Temperature Regulation PDF

Temperature Regulation Jennifer Connolly, PhD Email: [email protected] 1 Learning Objectives 1. Differentiate between core body temperature (Tb), skin temperature (Ts), ambient 2. 3. 4. 5. 6. 7. 8. temperature (Ta) and hypothalamic set-point temperature (Tset) Describe the circadian rhy...

Temperature Regulation Jennifer Connolly, PhD Email: [email protected] 1 Learning Objectives 1. Differentiate between core body temperature (Tb), skin temperature (Ts), ambient 2. 3. 4. 5. 6. 7. 8. temperature (Ta) and hypothalamic set-point temperature (Tset) Describe the circadian rhythm and temperature variability during the female menstrual cycle. Describe the mechanisms of heat production, heat storage and heat dissipation. Describe the mechanisms of heat transport from core of the body to skin. Describe normothermia, hypothermia and hyperthermia and regulatory mechanisms for maintaining normothermia. Describe the functions of the thermoregulatory center Describe how the body regulates the body temperature back to normal if body temperature is higher or lower than hypothalamic thermal set point. Define fever and describe the mechanisms of heat production and heat dissipation during fever and recovery. 2 Overview • Body heat is produced by muscular exercise, assimilation of • • • • • food & all of the vital processes that contribute to Basal Metabolic Rate (BMR) Body heat is lost by radiation, conduction, convection & by evaporation of water The balance between heat production & heat loss determines Body Temperature Chemical reactions & enzyme systems have narrow temperature ranges; thus, normal body function depends on a relatively constant body temperature Body temperature is tightly regulated by reflex adjustments in heat production & heat loss Thermoregulation is primarily under hypothalamic control BMR: basal metabolic rate 3 Regional body temperatures • “Normal” Core Body Temperature (Tb) o 37ᵒC (98.6ᵒF) o Range: 36 - 37.5ᵒC (97 - 99.5ᵒF) o Tb is homeostatically regulated • Skin temperature (Ts) o Varies according to: • Ambient Temperature (Ta) • Cutaneous blood flow Tb: Core Body Temperature Ts: Skin Temperature Ta: Ambient (environmental) Temperature 4 Variations in regional temperatures • Rectal temp ↑ ~0.5°C compared to oral o Rectal > ear > oral > axillary • Tb varies with activity & Ta o ↑ during exercise : ~40°C o ↓ extreme cold weather : ~35°C • Skin temperature (Ts) varies widely with changes in Ta • Naked individual at rest in a room exposed to Ta ~23°C to 35°C in dry air can maintain an almost constant core Tb despite wide changes in Ta & Ts Note: In reference to the data on this chart, despite changes in ambient (environmental) temperature of 23-35°C , core body temperature (rectal temperature) remain relatively stable (around 37°C) while skin temperature fluctuates. Alterations in skin temperature reflect the degree of blood flow to the skin, i.e., as ambient temperature increases blood flow to the skin increases, increasing skin temperature. This is one mechanism by which heat is lost from the body in order to maintain constant core body temperature. 5 Rhythmic changes in body temperature (Tb) Circadian (diurnal) rhythm Female monthly rhythm 37±0.6ᵒC (98.6±1ᵒF) +0.5ᵒC during luteal phase of menstrual cycle Post-ovulation (due to progesterone) Pre-ovulation The normal core body temperature (Tb) in adults undergoes a regular circadian (24hr cycle) fluctuation ~0.6ᵒC, where body temperature is usually lowest at around 6am and highest around 6pm. In women, an additional monthly cycle of temperature variation is characterized by a rise in Tb in the immediate post-ovulation period. Tb increases by ~0.5ᵒC in the postovulatory period owing to the action of the hormone PROGESTERONE which is secreted from the ovarian corpus luteum. 6 Importance of maintaining a stable core body temperature Skin vasoconstriction Skin vasodilation 7 Basic mechanism of heat balance • • • • • Metabolism Muscular activity Food intake Brown adipose tissue Environment • • • • Heat Gain Evaporation Conduction Convection Radiation Heat Loss Body temperature is constant when heat gain = heat loss Gain > Loss = ↑ Heat Storage (↑ Tb) Gain < Loss = ↓ Heat Storage (↓ Tb) Thermal balance: The temperature of the body is the result of a balance between heat gain and heat loss. When the body is in thermal balance the amount of heat produced and the amount of heat lost (or dissipated) are equal, such that the Tb does not change; it remains constant. When the rate of heat production in the body is greater than the rate at which heat is being lost, heat builds up in the body (i.e., it is stored in the body) and body temperature (Tb) rises. Conversely, when heat loss is greater than heat production, both body heat and body temperature decreases. When the rate of heat production = rate of heat loss, heat storage is negligible. 8 Heat storage Heat capacity • Energy required to change the temperature of 1 kg of a substance by 1ᵒC • Rate at which the body temperature rises or falls as its heat content ↑ or ↓ • Water has a high heat capacity ➢ 1 kcal of heat energy is required to ↑ temperature of 1 kg of water by 1ᵒC • Body is ~70% water: ➢ ~1 kcal of heat energy is required to ↑ temperature of 1 kg of the body by 1ᵒC ➢ ~70 kcal of heat energy is required to ↑ body temperature of 70 kg individual by 1ᵒC • Varies little between individuals The specific heat capacity of a substance is the amount of energy needed to change the temperature of 1 kg of the substance by 1°C. Water has a particularly high heat capacity. This means that water can absorb large amounts of heat energy before its temperature raises. This makes water useful for storing heat energy. 1 kcal of heat energy is required to increase the temperature if 1 kg of water by 1°C. Thus, for a 70 kg individual, a 70 kcal increase in heat energy will increase Tb by 1°C. 9 Mechanisms of heat production • Catabolism liberates energy from organic molecules & the energy liberated is used to do work (40%) or is released as heat (60%) Metabolism • Basal Metabolic Rate (BMR): minimum level of energy required to exist accounts for 50-70% of daily energy expenditure • BMR: i.e. heat production rate, averages ~70 kcal/hr = ~1ᵒC/hr • BMR is influenced by a number of factors: • Age: MR declines with age • Sex: 5-10% ↑ metabolic rate in men • Hormones: Thyroid hormone & catecholamines ↑ cellular MR (chemical thermogenesis) • Digestive state: 10-20% post-prandial ↑ metabolic rate (thermal effect of food) Heat production is a principal by-product of metabolism. BMR, defined as the minimum level of energy required to exist, is measured in a controlled environment in a fasted, rested individual. BMR accounts for 50-70% of daily energy expenditure and normally averages ~70 kcal/hr in a 70 kg male. BMR decrease with age and in women is most likely due to decreased muscle mass & increased adipose tissue, which has a lower rate of metabolism. Also, testosterone can increase MR by 10-15%. Thyroid hormone (TH) (by increasing the rates of chemical reactions within many cells) can increase MR by 50-100%, while total loss of thyroid secretion decreases MR to 40-60% of normal. After a meal is ingested, MR increases as a result of the different chemical reactions associated with digestion, absorption, and storage of food in the body. 10 Mechanisms of heat production Muscular activity Voluntary or involuntary muscle activity = ↑ energy consumption rate = ↑ metabolic heat production Heat generated in active muscle… is convected to the blood…. & conducted to the skin… Thus, active muscle = ↑ Tb Physical activity: • • 75% of energy is released as heat Moderate exercise (e.g., jogging) ↑ metabolic rate ~ 500 kcal/hr = ~6ᵒC/hr Shivering: • Asynchronous involuntary skeletal muscle contraction, ↑ muscle tone & tremors • ↑ rate of heat production X 5 BMR During physical exercise, the rate of energy consumption and hence heat generation increases in proportion to the intensity of the exercise. Shivering is an involuntary somatic motor response that occurs in skeletal muscles to produce heat 11 Mechanisms of heat production Non-shivering thermogenesis • Occurs in Brown Adipose Tissue (BAT) • Stored in depots • Quantity ↓ with age,↑ with chronic exposure to cold • NE stimulates lipase & release of FFAs • Thyroid hormone stimulates upregulation of mitochondrial UCP1 (thermogenin) • Respiration uncoupled to ATP production→ heat release • ↑ rate of heat production by 10-15% NE: norepinephrine FFAs: free fatty acids UCP1: uncoupling protein 1 (thermogenin) NE & thyroid hormone (TH) work synergistically to stimulate non-shivering thermogenesis in brown adipose tissue (BAT). Briefly, NE released from sympathetic nerves binds to b3 adrenergic receptors on brown fat cells. This stimulates a lipolytic cascade characterized by lipase-mediated degradation of triglycerides. FFAs are released into the cytosol, transported across the mitochondrial membrane and release protons. Concomitantly, thyroid hormone crosses the cell and stimulates the upregulation of mitochondrial UCP1. The protons are then circulated through electron transport through the UCP1 pump (instead of ATPase), resulting in the release of heat (instead of ATP synthesis). Heat production in this manner is particularly important for neonates. 12 Mechanisms of heat loss • • • • RADIATION : heat transfer in the form of electromagnetic waves between solid objects Amount & direction of heat transfer is determined by the temperature of the radiator Heat net-radiates from the body to solid objects which are cooler than Ts (e.g. walls) Heat net-radiates to the body from objects that are warmer than Ts (e.g. sun) • CONDUCTION: transfer of heat between objects which are in direct contact (e.g. chair) • Conduction of heat requires a temperature gradient • CONVECTION: transfer of heat to the environment by a moving fluid (e.g. air or water) • Convective heat loss is proportional to the temperature gradient & the velocity of the liquid • • • EVAPORATION of 1 L of water from the skin surface removes 580 kcal of heat Primary mechanism of heat loss at high Ta & during strenuous physical activity Rate of evaporation depends on ambient humidity:↑ humidity = ↓ evaporation Remember: heat flows from areas of higher temperature to areas of lower temperature, i.e., a temperature gradient is required for heat to be transferred. 13 Heat transfer between the core & the environment Heat produced in the body enters the blood & is conveyed to the body surface from where heat is dissipated/lost Heat transfer occurs from area of high temperature to area of lower temperature. For heat loss, surface temperature must be lower than at the core. Almost all cellular processes of the body will ultimately result in production of heat. The more metabolically active the tissue, the more heat it produces. The organs which produce the most heat are the brain, skeletal muscle, and the visceral organs, particularly the liver and kidneys. At rest, approx. 56% of total heat production occurs in the internal organs and about 18% in the muscles and skin. During physical exercise, heat production increases several fold, and the percentage of heat produced by muscular activity can rise to as much as 90%. To maintain normal body temperature, heat loss to the environment must be balanced by heat generated through metabolism. This is the situation when body temperature is stable. Note that, even at rest, the body is constantly losing heat. This loss is necessary in order to maintain Tb ~37ᵒC. This is mediated predominantly by heat loss through the skin. 14 Heat transfer from the core to the skin • Heat is transferred to the skin by convection (mostly) & conduction (minor) • Rate of heat transfer by conduction across the subcutaneous fat is relatively constant • Rate of heat transfer by convection depends on cutaneous blood flow • Blood flow to the skin varies from 0-30% of CO • Vasoconstriction → Heat storage • Vasodilation → Heat loss Heat produced by the body is absorbed by the bloodstream and conveyed to the body surface. In order for the internal flow of heat to occur, temperature of the body surface must be lower than that of the body interior. The blood supply to the skin is the chief determinant of heat transfer to the skin. The rate of blood flow into the skin venous plexus can vary tremendously—from barely above zero to as great as 30% of the total cardiac output. 15 Heat dissipation at low Ta Heat dissipation at high Ta Regulation of skin temperature (Ts) Controlled by the ANS ↑ Sympathetic activity (NE via a1 adrenoceptors) → vasoconstriction → heat storage ↑ SYMPATHETIC NERVOUS ACTIVITY ↓ SYMPATHETIC NERVOUS ACTIVITY ↓Sympathetic tone → vasodilation → heat loss Heat conduction to the skin by the blood is regulated by the degree of vasoconstriction of the cutaneous blood vessels. This vasoconstriction is controlled almost entirely by the sympathetic nervous system in response to changes in core Tb and changes in environmental temperature. In normothermia, there is a baseline level of vasoconstrictive tone of the cutaneous blood vessels. This is mediated by the sympathetic nervous system and is called cutaneous sympathetic tone. In response to cold, increased sympathetic tone constricts arterioles and reduces cutaneous blood flow, thereby reducing heat loss from the skin surface. In response to heat, sympathetic nervous activity withdrawal leads to passive vasodilation of blood vessels and increased cutaneous blood flow. This permits large increases in cutaneous blood flow and heat loss. 16 Heat transfer between the core & the environment Naked individual in a room with Ta of 20ᵒC, loses heat predominantly by radiation to surrounding solid objects. At Ta of 30ᵒC, evaporative heat loss increases. Radiative heat loss decreases owing to smaller gradient between Ts & Ta At Ta >36ᵒC or so, heat loss occurs by evaporation only, owing to loss of thermal gradient for conduction & radiation Heat transfers from areas of high temperature to areas of lower temperature, provided there is a thermal gradient. 17 Regulation of sweat production • Loss of heat by evaporation of water from the skin surface is regulated by controlling the rate of sweat production • Evaporation of 1 L of water from the skin surface removes 580 kcal of heat • ~600 mL/day of water evaporates from skin & respiratory surfaces - “Insensible heat loss” Sweat glands: • are innervated by the sympathetic cholinergic nerves (ACh) • can deliver up to 6L fluid/hr to skin surface • Evaporation rate depends on ambient temperature & humidity ↑ Ambient humidity = ↓evaporation = ↓ heat loss = ↑ heat storage Eccrine glands produce sweat at a basal rate of about 600 mL/day. With increased Ta (approx >30ᵒC in a resting individual) or with increased physical activity, the rate of sweat production can increase to levels exceeding 1-2 L/hr. Sympathetic cholinergic fibers innervate sweat glands & stimulation of these glands (with ACh) leads to an increase in sweat production mediated via muscarinic M3 receptors. When heat production/gain exceeds heat loss, Tb rises, sweating is initiated & large quantities of sweat are produced and released from eccrine glands. As long as the air is dry, the evaporation of sweat from the skin surface is an efficient means of losing heat form the body. Note is not simply the act of sweating that helps to lower body temperature, but the vaporization of water from the skin surface that removes heat. If sweat id produced but cannot evaporate from skin surface (e.g., in high humidity), the effectiveness of sweating as a heat loss mechanism is decreased. If ambient humidity is high, the water vapor pressure gradient between skin & air will be low, slowing evaporation and increasing the body’s tendency to accumulate excess heat produced during exercise. Evaporation is the principal mechanism of heat loss in a hot environment but becomes ineffective above a relative humidity of 75 %. The other major methods of heat dissipation (conduction, convection, radiation) cannot efficiently transfer heat when environmental temperature exceeds skin temperature. 18 Heat transfer between the core & the environment At high Ta with high ambient humidity, evaporation rate declines, the body cannot effectively lose heat and, thus ↑Tb >37ᵒC Humidity >75% Evaporation rate approaches 0 & Tb rises Heat transfers from areas of high temperature to lower temperature. Heat is gained if surface temperature exceeds core temperature. This is particularly relevant in conditions of high Ta & high humidity Ta: Ambient (environmental) Temperature 19 Heat balance equation • If Tb is to remain unchanged, ↑ or ↓ heat production must be balanced with ↑ or ↓ in heat loss resulting in negligible heat storage within the body • In equilibrium: • Capabilities of thermoregulatory machinery are not limitless • Shifts in heat storage can shift the balance from normothermia to hypothermia or hyperthermia 20 • The thermoregulatory center is located in the anterior hypothalamus. It determines the Temperature Set Point (Tset) • It receives information about ambient temperature from cold & warmth thermoreceptors in the skin & about core Tb from thermoreceptors in the spinal cord & anterior hypothalamus itself • It compares actual core Tb with Tset & initiates measures to counteract any deviations Thermoregulatory center Hypothalamic temperature As can be seen in the graph, at core Tb of 37.1°C, the rate of heat loss > production. At core Tb of 36.9°C, the rate of heat production > loss. Thus, temperature control mechanisms continually attempt to bring the body temperature back to 37°C – this crucial temperature is called the “set-point” (Tset). This level is set in the thermoregulatory center located in the preoptic anterior hypothalamus (POAH). The hypothalamic thermoregulatory center contains the thermoregulatory integration and control center. It receives information about environmental temperature (Ta) from thermoreceptors in the skin and about core temperature from thermoreceptors in the hypothalamus itself. The center then orchestrates the appropriate responses, which may involve heat-generating or heat-dissipating mechanisms. If Tb < Tset, heat generating and heat retaining mechanisms are activated. These include increased MR, shivering, vasoconstriction of BVs of the skin. If Tb > Tset, heat dissipating mechanisms are activated. These mechanisms include vasodilation of BVs of the skin (decreased sympathetic tone) and increased activity of sympathetic cholinergic fibers to sweat glands. 21 Hypothalamic control of thermoregulation cholinergic Heat loss by evaporation a1- adrenergic Cutaneous vasoconstriction b3- adrenergic Non-shivering thermogenesis cholinergic Heat production by shivering 22 Skin blood vessels dilate: capillaries becomes flushed with warm blood; heat is lost from skin surface Thermoregulatory responses to changes in core Tb Activates heat-loss center in hypothalamus Blood warmer than hypothalamic set-point Sweat glands activated & sweat production ↑ evaporation of fluid from the skin enhances heat loss greatly Stimulus: ↓ Tb (cold Ta, exposure to cold water) Stimulus:↑Tb (during exercise, high Ta) Skin blood vessels constrict, blood is diverted from skin capillaries; minimizes overall heat loss from the skin Skeletal muscles contraction activated, shivering begins Blood cooler that hypothalamic set-point Activates heat-promoting center in hypothalamus 23 When heat transfer to or from the environment overwhelms the body’s regulatory capacity: Hypothermia & Hyperthermia 24 Hyperthermia • Elevation of Tb > normal Tset range (36-37.5ᵒC) due to overwhelming of thermoregulatory mechanisms • Environmental conditions: Prolonged exposure to heat (↑Ta), high ambient humidity, physical exertion Thermoregulatory mechanisms become overwhelmed & fail; sweating ceases Inability to maintain adequate CO • Heat Collapse: inability to maintain CO leads to transient collapse • Heat Stroke: thermoregulatory failure (sweating ceases), CNS dysfunction (disorientation, headache, irritability, confusion, coma, seizures), death. Malignant Hyperthermia: Hypermetabolic crisis characterized by excessive accumulation of calcium in skeletal muscle & resultant sustained contraction following exposure to certain volatile anesthetic agents (e.g. isoflurane) in susceptible (MHS) individuals. Hyperthermia is basically an increase in core Tb above the normal 36-37.5ᵒC range owing to an inability of the body to dissipate heat at a rate equal to that at which it is being produced/gained. The most common environmental conditions that result in hyperthermia are prolonged exposure to heat + high ambient humidity, particularly when accompanied by physical activity. As such, athletes exercising in hot, humid environments over long periods of time (e.g., golfers, marathon runners) are at particularly high risk of hyperthermia. A sustained increase in Tb to 38-40ᵒC results in heat collapse (also known as heat exhaustion), characterized by inability to maintain adequate cardiac output (CO) owing to hypovolemia (caused by dehydration) and vasodilation. It manifests clinically as weakness, profuse sweating, nausea, vomiting, diarrhea, dizziness, muscle cramping and eventually, collapse. It is also associated with hyperventilation, elevated heart rate & hypotension. Symptoms resolve quickly with rest, cooling and rehydration with isotonic solutions. A prolonged increase in Tb>40ᵒC results in heat stroke. At such high Tb, the thermoregulatory center fails & sweating ceases (skin is dry and hot). Cerebral edema with accompanying damage to the CNS manifests as disorientation, headache, irritability, confusion, seizures, and if untreated by cooling and fluid replacement, may progress to coma and death. 25 Hypothermia I. Mild Hypothermia (32-35ᵒC) II. Moderate Hypothermia (28-32ᵒC) III. Severe Hypothermia (<28ᵒC) Most common environmental cause is prolonged immersion in cold water. The convective heat transfer coefficient (h) in water is ~100X that of air Frostbite: Perfusion of extremities (ears, nose, cheeks, chin, fingers & toes) reduced markedly even with mild hypothermia. Prolonged cold exposure leads to freezing of tissue & cold injury (loss of sensation → blister formation → extensive tissue necrosis) Induced hypothermia: use of sedatives to depress the hypothalamic temperature controller & ice packs to reduce Tb < 34ᵒC. Permits ↓HR & ↓MR without tissue damage for periods 30-60 mins during surgery. If there is a danger of core temperature dropping, thermoregulatory mechanisms are activated to stimulate heat production (shivering) and prevent heat loss (cutaneous vasoconstriction). Cooling also triggers behavioral changes (e.g., adding clothes, leaving the swimming pool, leaving an air-conditioned space). If these preventative reactions do not occur, due to inability to leave the situation (e.g., immersion in cold water, accident at sea, falling through ice, snow avalanche, sleeping rough), core Tb can drop < 35ᵒC and hypothermia ensues. I. Maximal shivering, ↑ MR, ↑ glucose utilization & O2 consumption increases up to 6-fold. Tachycardia & vasoconstriction cause a rise in BP. Peripheral vasoconstriction (fingers & toes) causes pain. Patient is at first fully awake, later confused, apathetic and ultimately judgement becomes impaired. II. Sources of glucose become exhausted (hypoglycemia), bradycardia, arrhythmia, depressed breathing, person hallucinates, soon losing consciousness & no longer feeling pain. III. Coma, no pupillary reflexes, no sign of brain death; ultimately leading to ventricular fibrillation, asystole and apnea. 26 Fever • Fever is an elevation of Tb due to resetting of the hypothalamic thermoregulatory set-point to a higher level (↑37ᵒC) RISING PHASE FALLING PHASE PLATEAU Fever (or pyrexia) is an elevation of normal Tb not related to work or to exposure to hyperthermic conditions. The development of fever involves an elevation of Tset. Since the aim of thermoregulation is to maintain the Tb at the level designated by Tset, in fever, the thermoregulatory mechanisms are activated to increase Tb to the new raised Tset. During the rising phase of fever (i.e., when Tb < Tset), thermoregulatory mechanisms are activated in order to increase Tb to the elevated Tset. During this phase, the individual complains of feeling cold, the individual is shivering, cutaneous blood flow is decreased, and the skin feels cool to touch. The thermoregulatory mechanisms activated to produce & retain heat continue until Tb reaches the elevated Tset. During the plateau phase of fever, Tb = Tset. Both Tb & Tset are elevated at this stage. During this phase, shivering has ceased, the skin feels warm, the individual has an increased heart rate and respiratory rate, they are drowsy, weak and complain of aching muscles and thirst. During the falling phase of fever, Tset falls back to its normal level. At this stage, Tb > Tset. Thermoregulatory mechanisms are now activated to facilitate heat loss and reduction of Tb back to 37ᵒC. Cutaneous blood flow increases, and sweating is induced. During this phase of fever, the individual complains of feeling hot, they are sweating, they actively try to reduce their temperature by kicking off blankets and removing clothes, they are hyperemic (skin is red) and their skin feels hot and clammy to touch. 27 1. In response to a variety of infectious & inflammatory stimuli, macrophages & lymphocytes release cytokines into the circulation 2. Cytokines cross the BBB & stimulate PGE2 release from endothelial cells 3. PGE2 acts on the POAH to elevate thermoregulatory set-point resulting in fever • Cytokines are endogenous pyrogens & mediate their fever-inducing effects via stimulation of PG production. Inhibitors of PG synthesis (e.g. NSAIDs, aspirin) thus help to reduce temperature in fever • Fever is beneficial? • ↑ Tb = ↓micro-organism growth, ↑ AB production, slows the growth of some tumors • Prolonged Tb > 41°C = hyperthermia...death POAH: preoptic anterior hypothalamus PGE2: prostaglandin E2 Fever accompanies disease so frequently and is such a reliable indicator of the presence of disease that body temperature is probably the most commonly measured clinical index. In response to a variety of exogenous pyrogens (e.g., the lipopolysaccharide complexes (endotoxins) of gram-negative bacteria), immune cells (macrophages, monocytes) are activated and release numerous cytokines among them the endogenous pyrogens (e.g., IL1, IL6, TNFa). These circulating cytokines reach the circumventricular organs of the brain which do not possess a blood-brain barrier, and triggers release of prostaglandin E2 (PGE2) from endothelial cells. PGE2 diffuses into the hypothalamus & stimulates an elevation in Tset. As a consequence of fever, heart rate and energy metabolism increase resulting in fatigue, joint aches, headache, disturbances of consciousness and of the senses, and seizures may also occur. 28 By the end of this lecture, you should be able to answer the following questions: • • • • • • • • • • • • • • • • • • What are the primary mechanisms by which heat is lost from the body? During what phase of fever is Body temperature equal to Set-point temperature? Vasoconstriction of cutaneous blood vessels in response to changes in ore body temperature is controlled by what hormone/ neurotransmitter? At increased ambient temperatures, increased sweat production is achieved by stimulation of what receptor? What effect does intensive exercise have on temperature set-point? What are the most common causes of hypothermia and heatstroke? If core body temperature decreases, what 2 mechanisms that are activated to help bring temperature back to normal. By what brain center is the temperature set-point set and monitored? At room temperature, what is the primary mechanism by which heat is lost from the body? To diagnose heat stroke, core body temperature must exceed what temperature (in degree C)? If someone has a fever and is shivering, what phase of fever are they most likely in? At what core body temperature can hypothermia be diagnosed? Vasoconstriction of cutaneous blood vessels in response to changes in ore body temperature is mediated by binding of a hormone/ neurotransmitter to what receptor? During the falling phase of fever, which is highest – body temperature or set point temperature? If core body temperature increases, what 2 mechanisms that are activated to help bring temperature back to normal. What hormone is responsible for increasing female body temperature by 0.5 degree C during the luteal phase of the menstrual cycle? At ambient temperature approaches body temperature, what is the primary heat loss mechanism used by the body to maintain normal core body temperature? Increased sympathetic stimulation of blood vessels in the skin increases heat loss or heat storage? Which of the following temperatures (core body temperature, skin temperature, temperature set-point) is monitored and homeostatically regulated by thermoregulatory responses? 29