Regulation Quiz.text - - 6/8/99 QUESTION 1: What normally happens to core temperature during exercise? ANSWER: During exercise core temperature rises. How much it rises depends on the level of exercise. With prolonged strenuous exercise it may approach 39°C. QUESTION 2: How long does it take for core temperature to stabilize during maintained exercise? ANSWER: About 30 to 60 minutes at moderate levels of exercise. With more strenuous exercise, it may not stabilize (hopefully you stop exercising because of exhaustion, before you die of hyperthermia). QUESTION 3: What happens to skin blood flow during maintained exercise? What causes this and what purpose does it serve? ANSWER: Initially skin blood flow drops (due to activation of vasoconstrictor nerves supplying cutaneous arterioles), but then it rises. The delayed rise (due to inhibition of the output from sympathetic vasoconstrictor nerves & release of bradykinin from activated sweat glands) serves to increase heat dissipation from the skin. However, if excessive vasodilatation begins to threaten maintenance of mean arterial blood pressure, cutaneous vasoconstriction may again occur (blood pressure regulation over-rides temperature regulation). QUESTION 4: Does the initial cutaneous vasoconstriction at the beginning of exercise serve any useful purpose? ANSWER: This is a very interesting question. It could be just an incidental effect of a generalized increase in sympathetic nervous output. However, it could be taken as evidence that temperature is regulated at a higher set-point during exercise (the current view is that set-point doesn't change in exercise). QUESTION 5: From which cutaneous blood vessels is most heat lost and why? ANSWER: The veins. They have a large volume and a low linear velocity* of blood flow, allowing plenty of time for heat loss to occur. They are also close to the surface of the skin, facilitating loss of heat to environment. * This is different from flow in terms of volume/time: eg. a narrow river with a high linear velocity of flow can run into a deep, wide pool with a very low linear velocity of flow. Yet the total flow as volume/time may be constant. QUESTION 6: Which parts of the nervous system are most important in automatic (involuntary) temperature regulation during exercise? ANSWER: The hypothalamus (thermoregulatory integrating "centre" and location of central thermoreceptors), the sympathetic nervous system (controls cutaneous arterioles and sweat glands) and cutaneous thermoreceptors (provide additional input to hypothalamus). QUESTION 7: At high work rates, particularly under warm conditions, the skin may become vasoconstricted. Suggest why. ANSWER: Temperature regulatory responses, driven by the combined effects of excessive heat production and ambient heat gain, may compromise the maintenance of adequate mean arterial pressure. The blood pressure regulatory system then kicks in, causing a degree of vasoconstriction and thereby increasing total peripheral resistance (TPR). This helps to increase mean arterial pressure (proportional to TPR x Cardiac Output). QUESTION 8: Suggest why exercise may be more tiring when it is performed under warm conditions than under cool conditions, at the same work rate? ANSWER: Under warm conditions, vasoconstriction may be initiated by the blood pressure regulatory reflexes, over-riding the thermoregulatory reflexes (which cause vasodilatation). Under these conditions, blood flow to exercising muscle may not be optimal for the purpose of oxygen supply. This may lead to use of anaerobic metabolism and the accumulation of lactic acid. Lactic acid may contribute to feelings of fatigue for a number of reasons. For example, the increased intracellular hydrogen ion competes with calcium, decreasing the efficiency of muscle contraction. It may also contribute to sensations of discomfort by activating nociceptors. QUESTION 9: What happens to a rat's weight during and after you temporarily deprive it of food? What does this suggest regarding regulation of body weight? ANSWER: The rat's weight drops during food deprivation and subsequently rises to a level comparable to its litter-mates. This suggests that body weight is regulated to a predetermined "set-point". QUESTION 10: What happens to appetite and basal metabolism when you are deprived of food? ANSWER: Appetite is increased (hunger) and the basal metabolic rate is reduced (all other things being equal). QUESTION 11: What happens to a rat when you destroy the ventromedial nucleus of its hypothalamus? ANSWER: It gets very fat, perhaps more than doubling in weight. It may also become a "finicky" eater and unusually aggressive. QUESTION 12: What happens to a rat when you destroy the lateral areas of its hypothalamus? ANSWER: It becomes anorexic and may even starve to death if not forced to eat. QUESTION 13: What factors are thought to be important in short-term regulation of feeding? ANSWER: Mechanical stimuli such as passage of food through the mouth and stretch of the stomach (activates sensory nerves), and entry of chyme into the duodenum (releases cholecystokinin). Stretch and CCK act on the hypothalamus to decrease appetite. QUESTION 14: What factors are thought to be important in medium-term regulation of feeding? ANSWER: Entry of the products of digestion and associated hormones into the bloodstream (eg. glucose and insulin, which act on the hypothalamus to decrease appetite). QUESTION 15: What factors are thought to be important in long-term regulation of feeding? ANSWER: A hormone (leptin) released from adipose tissue is very important. It acts on the hypothalamus to decrease appetite and increase basal metabolic rate. QUESTION 16: What is the role of neuropeptide Y in control of appetite and body weight? ANSWER: It is a neurotransmitter released in the hypothalamus which has a very potent stimulatory effect on appetite. It also acts to decrease basal metabolism. QUESTION 17: What is the relationship between leptin and neuropeptide Y? ANSWER: Leptin appears to inhibit the release of neuropeptide Y. QUESTION 18: What is the Ob gene? ANSWER: The Ob gene normally produces leptin. A mutant form of the gene is responsible for a recessive obesity disorder in rats (Ob-Ob mutant). QUESTION 19: Are morbidly obese humans deficient in leptin? ANSWER: This is a active field of research. To date (1997), studies of obese human subjects have found only normal or high levels of plasma leptin. The obesity problem is therefore hypothesized as due to a deficiency in the leptin receptor or something further along the chain of communication. Or it may have nothing to do with leptin...