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Humans live their entire lives within a very small, fiercely protected range of internal body temperatures. To maintain internal temperature within these limits, people have developed very effective and in some instances specialized physiological responses to acute thermal stresses. By far, the largest source of heat imparted to the body from metabolic heat production M. At rest, a metabolic rate of ml O 2 per minute creates a heat load of approximately Watts. Even at such a mild to moderate work intensity, body core temperature would rise approximately one degree centigrade every 15 min were it not for an efficient means of heat dissipation.
In fact, very fit individuals can produce heat in excess of 1, W for 1 to 3 hours without heat injury Gisolfi and Wenger Heat can also be gained from the environment via radiation R and convection C if the globe temperature a measure of radiant heat and air dry-bulb temperature, respectively, exceed skin temperature. These avenues of heat gain are typically small relative to M, and actually become avenues of heat loss when the skin-to-air thermal gradient is reversed.
These relations are discussed elsewhere in this chapter. Under cool to thermoneutral conditions, heat gain is balanced by heat loss, no heat is stored, and body temperature equilibrates; that is:. Core temperature T c represents internal or deep body temperature, and can be measured orally, rectally or, in laboratory settings, in the oesophagus or on the tympanic membrane eardrum. The temperature of the shell is represented by mean skin temperature T sk.
The average temperature of the body T b at any time is a weighted balance between these temperatures, that is. When confronted with challenges to thermal neutrality heat or cold stressesthe body strives to control T c through physiological adjustments, and T c provides the major feedback to the brain to coordinate this control. In this region are nerve cells which respond to both heating warm-sensitive neurons and cooling cold-sensitive neurons.
This area dominates control of body temperature by receiving afferent sensory information about body temperature and sending efferent als to the skin, the muscles and other organs involved in temperature regulation, via the autonomic nervous system.
Other areas of the central nervous system posterior hypothalamus, reticular formation, pons, medulla and spinal cord form ascending and descending connections with the POAH, and serve a variety of facilitory functions. When body temperature falls below the set point, heat gain responses decreasing skin blood flow, shivering are initiated.
Much work is yet to be done toward a full understanding of the mechanisms associated with the thermoregulatory set point. Whatever its basis, the set point is relatively stable and is unaffected by work or ambient temperature. In fact, the only acute perturbation known to shift the set point is the group of endogenous pyrogens involved in the febrile response.
A core temperature below the set point creates a negative load error, resulting in heat gain shivering, vasoconstriction of the skin being initiated. A core temperature above the set point creates a positive load error, leading to heat loss effectors skin vasodilatation, sweating being turned on. In each case, the resultant heat transfer decreases the load error and helps return the body temperature to a steady state.
Temperature Regulation in the Heat As mentioned above, humans lose heat to the environment primarily through a combination of dry radiation and convection and evaporative means.
While skin vasodilatation often in small increases in dry radiative and convective heat loss, it functions primarily to transfer heat from the core to the skin internal heat transferwhile evaporation of sweat provides an extremely effective means of cooling the blood prior to its return to deep body tissues external heat transfer.
By contrast, under conditions of severe hyperthermia such as high-intensity work in hot conditions, the core-to-skin thermal gradient is smaller, and the necessary heat transfer is accomplished by large increases in SkBF. Active vasodilatation involves sympathetic nerve als from the hypothalamus to the skin arterioles, but the neurotransmitter has not been determined. T c rises as muscular work is initiated and metabolic heat production begins, and once some threshold T c is reached, SkBF also begins to increase dramatically.
This basic thermoregulatory relationship is also acted upon by non-thermal factors. This second level of control is critical in that it modifies SkBF when overall cardiovascular stability is threatened. The veins in the skin are very compliant, and a ificant portion of the circulating volume pools in these vessels.
This aids in heat exchange by slowing the capillary circulation to increase transit time; however, this pooling, coupled with fluid losses from sweating, may also decrease the rate of blood return to the heart. Among the non-thermal factors which have been shown to influence SkBF during work are upright posture, dehydration and positive-pressure breathing respirator use.
These act through reflexes which are turned on when cardiac filling pressure is decreased and stretch receptors located in the large veins and right atrium are unloaded, and are therefore most evident during prolonged aerobic work in an upright posture. These reflexes function to maintain arterial pressure and, in the case of work, to maintain adequate blood flow to active muscles.
Thus, the level of SkBF at any given point in time represents the aggregate effects of thermoregulatory and non-thermoregulatory reflex responses. The need to increase blood flow to the skin to aid in temperature regulation greatly impacts on the ability of the cardiovascular system to regulate blood pressure. For this reason, a coordinated response of the entire cardiovascular system to heat stress is necessary. What cardiovascular adjustments occur that allow for this increase in cutaneous flow and volume?
At higher levels of work, maximal heart rate is reached, and this tachycardia is therefore incapable of sustaining the necessary cardiac output. The second way in which the body supplies a high SkBF is by distributing blood flow away from such areas as the liver, kidneys and intestines Rowell This redirection of flow can provide an additional to 1, ml of blood flow to the skin, and helps offset the detrimental effects of peripheral pooling of blood.
Thermoregulatory sweat in humans is secreted from 2 to 4 million eccrine sweat glands scattered non-uniformly over the body surface. Unlike apocrine sweat glands, which tend to be clustered on the face and hands and in the axial and genital regions and which secrete sweat into hair follicles, eccrine glands secrete sweat directly onto the skin surface.
This sweat is odourless, colourless and relatively dilute, since it is an ultrafiltrate of plasma. Thus it has a high latent heat of vaporization and is ideally suited for its cooling purpose. As an example of the effectiveness of this cooling system, a man working at an oxygen cost of 2. With efficient evaporation of about 16 g of sweat per minute a reasonable ratethe rate of heat loss can match the rate of heat production, and body core temperature can be maintained at a steady state; that is.
Eccrine glands are simple in structure, consisting of a coiled secretory portion, a duct and a skin pore. The volume of sweat produced by each gland is dependent upon both the structure and the function of the gland, and total sweating rate in turn depends on both the recruitment of glands active sweat gland density and sweat gland output. The fact that some people sweat more heavily than others is attributable mainly to differences in sweat gland size Sato and Sato Heat acclimation is another major determinant of sweat production.
With ageing, lower sweating rates are attributable not to fewer activated eccrine glands, but to a decreased sweat output per gland Kenney and Fowler This decline probably relates to a combination of structural and functional alterations which accompany the ageing process. Like vasomotor als, nerve impulses to the sweat glands originate in the POAH and descend through the brainstem. The fibres which innervate the glands are sympathetic cholinergic fibres, a rare combination in the human body. While acetylcholine is the primary neurotransmitter, adrenergic transmitters catecholamines also stimulate eccrine glands.
In many ways, control of sweating is analogous to control of skin blood flow. Both have similar onset characteristics threshold and linear relationships to increasing T c. The back and chest tend to have earlier onsets of sweating, and the slopes for the relationship of local sweat rate to T c are steepest for these sites. Like SkBF, sweating is modified by non-thermal factors such as hypohydration and hyperosmolality. Such areas of skin, due to their continuously wet state, decrease sweat output. This serves as a protective mechanism against continued dehydration, since sweat which stays on the skin rather than evaporating serves no cooling function.
If sweating rate is adequate, evaporative cooling is determined ultimately by the water vapour pressure gradient between the wet skin and the air surrounding it. Thus, high humidity and heavy or impermeable clothing limit evaporative cooling, while dry air, air movement about the body and minimal, porous clothing facilitate evaporation.
One important difference in the way humans respond to cold compared to heat is that behaviour plays a much greater role in thermoregulatory response to cold. A second difference is the greater role played by hormones during cold stress, including the increased secretion of catecholamines norepinephrine and epinephrine and thyroid hormones. An effective strategy against heat loss from the body through radiation and convection is to increase the effective insulation provided by the shell. Constriction of the cutaneous vessels is more pronounced in the extremities than on the trunk.
Like active vasodilatation, skin vasoconstriction is also controlled by the sympathetic nervous system, and is influenced by T cT sk and local temperatures. The effect of skin cooling on the heart rate and blood pressure response varies with the area of the body which is cooled, and whether the cold is severe enough to cause pain. To further confound the complexity of the overall response to cold, there is a wide range of variability in responses from one person to another.
If the cold stress is of sufficient magnitude to decrease body core temperature, HR may either increase due to sympathetic activation or decrease due to the increased central blood volume. A specific case of interest is termed cold-induced vasodilatation CIVD. When the hands are placed in cold water, SkBF initially decreases to conserve heat. As tissue temperatures drop, SkBF paradoxically increases, decreases again, and repeats this cyclical pattern.
It has been suggested that CIVD is beneficial in preventing tissue damage from freezing, but this is unproven. Mechanistically, the transient dilation probably occurs when the direct effects of the cold are severe enough to decrease nerve transmission, which transiently overrides the effect of the cold on the blood vessel sympathetic receptors mediating the constrictor effect. As body cooling progresses, the second line of defence is shivering.
Shivering is the random involuntary contraction of superficial muscle fibres, which does not limit heat loss but rather increases heat production. Since such contractions do not produce any work, heat is generated. A resting person can increase his or her metabolic heat production about three- to fourfold during intense shivering, and can increase T c by 0.
The als to initiate shivering arise principally from the skin, and, in addition to the POAH region of the brain, the posterior hypothalamus is also involved to a large extent. Although many individual factors contribute to shivering and cold tolerance in generalone important factor is body fatness. When a person is exposed to warm environmental conditions the physiological heat loss mechanisms are activated in order to maintain normal body temperature. Heat fluxes between the body and the environment depend on the temperature difference between:. The surface temperature of the person is regulated by physiological mechanisms, such as variations in the blood flow to the skin, and by evaporation of sweat secreted by the sweat glands.
Also, the person can change clothing to vary the heat exchange with the environment. The warmer the environmental conditions, the smaller the difference between surrounding temperatures and skin or clothing surface temperature. At environmental temperatures above the surface temperature, heat is gained from the surroundings. In this case this extra heat together with that liberated by the metabolic processes must be lost through evaporation of sweat for the maintenance of body temperature. Thus evaporation of sweat becomes more and more critical with increasing environmental temperature.
Given the importance of sweat evaporation it is not surprising that wind velocity and air humidity water vapour pressure are critical environmental factors in hot conditions. If the humidity is high, sweat is still produced but evaporation is reduced.
Sweat which cannot evaporate has no cooling effect; it drips off and is wasted from a thermoregulatory point of view. About one-third of the water in the body, the extracellular fluid, is distributed between the cells and in the vascular system the blood plasma.
The remaining two-thirds of the body water, the intracellular fluid, is located inside the cells. The composition and the volume of the body water compartments is very precisely controlled by hormonal and neural mechanisms. Sweat is secreted from the millions of sweat glands on the skin surface when the thermoregulatory centre is activated by an increase in body temperature. The sweat contains salt NaCl, sodium chloride but to a lesser extent than the extracellular fluid.
Thus, both water and salt are lost and must be replaced after sweating. In neutral, comfortable, environmental conditions, small amounts of water are lost by diffusion through the skin. This is seen by a rise in heart rate HR HR increases about five beats per minute for each per cent loss of body water and a rise in body core temperature. This is partly due to the loss of fluid from the vascular system figure A loss of water from the blood plasma reduces the amount of blood which fills the central veins and the heart.
Each heart beat will therefore pump a smaller stroke volume. As a consequence the cardiac output the amount of blood which is expelled by the heart per minute tends to fall, and the heart rate must increase in order to maintain the circulation and the blood pressure.
A physiological control system called the baroreceptor reflex system maintains the cardiac output and blood pressure close to normal under all conditions. The reflexes involve receptors, sensors in the heart and in the arterial system aorta and carotid arterieswhich monitor the degree of stretching of the heart and vessels by the blood which fills them.
Impulses from these travel through nerves to the central nervous system, from which adjustments, in case of dehydration, cause a constriction in the blood vessels and a reduction in blood flow to splanchnic organs liver, gut, kidneys and to the skin. In this way the available blood flow is redistributed to favour circulation to the working muscles and to the brain Rowell Severe dehydration may lead to heat exhaustion and circulatory collapse; in this case the person cannot maintain the blood pressure, and fainting is the consequence.
In heat exhaustion, symptoms are physical exhaustion, often together with headache, dizziness and nausea. The main cause of heat exhaustion is the circulatory strain induced by water loss from the vascular system. The decline in blood volume le to reflexes which reduce circulation to the intestines and the skin. The reduction in skin blood flow aggravates the situation, since heat loss from the surface decreases, so the core temperature increases further. The subject may faint due to a fall in blood pressure and the resulting low blood flow to the brain. The lying position improves the blood supply to the heart and brain, and after cooling and having some water to drink the person regains his or her well-being almost immediately.
The gradual reduction in skin circulation makes the temperature rise more and more, and this le to a reduction, even a stop in sweating and an even faster rise in core temperature, which causes circulatory collapse and may result in death, or irreversible damage to the brain. Changes in the blood such as high osmolality, low pH, hypoxia, cell adherence of the red blood cells, intravascular coagulation and damage to the nervous system are findings in heat stroke patients.
The reduced blood supply to the gut during heat stress can provoke tissue damage, and substances endotoxins may be liberated which induce fever in connection with heat stroke Hales and Richards The sweat contains less salt than the body fluid compartments. This means that they become more salty after sweat loss.Who wants to exchange body heat
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Methods of Heat Transfer