body temperature decreases below 77°F. In some very extreme cases, individuals have survived internal temperatures as low as 64.4°F , and in one case occurring in 1958, a woman was deliberately cooled to an internal temperature of 48.2°F under anesthesia and was finally revived after a cardiac arrest lasting about 60 minutes .
With these extreme cases aside, the body begins to lose hypothalamal control over thermoregulation once the internal temperature drops below 94.1°F. Control is completely lost once internal temperature drops below 85.1°F. This loss of function is associated with the slowdown of metabolic reactions to one half their normal rates for every 18°F decrease in cellular temperature. As a result, the cooling of the body can result in a coma and then death.
Excessive exposure to cold environments can cause damage to both peripheral tissues and the life-supporting cardiovascular and respiratory systems. The most significant affect of hypothermia is on the heart. Deaths associated with hypothermia are a result of cardiac arrest while respiration was still somewhat functional. Cooling of the internal cavity influences the sinoatrial node, which controls the nerve impulses leading to the heart to set heart rate. Cooling of heat tissue leads to a progressive decline in heart rate and then to cardiac arrest . A decrease in core temperature, coupled with a decrease in heart rate, significantly lowers cardiac output.
There is some question as to whether or not rapid, deep breathing (as in exercise) in cold environments can damage the respiratory tract; however, it has been shown that the cold air is rapidly warmed in the trachea, even when the air inhaled is less than –13°F . Even at this temperature, the air can be almost instantaneously warmed to an adequate 59°F by the time it has traveled about 5 cm into the nasal passage. Therefore, there is absolutely no shred of damage posed by inhalation of cold air, although heavy breathing through the mouth has been shown to cause a minor degree of irritation to the mouth, pharynx, trachea, and even bronchi when the air temperature is below 10°F. Nonetheless, no major damage is incurred. Excessive exposure to cold environments can also affect respiratory function by decreasing the rate and volume of respiration.
Treatment of hypothermia includes protecting the victim from further exposure to the cold and providing dry clothing and warm beverages. Cases of severe hypothermia must be handled with caution to help prevent a cardiac arrhythmia. This requires the victim to be slowly warmed.
Skin exposed directly to a cold environment can freeze when external temperatures reach just below 32°F. Due to the heat retention mechanisms the body initiates during exposure to cold environments, the air temperature actually required to freeze body parts such as the fingers, nose and ears is about –20°F. During this type of extreme cold, vasoconstriction in the skin will become so effective that blood flow to the extremities may cease, causing the tissues to die from a lack of oxygen and nutrients. This is known as frostbite. If not treated promptly, frostbite can lead to conditions such as gangrene and a loss of tissue (forced amputation). Frostbitten body parts must be left untreated until given a chance to thaw.
Acclimatization to Exercise in Cooled Environments
To date, information about acclimatization to cold environments is somewhat limited; however, the available data suggests that chronic daily exposure to cold water will increase subcutaneous body fat . Most of the research regarding cold acclimatization originates from the study of Australian Aborigines who are normally exposed to low temperatures at night and high temperatures during the day . Compared with individuals who are unacclimatized, the Aborigines were able to sleep more comfortably in the cold with little protection from the environment, and only minor changes in their metabolism and internal temperatures were recorded. The unacclimatized subjects, on the other hand, experienced significant distress and considerable difficulty in maintaining a constant body temperature.
Some data suggests that chronic exposure to cold environments alters peripheral blood flow and overall skin temperatures, yet other studies suggest that appendages (such as the hands) that are chronically exposed to cold temperatures show an increase in vasodilation and local warming of the exposed skin.
Maintaining homeostasis is of prime importance when exercising in both hot and cold environments. Failing to do so will result in a decrease in performance and an increase in the risk of developing potentially fatal situations. These conditions are amplified in athletes such as bodybuilders, due to the intensity of training, the pre-contest water depletion and the larger than average surface area of bodybuilding athletes. All heat- and cold-related illnesses are completely preventable, and there is no reason an athlete should become predisposed to said illnesses due to a lack of fluid ingestion.
By gaining an understanding of how the body’s thermoregulatory mechanisms act, the well-informed athlete can make better decisions when it comes to training in extreme environments to ensure operation at peak performance in the safest possible manner. Bodybuilders are known for going to extremes to achieve seemingly inhuman physiques, but there is no reason to go to such extremes when it comes to proper fluid ingestion.
Keep it hardcore!
Joe “Yu Yevon” King
Administrator of Hyperplasia Research
Writer for the Journal of Hyperplasia Research
Sources Cited and References/Research Credited:
1. God: The Bible.
2. American College of Sports Medicine. Heat and cold illnesses during distance running: ACSM position stand. Med Sci in Sports and Exerc, 28(12):I-x, 1995.
3. American College of Sports Medicine: position stand on exercise and fluid replacement, Med and Sci Sports Exerc 28(17), 1996.
4. Armstrong LE, Epstein Y, Greenleaf JE: Heat and cold illnesses during distance running, Med Sci Sports Exerc 28(12), 1996.
5. T. H. Benzinger. Heat regulation: homeostasis of central temperature in man, Physiol Rev, Oct 1969; 49: 671 - 759.
6. Bernard TE: Risk management for preventing heat illness in athletes, Ath Ther Today 1(4):19, 1996.
7. Bodine KL: Avoiding hyopthermia: caution, forethought and preparation, Sports Medicine Alert 6(1):6, 2000.
8. Brzozowski-Gardner C: New options under foot. Ath Management 13(3):47, 2001.
9. Casa DJ, Armstrong LE, Hillman S: National Athletic Trainers’ Association position statement: fluid replacement for athletes, J Ath Train 35(2):212, 2000.
10. Casa DJ: Exercise in the heat. I. Fundamentals of thermal physiology, performance implications, and dehydration, J Ath Train 34(3):246, 1999.
11. Casa DJ: Exercise in the heat. II. Critical concepts in rehydration, exertional heat illnesses, and maximizing athletic performance, J Ath Train 34(3):253, 1999.
12. Constance R. Chu, Lee D. Kaplan, Freddie H. Fu, Lawrence S. Crossett, and Rebecca K. Studer. Recovery of Articular Cartilage Metabolism Following Thermal Stress Is Facilitated by IGF-1 and JNK Inhibitor, Am. J. Sports Med., Jan 2004; 32: 191 - 196.
13. Cooper KE: Molecular Biology of Thermoregulation: Some historical perspectives on thermoregulation, J Appl Physiol, Apr 2002; 92: 1717 - 1724.
14. Costill DL: Inside running, Basics of Sports physiology. Indianapolis: Benchmark Press, 1986.
15. Costill DL, Kammer WF, Fisher A: Fluid ingestion during distance running. Archives of environmental health, 21, 520-525, 1970.
16. Coyle E: Fluid and carbohydrate replacement during exercise: how much and why? Sports Sci Exchange 7(50):1, 1994.
17. Davis M: Ultraviolet therapy. In Prentice W, editor: Therapeutic modalities in sports medicine, St Louis, 2003, McGraw Hill.
18. Embleton P, Thorne G: Anabolic Primer. MuscleMag International, 1998.
19. Epstein Y, Moran D, Shapiro Y: Exertional heat stroke: a case series, Med Sci Sports Exerc 31(2):224, 1999.
20. Faulkner JA, Claflin DR, McCully KK: Muscle function in the cold. In JR Sutton, CS Houston, G Goates, editors: Hypoxia and the cold. New York, Praeger, 1987.
21. Febbraio MA: Does muscle function and metabolism affect exercise performance in the heat? Exer Sports Sci Reviews, 28, 171-176, 2000.
22. Fink W, Costill DL, Van Handel P, Getchell L: Leg muscle metabolism during exercise in the heat and cold. European J of Appl Physiol, 34, 183-190, 1975.
23. FLOREZ M, ROGER B. McDONALD. Cold-Induced Thermoregulation and Biological Aging, Physiol Rev, Apr 1998; 78: 339 - 358.
24. Fritz R, Perrin D: Cold exposure injuries: prevention and treatment. In Ray R, editor: Clinics in sports medicine, Philadelphia, 1989, Saunders.
25. Gisolfi CV, Wegner CB: Temperature regulation during exercise: Old concepts, new ideas. Exer and Sport Sci Reviews, 12, 339-372, 1984.
26. Gutierrez G: Solar injury and heat illness, Physician Sportsmed 23(7):43, 1995.
27. Hayward JN: Functional and morphological aspects of hypothalamic neurons, Physiol Rev, Jul 1977; 57: 574 - 658.
28. Hayward MG, Keatinge WR: Roles of subcutraneous fat and thermoregulatory reflexes in determining ability to stabilize body temperature in water. J Apply Physiol, 320, 229-251, 1981.
29. Hecht P, Kei Hayashi, A. James Cooley, Yan Lu, Gary S. Fanton, George Thabit, III, and Mark D. Markel. The Thermal Effect of Monopolar Radiofrequency Energy on the Properties of Joint Capsule: An In Vivo Histologic Study Using a Sheep Model, Am. J. Sports Med., Nov 1998; 26: 808 - 814.
30. Hunter SL et al: Malignant hyperthermia in a college football player, Physician Sportsmed 15(12):77, 1987.
31. Kang BS, Song SH, Suh CS, Hong SK: Changes in body temperature and basal metabolic rate of the ama. J Apply Physiol, 18, 483-488, 1963.
32. Kanzanbach TL, Dexter WW: Cold injuries: Protecting your patients from the dangers of hypothermia and frostbite, Post Graduate Medicine 105(1):72, 1999.
33. Kapit W, Robert I. Macey, and Esmail Meisami, The Physiology Coloring Book, Second Edition. Addison Wesley Longman, Inc. San Francisco, CA. 2000.
34. Kay D, Marino FE: Fluid ingestion and exercise hyperthermia: implications for performance, thermoregulation, metabolism, and development of fatigue, J Sports Sci 18(2):71, 2000. Johnson R, Tulin 35. B: Travel fitness, Champaign, Ill, 1995, Human Kinetics.
36. King DS, Costill DL, Fink WJ, Hargreaves M, Fielding RA: Muscle metabolism during exercise in the heat in unacclimatized and acclimatized humans. J Apply Physiol 59, 1350-1354, 1985.
37. King JD: Endocrine Insanity Part 1. J Hyper Res, 2003.
38. King JD: Endocrine Insanity Part 2. J Hyper Res, 2003.
39. Knochel JP: Management of heat conditions, Ath Ther Today 1(4):30, 1996.
40. Knowlton FP, Starling EH. The influence of variations in temperature and blood pressure on the performance of the isolated mammalian heart. J Apply Physiol, 44, 206-219, 1912.
41. Kuznetz LH: A two-dimensional transient mathematical model of human thermoregulation, Am J Physiol Regulatory Integrative Comp Physiol, Nov 1979; 237: R266 - 277.
42. McArdle WD, Katch Fl, Katch VL: Exercise physioloy, Philadelphia, 2001, Lea & Febiger.
43. McCann DJ, Adams WC: Wet Bulb globe temperature index and performance in competitive distance runners, Med Sci Sports Exerc 29(7):955, 1997.
44. McDonald, C. Day, K. Carlson, J. S. Stern, and B. A. Horwitz: effect of age and gender on thermoregulation. J Physiol Regulatory Integrative Comp Physiol, Oct 1989; 257: R700 - 704.
45. Mellion MB, Shelton GL: Thermoregulation, heat illness, and safe exercise in the heat. In Mellion MB, editor: Office sports medicine, ed 2, Philadeplhia, 1996, Hanley & Belfus.
46. Molnar GW. Survival of hypthermia by man immersed in the ocean. J of Amer Med Association, 131, 1046-1050, 1946.
47. Montain SJ, Maughan RJ, Sawka MN: Fluid replacement strategies for exercise in hot weather, Ath Ther Today 1(4):24, 1996.
48. Murray B: Fluid replacement: the American College of Sports Medicine position stand. Sports Sci Exchange 9(4):1, 1996.
49. Murray R: Dehydration, hyperthermia, and athletes: Science and practive, J Ath Train 31(3):248, 1996.
50. Murray R: Guidelines for fluid replacement during exercise. Australian Journal of Nutrition and Dietetics 53(4 suppl):S17, 1996.
51. Murray R: Practical advice for exercising in cold weather. In Murray R: Endurance training for performance, Barrington, Ill, 1995, Gatorade Sports Medicine Institute.
52. NCAA sports medicine handbook, 2001-2002, Indianapolis, 2001, National Collegiate Athletic Association.
53. Newburgh LH: Physiology of heat regulation. Philadelphia: Saunders, 1949.
54. Newmark SR, FR Toppo, and G Adams. Fluid and electrolyte replacement in the ultramarathon runner, Am. J. Sports Med., Jul 1991; 19: 389 - 391.
55. Niazi SA, Lewis FJ. Profound hypothermia in man. Annals of Surgery, 147, 264-266, 1958.
56. Palca JW, J. M. Walker, and R. J. Berger: Thermoregulation, metabolism, and stages of sleep in cold-exposed men, J Appl Physiol, Sep 1986; 61: 940 - 947.
57. Pandolf K: Avoiding heat illness during exercise. In Torg J, Shephard R, editors: Current therapy in sports medicine, St Louis, 1995, Mosby.
58. Pendergast DR: The effect of body cooling on oxygen transport during exercise. Med Sci in Sports Exerc, 20(suppl):S171-S176,1988.
59. Prentice WE: Arnheim’s Principles of Athletic Training, ed. 11. Prentice WE, editor: McGraw Hill, 2003.
60. Pugh LG, Edholm DG: The physiology of channel swimmers. Lancet 2, 761-767, 1955.
61. Rennie DW. Tissue heat transfer in water: Lessons from the Korean divers. Med Sci Sports Exerc, 20, S177, 1988.
62. Robinson S: Physiological adjustments to heat. In LH Newburgh, editor: Physiology of heat regulation and the science of clothing. Philadelphia, Saunders, 1949.
63. Romanovsky AA, O. Shido, S. Sakurada, N. Sugimoto, and T. Nagasaka. Endotoxin shock: thermoregulatory mechanisms, Am J Physiol Regulatory Integrative Comp Physiol, Apr 1996; 270: R693 - 703.
64. Sandor RP: Heat illness: on-site diagnosis and cooling. Physician Sportsmed 25(6):35, 1997.
65. Sawka MN. R. Gonzalez, A. J. Young, S. R. Muza, K. B. Pandolf, W. A. Latzka, R. C. Dennis, and C. R. Valeri: Polycythemia and hydration: effects on thermoregulation and blood volume during exercise-heat stress, Am J Physiol Regulatory Integrative Comp Physiol, Sep 1988; 255: R456 - 463.
66. Schmidt I. and E. Simon. Negative and positive feedback of central nervous system temperature in thermoregulation of pigeons, Am J Physiol Regulatory Integrative Comp Physiol, Sep 1982; 243: R363 - 372.
67. Scholander PF, Hammel HT, Hart JS, Lemessurier DH, Steen J. Cold adaptation in Australian aborigines. J Appl Physiol, 13, 211-218, 1958.
68. Simon E, F. K. Pierau, and D. C. Taylor. Central and peripheral thermal control of effectors in homeothermic temperature regulation, Physiol Rev, Apr 1986; 66: 235 - 300.
69. Sparling PB, Milford-Stafford M: Keeping sports participants safe in hot weather, Physician Sportsmed 27(7):27, 1999.
70. Thein L: Environmental conditions affecting the athlete, J Orthop Sports Phys Ther 21(3):158, 1995.
71. Thompson RL, Hayward JS: Wet-cold exposure and hyperthermia: Thermal and metabolic responses to prolonged exercise in the rain, J Appl Physiol 81(3):1128, 1996.
72. Trappe TA, Starling RD, Jozsi AC, Goodpaster BH, Trappe SW, Nomura T, Obara S, Costill DL: Thermal responses to swimming in three water temperatures: Influence of a wet suit. Med Sci Sports Exerc, 27, 1214-1221, 1995.
73. Vellerand A: Exercise in the cold. In Torg J, Shephard R, editors: Current therapy in sports medicine, St Louis, 1995, Mosby.
74. Venom: Effect of plasma volume on myofibril hydration, nutrient delivery, and athletic performance. J Hyper Res, 2004.
75. Webb P: Air temperature in respiratory tracts of resting subjects in the cold. J Apply Physiol 4, 378-382, 1951.
76. Wyndham CHJ: The physiology of exercise under heat stress. Annual Rev of Physiol, 35, 193-2.., 1973.
77. Young AJ, Sawka MN, Neufer PD, Muza, SR, Askew EW, Pandolf KP: Thermoregulation during cold water immersion is unimpaired by low muscle glycogen levels. J Appl Physiol, 66, 1809-1816, 1989.