YR1 Lecture 1H - Thermoregulation - Dr Alex Burton 2020 (2).pdf

thermoregulation Alexander Burton Adjunct Fellow School of Medicine Western Sydney University Learning objectives: Describe the maintenance of body temperature and the control of body fluid balances in the face of high temperatures and lack of fluid intake. Describe the organisation, distribution, f...

thermoregulation Alexander Burton Adjunct Fellow School of Medicine Western Sydney University Learning objectives: Describe the maintenance of body temperature and the control of body fluid balances in the face of high temperatures and lack of fluid intake. Describe the organisation, distribution, function and control of sweat glands in relation to body fluid and temperature homeostasis. Thermoregulation Control of body temperature Poikilothermy: “poikilos” [Greek] = changeable “therme” [Greek] = heat Reptiles and amphibians adjust body temperature largely by heat gain or loss from the environment Homeothermy: “homoios” [Greek] = like, same Humans and other mammals, and birds, maintain a constant body temperature, in which net heat production = net heat loss Control of osmolality Molecular Physiology of Water Balance Knepper, et al. N Engl J Med 2015; 372:1349-1358 Human thermogenesis In neonates, a special type of fat - brown fat, located around the neck and midline of the back - is largely responsible for the generation of heat through metabolic processes. Brown fat has a very high density of mitochondria, in which ATP production is inefficient: heat is produced In adults, residual brown fat is located primarily under the shoulder blades (subscapular brown fat) and plays a negligible role in thermogenesis Human thermogenesis Heat production is a by-product of normal metabolic processes that involve the generation of ATP Core temperature (~37 oC) varies by ~1 oC during the course of a day: lowest between 3-6 am, highest between 3-6 pm The basal metabolic rate (BMR) is lower in older people Abrupt increase in body temperature (~0.15 - 0.45 oC) in women accompanies ovulation Human thermogenesis during exercise Physical activity increases energy expenditure (and hence heat production), largely from active skeletal muscle Heat production increases from ~80 kcal/h at rest to ~600 kcal/h during moderate exercise (e.g. jogging) Unless this excess heat is dissipated core temperature will increase by 1 oC every 10 min, limiting the duration of exercise to 30 min (core temperature 40 oC) Body temperature is determined by metabolic heat production and environmental heat gain and loss Heat loss to, or gain from, the environment is determined by: Radiation Heat loss to, or gain from, the environment is determined by: Radiation Conduction Heat loss to, or gain from, the environment is determined by: Radiation Conduction Convection Heat loss to, or gain from, the environment is determined by: Radiation Conduction Convection Evaporation Comparative physiology: Different animals use different means to liberate excess heat Radiation of heat following dilation of cutaneous blood vessels (e.g. rat tail, elephant ears) Evaporative heat loss from mouth during panting (dog) Evaporative heat loss from nasal heat exchanger (sheep) Evaporative heat loss from licking forearms (kangaroo) Evaporative heat loss from sweating (horse, human) Evaporative heat loss in humans: Evaporation of sweat can liberate most of the heat produced during exercise During exercise sweating is the most important means of liberating heat Eccrine Sweat Glands Apocrine Sweat Glands Apoeccrine Sweat Gland Evaporative heat loss in humans: Evaporation of sweat can liberate most of the heat produced during exercise The cooling effect is due to the latent heat of evaporation of water (energy is required to convert liquid water to vapour) Dependent on a water-vapour pressure gradient between the skin and the atmosphere (gradient is low when air humidity is high) Sweat release is controlled by cutaneous sympathetic sudomotor neurones Cutaneous vasodilatation in humans In glabrous (non-hairy) skin blood flow is controlled by sympathetic cutaneous vasoconstrictor neurones: noradrenaline (NA) is the neurotransmitter Vasodilatation is brought about by a decrease of cutaneous vasoconstriction, which allows the vascular smooth muscle to relax and the vessels to dilate In non-glabrous (hairy) skin blood flow is also controlled by sympathetic active cutaneous vasodilator neurones: acetylcholine (ACh) is the neurotransmitter, so these neurones may well be sudomotor neurones ACh acts on blood vessels to cause relaxation, partly via release of nitric oxide (NO) Cutaneous vasodilatation in humans In normothermic conditions skin blood flow is approximately 5% of cardiac output During heating blood flow in non-glabrous skin increases due to withdrawal of active noradrenergic cutaneous vasoconstriction As heating increases sweat release and active cholinergic vasodilatation occurs in non-glabrous skin In heat stress skin blood flow can increase to ~60% of cardiac output Cutaneous vasodilatation An increase in skin blood flow brings hot blood from the core to the surface, allowing cooling by convection and radiation to the atmosphere Skin blood flow is controlled by cutaneous vasoconstrictor neurones in the raphe nucleus of the medulla Cutaneous vasoconstriction A decrease in skin blood flow keeps warm blood near the core Sweating is abolished Human thermoregulation Temperature is sensed by two sets of thermoreceptors peripheral and central Peripheral thermoreceptors are located over the body surface, and detect changes in temperature of the skin Skin temperature is detected by two sets of thermoreceptors: cold receptors and warmth receptors Human thermoregulation Temperature is sensed by two sets of thermoreceptors peripheral and central Peripheral thermoreceptors are located over the body surface, and detect changes in temperature of the skin Core temperature is sensed by thermoreceptors in the preoptic anterior hypothalamus Both peripheral and central thermoreceptors contribute to temperature regulation Both core temperature and skin temperature contribute to the temperature set point, but core temperature is more important A fever is an increase in the temperature set-point as a result of an infection Pyrogenic hyperthermia: Sympathetic cutaneous vasoconstrictor neurones are deactivated and sympathetic sudomotor neurones are activated, resulting in hot sweaty skin The change in set point results in a perception of being cold, despite the high temperature Shivering occurs in an attempt to increase the core temperature Once the core temperature has increased beyond the set point sweating commences in an attempt to decrease core temperature Conclusions: Body temperature is generated as a byproduct of biochemical energy-generating processes Additional heat is generated by active muscle contraction Body temperature is detected by peripheral (cutaneous) and central (hypothalamic) thermoreceptors The skin is the largest organ of the body and is highly vascularized Conclusions: Loss of heat to the environment is brought about by an increase in sympathetic sudomotor (sweating) activity, a decrease in cutaneous vasoconstrictor activity and increase in active cutaneous vasodilatation Gain of heat is brought about by an increase in cutaneous vasoconstriction and increase in activity of the skeletal muscles (shivering) A pyrogenic fever results in an increase in temperature set point: shivering occurs to increase core temperature, with sweating occurring once core temperature has exceeded the set point Questions? 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