Recent advances in hormonal response to exercise

Comp. Biochem. Physiol. Vol. 9311,No. 4, pp. 727-739, 1989 Printed in Great Britain

0305-0491/89$3.00+ 0.00 © 1989PergamonPress plc

MINI-REVIEW RECENT ADVANCES IN HORMONAL RESPONSE TO EXERCISE S. E. TERBLANCHE Department of Biochemistry, University of Zululand, Private Bag X1001, KwaDlangezwa 3886, South Africa (Tel: 0351 93911; Fax 0351 93735) (Received 19 December 1988) A~tract--1. This is an article concerning the maintenance of homeostasis during varying metabolic responses to different forms of physical stress. This can be considered the task of the nervous and endocrine systems. 2. Research during the past decade in the field of hormonal response to exercise (as a form of stress) in both exercise-trained and untrained subjects (mostly in the human and rat) is discussed. 3. The responses of the various hormones are discussed in three categories according to the broad chemical classification of the hormones, viz. the polypeptides, the amines and the steroids, although of course, these responses are highly integrated. 4. From the literature it is evident that exercise-trained individuals maintain homeostasis more efficiently than untrained individuals because of an improved integrated endocrine response to changes in homeostatic balance. 5. There seems to be insufficientresearch being conducted into the steroid hormones---especiallyin view of the increasing misuse of anabolic steroids in enhancing sports performance these days.

l. HISTORIC BACKGROUND

The control and integration of vital life functions in higher animals is the task of the co-ordinated functioning of the nervous and endocrine systems. By a system of sensor and feedback mechanisms the intra-cellular homeostatic balance of the organism is maintained such that the composition of body fluids is protected against marked changes, and the levels of various regulatory hormones remain appropriate to the rates of the various metabolic processes involved in the dynamically changing needs of the whole organism. The feedback mechanisms of the different hormones interact to achieve integrated functioning resulting in homeostasis. Investigations into the energy metabolism of trained and untrained individuals have shown that exercise-trained individuals maintain homeostasis better than untrained (Hellemans, 1978). The reason for this must be an improved integrated endocrine response to changes in homeostatic balance. Different levels of stress affect plasma hormone levels. The observed metabolic response to exercise is a rise in levels of certain hormones e.g. glucagon, growth hormone, vasopressin, prolactin, luteinizing hormone, cortisol, adrenocorticotropin, epinephrine and norepinephrine, and a drop in levels of other hormones e.g. insulin and testosterone. However, the intensity and duration of the exercise is a significant factor affecting these levels. The response of certain other hormones only becomes marked on intense and prolonged exercise e.g. the steroid hormones. Research into the endocrine response to various levels of exercise in both trained and untrained C.B.P 93/4B~A

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individuals reveals that cardiorespiratory fitness is an important determinant of hormonal and metabolic response to submaximal exercise (Sutton, 1978). Exercise trained individuals show a blunted hormonal response to exercise i.e. there is a training induced decrement in the plasma levels of glucagon and catecholamines (Winder et al., 1979; Koivisto et al., 1982) and of the ovarian hormones (Bonen et al., 1979) as well as insulin (Krzentowski et al., 1983; LeBianc et al., 1983) together with a reduction in the fluid-endocrine response (Convertino et al., 1983). This includes the pancreatic hormones insulin and glucagon, the hypothalamic releasing factors, the pituitary hormones as well as the parathyroid hormones and those of the gastro-intestinal tract. The results of such research into the body's endocrine responses to exercise have application not only in an improved understanding of the integrated functioning of the endocrine system and in the fields of health care and sport but also into aspects of aging, stress, obesity and diseases caused by disturbed endocrine function as in diabetes mellitus and amenorrhea, diseases affecting cardiovascular fitness such as coronary heart disease and atherosclerosis, in all of which exercise can be a therapeutic as well as a diagnostic tool. For the purposes of this review article, the responses of the three main types of hormones viz. the polypeptide hormones, the amine hormones and the steroid hormones, to exercise will be discussed separately, although of course, in the highly integrated endocrine network, no single hormone operates independently of another. Only a selection of hormones will be discussed, those which have figured prominently in the research in this field since 1976.

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S.E. TERBLANCHE 2. T H E P O L Y P E P T I D E H O R M O N E S

These include the pancreatic hormones insulin and glucagon, the hypothalamic releasing factors and the pituitary hormones as well as the parathyroid hormones and those of the gastro-intestinal tract. 2. I. The pancreatic hormones insulin and glucagon

The co-ordinated control of the secretory rates of the two main islet cell hormones, insulin and glucagon, is the result of an interplay of a variety of factors. One important regulatory factor is the blood level of glucose. A rise in blood glucose stimulates insulin secretion, a drop stimulates glucagon secretion. The levels of glucose during exercise therefore play an important role in pancreatic response. 2.1.1. Insulin. The role of insulin in homeostasis and metabolic response to exercise is a vital one. The glucose/insulin ratio is a major determining factor of general metabolic response. The level of physical fitness is positively related to glucose tolerance (Lindgarde et al., 1983). Resting levels of insulin are higher in untrained subjects and lower in exercise-trained subjects, without any impairment of glucose tolerance. LeBlanc et al. (1983) observed reduced insulin requirements of about 40% in physically trained persons in comparison with sedentary subjects. James et al. (1983) report an exercise-training induced lowering of the glucose stimulated insulin response curve in rats, and Krzentowski et al. (1983) report that insulin response to an oral glucose load in healthy males was decreased by 24% due to a 6-week training period. 2.1.1.1. Response ~?[" insulin to exercise. Insulin levels fall in all normal subjects as a result of exercise. This drop is greater in untrained subjects than in trained subjects. Endurance training brings about a blunting of the insulin response to exercise (Gyntelberg et al., 1977; Wirth et al., 1981; Lohmann et al., 1978). Researchers have reported similar blunting of hormonal response to exercise in trained rats (Galbo et al., 1977c; Zawalich et al., 1982). Investigations into the reasons to account for the blunted response due to training have revealed an increase in insulin binding to the insulin receptors on the plasma membrane which transport insulin into the cell. During rest, insulin binding to monocytes was found by Koivisto et al. (1979) to be 69% higher in athletes than in sedentary controls and was correlated with maximum aerobic power. The increase was primarily due to an increase in binding capacity. During acute exercise this insulin binding fell by 31% in the athletes but rose by 35% in the controls. Many researchers document the enhanced sensitivity to insulin of trained subjects (LeBlanc et al., 1984; Kita et al., 1982; Berntorp et al., 1984; Tremblay et al., 1985). Lampman et al. (1985) report an improvement of in vivo insulin sensitivity of 25 _+ 6.1% following moderate training. Walberg et al. (1984) confirm this increased insulin sensitivity in moderate exercise training with obese Zucker rats. This increased insulin sensitivity lapses if exercise training lapses e.g. Heath et al. (1983) found that after 10 days without exercise, trained individuals showed a 100% higher maximum rise in plasma insulin concentration in response to a 100g oral

glucose load than when exercising regularly. However, one bout of exercise then returned insulin binding and insulin and glucose responses almost to the initial trained value. Tremblay et al. (1983) found that although there was a decrease in insulin sensitivity in subjects inactive for 3 days, the insulin sparing effect of exercise training is retained if this period of inactivity is preceded by 2 days of fast with exercise. Galbo et al. (1981a) found that insulin availability before, but not during, exercise apparently is an important determinant of the hormonal response to exercise. Ivy et al. (1983) found that in rats, the difference in trained and untrained rats" hindlimb muscle glucose uptake are due to the residual effects of the last exercise session and that training does not result in a long term adaptive increase in sensitivity of muscle to insulin. Michel et al. (1984) found that insulin receptor affinity decreased after exhaustive exercise in monocytes and erythrocytes. After moderate exercise, however, binding to monocytes was enhanced due to increased receptor affinity. Subsequently they reported that acidosis diminished insulin binding, and may account for some of the decrease in cellular insulin binding observed after exhaustive exercise (Michel et al., 1985). Various proposals have been made to account lbr the marked increase in whole body insulin sensitivity in exercise-trained subjects. Vinten et al. (1985) report that the number of glucose transporters in the plasma membrane fractions from maximally insulin stimulated fat cells was larger in trained rats than in control rats. Woodhouse et al. (1984) suggest that increased muscle tissue in particular may contribute to this training induced decrease in serum insulin in humans. Miller et al. (1984) found that increased muscle mass as a result of strength training was responsible for an attenuated insulin response to a glucose challenge. James et al. (1985a) relates increased whole body insulin sensitivity in rats to an increased glucose oxidation in skeletal muscle. Richter et al. (1982), adding insulin to fast-twitch fibres of exercised red gastrocnemius muscle of rats, found a marked stimulation of glycogen synthesis in comparison with the same muscle of non-exercised rats. In contrast. insulin only minimally increased glycogen synthesis in the fast-twitch white gastrocnemius fibres that had not been glycogen-depleted on exercise. Thus the increase in insulin sensitivity occurs predominantly in muscle fibres deglycogenated during exercise. Krotkiewski et al. (1983) working wilh obese women found significantly negative correlations between plasma insulin levels and the number of capillaries in contact with slow-twitch muscle fibres and fast-twitch oxidative fibres before training. The capillary density around those fibres could predict 80% of the expected variance of plasma insulin levels. They suggest an important regulatory role of muscle in insulin-glucose levels because of the strong association they found between muscle morphology together with capillarization, enzyme activities, glucose and insulin concentrations, and their changes after training. Zorzano et al. (1985) report that the ability of insulin to stimulate processes other than glucose transport and glycogen synthesis is enhanced in

Hormonal response to exercise skeletal muscle in the rat after exercise, and this is not due to an alteration in insulin binding. Lower insulin levels in rats due to training were found by Zawalich e t a ! . (1982) and Galbo et al. (1981b) to be due to a decreased sensitivity of the pancreatic /~-cells to the stimulatorY action of glucose. In this connection, it is interesting that Fujii et al. (1982) found that the recovery of E-cell function in non-insulin dependent diabetics with fasting hypoglycaemia and a low insulin response may be promoted by physical training. Noble and Ianuzzo (1985) found that exercise-training of diabetic rats mimicked the effects of insulin treatment. James et al. (1985b) found that in rats the pattern of exercisestimulated glucose metabolic rate in muscles of different fibre composition was similar to that seen with insulin stimulation. The connection between the condition of pancreatic islets and general fitness in rats has been investigated by Reaven and Reaven (1981a) who found that 1 yr old sedentary rats displaying hyperinsulinaemia had enlarged multilobulated fibrotic islets which showed significantly reduced glucoseinduced insulin release, whereas in 1 yr old exercised and/or caloric restricted rats with lower insulin levels, the islets were in youthful peak condition. There seems little doubt that exercise training may be used as a preventative or therapeutic measure in the case of glucose intolerance, hyperinsulinaemia, obesity and hypertriglyceridemia. Becker-Zimmermann et al. (1982) report that in the young fafa zucker rat, physical training may prevent a genetically predisposed deterioration of glucose tolerance and insulin sensitivity, and that in adult animals, mild physical training may improve in vitro glucose tolerance and insulin sensitivity. Indeed exercise-training can prevent the loss of insulin sensitivity seen in sucrose fed rats (Wright et al., 1983). In the problem of obesity, exercise training favourably alters body composition, adipose cellularity and plasma insulin of the obese rat (Walberg et al., 1982). Richard and LeBlanc (1980) say that reduced levels of plasma insulin in trained rats could be explained by a reduction of body mass caused by training. In 1982, Richard et al. report that exercise training prevents the elevation of basal as well as glucose challenged insulin levels induced by a high energy diet with high fat intake. They found a highly significant correlation between the size of adipocytes and the insulin response to a glucose load, suggesting that prevention of hyperinsulinaemia could be associated with the ability to prevent obesity. LeBlanc et al. (1981) found that a reduced insulin response to a glucose load in trained subjects could be retained on a restricted diet. They maintain that the ratio of caloric intake to caloric utilization is possibly the most important modulator of the action of exercise on insulin requirements. In the case of hypertriglyceridemia, Zavaroni et al. (1981) report that the ability of exercise training to inhibit carbohydrate induced hypertriglyceridemia is due to an increase in insulin sensitivity resulting from chronic exercise. Mondon et al. (1984) found that the serum triglyceride lowering effect of exercise training seems due to a combined effect of decreased hepatic triglyceride secretion secondary to a reduced sub-

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strate and insulin supply to the liver, plus increased removal by the muscle during exercise. Walberg et al. (1983) found that in exercise-trained rats, exercise and food restriction increased adipose and gastrocnemius lipoprotein lipase activity and depressed plasma insulin and triglyceride levels. Taskinen et al. (1980) also found that the muscle lipoprotein lipase increment in exercise training was significantly related to the fall of the insulin/glucagon ratio. During exercise, the skeletal muscle is apparently adapted for increased uptake of circulating triglycerides. Reaven and Reaven (1981 b), working on the blunting of hormonal responses in exercise-trained rats say that exercise training together with caloric restriction not only inhibits age-related rises in plasma insulin levels but also inhibits the usual age-related rise in plasma triglyceride concentrations. 2.1.2. Glucagon. Glucagon, secreted by the ~t-cells of the pancreatic islets is the second component of the coupled insulin-glucagon islet cell system which plays a dominant role in the control of fuel metabolism. Its action is to increase blood glucose by accelerating glycogenolysis in the liver, i.e. its action is antagonistic to that of insulin. 2.1.2.1. Response o f glucagon to exercise. On exercise, plasma glucagon levels rise. This rise is greater and remains elevated longer in untrained individuals (Bloom et al., 1976; Winder et aL, 1979). Winder et al. (1982) working with rats, suggest that lower glucagon levels in trained animals is due to the capacity of trained animals to maintain higher blood glucose levels. Gyntelberg et al. (1977) confirm that endurance training results in a similar blunting of plasma glucagon response as with the plasma insulin response. Ahlborg and Felig (1976) and Luyckx et al. (1978) found that glucose ingestion during prolonged exercise prevented a rise in glucagon levels, although a 4-fold rise occurred in controls. Terblanche et al. (1981) report that trained rats show a significant decrease in plasma glucagon concentration. The exercise-induced increase in plasma glucagon is lessened by increased plasma free fatty acids during exercise say Rennie et al. (1976) who found that glycogen concentration in the liver decreased by 83% in controls but only by 23% in rats with increased plasma free fatty acids during exercise. However, Galbo et al. (1976) found that neither stimulation of adrenergic receptors nor free fatty acids and alanine concentrations are major determinants for the exercised-induced glucagon secretion in man. They say that decreased glucose availability enhances the secretion of glucagon and epinephrine during prolonged exercise. However, glucagon does not seem to be a major determinant of lipolysis during exercise (Galbo et al., 1977c). It is, of course, difficult to isolate the effect of the glucose/ glucagon/insulin response to exercise and exercise training from the effects of epinephrine and norepinephrine and other hormones. For example as Richter et al. (1981a) report that in exercising rats, glucagon enhances hepatic glycogen depletion and that glucagon and the sympatho-adrenal system increase and decrease respectively the plasma insulin concentration. It is well documented that epinephrine supports glucagon action and is antagonistic to insulin in promoting lipolysis and glycogenolysis

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(Galbo et al., 1977a; 1977c). Koivisto et al. (1982) report that following training, the exercise-induced decline in glucose was 60% less than before training. This sparing of glucose, resulting in the ability of trained athletes to maintain higher glucose levels is well documented. N~veri et al. (1985) reports that liver glucose production during short-term exercise may be indirectly stimulated by catecholamines via enhanced glucagon secretion. 2.2. The p i t u i t a r y hormones

The pituitary gland or hypophysis has an anterior portion, the adenohypophysis, and a posterior portion, the neurohypophysis. The adenohypophyseal hormones, secreted in response to releasing factors from the hypothalamus, include thyrotropic hormone (TSH), adrenal corticotropin (ACTH), follicle stimulating hormone (FSH), luteinizing hormone (LH) (these hormones are discussed in this article in connection with the hormones of their target organs), growth hormone (GH) and prolactin (PL). The neurohypophyseal hormones, oxytocin (not discussed here) and vasopressin, are released in response to nerve impulses from the hypothalamus. 2.2.1. Growth hormone. Growth hormone (GH), another polypeptide hormone with a significant role in fuel homeostasis, is secreted by the adenohypophysis of the anterior pituitary. Its effects are not mediated via a secondary target (as is the case with the majority of the anterior pituitary hormones). However, as with other anterior pituitary hormones, secretion of GH is pulsatile, occurring in short bursts throughout the day, and is markedly accentuated during sleep. Exercise increases the secretion of G H as does sleep, stress, falling blood glucose, raised insulin levels and oestrogen levels, protein depletion, increased amino acids e.g. arginine and leucine, and higher vasopressin and glucagon levels. The action of G H in carbohydrate metabolism is complex. In general GH administration leads to elevated blood glucose levels, an anti-insulin effect, which appears to involve both decreased peripheral utilization of glucose and augmented production of glucose in the liver via gluconeogenesis. GH also has an insulinotropic effect in the pancreas and increases muscle and cardiac glycogen. G H has a lipid-mobilizing effect, thus augmenting release of fatty acids from adipose tissue. 2.2.1.1. Response o f g r o w t h hormone to exercise.

Most workers report an increase in GH levels on exercise (Janal et al., 1984; Ino, 1981; Karagiogos et al., 1979; Gambert et al., 1981). According to Frewin et al. (1976) GH response to exercise is to a large extent dependent on temperature. Exercise in the cold is not as conducive to increased GH levels as exercise at 4 0 C . Christensen et al. (1984) however, maintain that exercise, per se, does not stimulate GH secretion, but that it is core temperature and not cutaneous temperature which modulates GH release. Francesconi et al. (1984) found that preacclimation exercise in either the hot-wet or hot-dry environment resulted in significant increments in G H when euhydrated. Sidney and Shephard (1977) found that endurance training significantly augmented the GH response to a given work load and suggested that

higher concentrations of GH may help in either the mobilization of depot fat or the conservation of lean mass during exercise. Norris et al. (1978) noted an exaggerated rise in GH during exercise when fat mobilization was inhibited by nicotinic acid. Casanueva et al. (1981) showed that the GH secretion during exercise is completely blocked by an induced free fatty acid elevation (by intralipid and heparin). They found a threshold level of plasma free fatty acids, above which GH suppression was complete. Their data supports the role of plasma free fatty acids in GH regulation. Vanhelder et al. (1984) report that in their investigations involving intermittent weightlifting the load and frequency of the exercise are determinant factors in the regulation of GH levels. Steardo et al. (1985) suggest a gamma amine butyric acid ergic regulation of GH secretion in man. Their research showed that 600 mg sodium valproate blunted the exercise-induced increase in GH. Ino (1981) noted a higher response in GH secretion in males than females during exercise. During the period of elevated GH it was noted that blood sugar levels remained uniform. In a high carbohydrate fed group, GH secretion was lower on exercise than in both a high protein diet group and in fasting controls. In this article it is suggested that an increase of blood sugar partially inhibits secretion of GH during exercise. GH levels rise in response to stress. GH levels are higher during anaerobic exercise than aerobic exercise of equal duration (Vanhelder et al., 1985). Exercise at high altitudes led to greater response in GH, prolactin and ACTH levels (Utsunomiya et aL, 1984). Interestingly, Pertovaara et aL (1984) report a significant correlation between the release of GH during exercise and the dental pain threshold elevation. 2.2.2. Prolactin. Prolactin, the anterior pituitary polypeptide lactogenic hormone, is one of the so-called stress hormones or stress markers as are GH, cortisol and epinephrine. Prolactin secretion is increased by pregnancy, breast feeding, sleep and stress, including hypoglycemia. Thus exercise causing hypoglycemia and stress will increase plasma prolactin (PL) levels. 2.2.2.1. Response o f prolactin to exercise. Frewin et al. (1976) report that exercise at 40°C led to a small increase in PL levels, whereas exercise in the cold did not. Christensen et al. (1985) found that serum PL levels rose in response to the elevation of body temperature induced by external heating whereas in contrast temperature elevation of the same magnitude through exercise induced no change in PL secretion. They conclude that an increase in core temperature is a stimulus for serum prolactin secretion and suggest that exercise apparently inhibits the stimulatory effect. Rolandi et al. (1985) observed that exercise induced prolactin release was found in athletes only and suggest a possible role of training in conditioning the hypothalamopituitary exercise-induced secretion. Smallridge et al. (1985) suggest that increased prolactin response in trained males after treadmill running suggests an alteration in prolactin secretion in these male runners. De Meirleir et al. (1985) suggest

Hormonal response to exercise that augmented levels of PL during and after exercise are caused by increased pituitary secretion rather than decreased elimination. The response of PL secretion to stress was investigated by Nhu Uyen et al. (1982) who found that plasma PL levels increased with mental stress. Their investigations showed that PL levels were significantly higher during exercise before an academic examination (i.e. exercise together with mental stress) than the PL levels during exercise after the examination. The marked increment in plasma PL could be related to stress associated with the examination. Prolactin secretion could play a role in menstrual dysfunction in women athletes. Brisson et al. (1980) suggest that marked increments in blood PL in postpubescent girls with past and present sports history during exercise could probably furnish an explanation to findings of a significantly delayed menarche in athletic adolescents. They suggest that repeated heavy physical exercise could create a PL impregnation on the maturing ovary sufficient to delay any follitropin follicle-stimulating action giving a transient amenorrhic condition similar to the nursing mother. However, Chang et al. (1984) report that findings of a normal 24hr PL secretion and appropriate PL responses to dopamine in women runners with menstrual dysfunction do not support a role for PL in this disorder. Loucks and Horvath (1984) suggest that failure of PL to increase in response to exercise may be due to a lack of fl-estradiol. 2.2.3. Vasopressin. Arginine vasopressin (AVP) or vasopressin (VP), one of the two neurohypophyseal hormones is a polypeptide hormone involved in osmoregulation which is an important aspect of metabolic homeostasis. The secretion of vasopressin is influenced by, inter alia, the osmotic pressure of the blood, the "effective" circulating blood volume as well as nausea and emotional stress. Vasopressin has an antidiuretic action. Factors causing a rise in osmotic pressure of the blood e.g. dehydration or salt intake, augment VP secretion. 2.2.3.1.

Response

of

vasopressin

to

exercise.

Research on vasopressin response to exercise seems to show conflicting results at this stage. Many workers report an increase in VP levels on exercise, but Wade and Claybaugh (1980) concluded that this increase appears not to play a role in the concomitant antidiuresis. Melin et al. (1980) in their investigations with trained and untrained men during submaximal exercise to exhaustion, found that AVP levels displayed highly significant increases in both groups. Geyssant et al. (1981) and Convertino et al. (1981) maintain that an exercise intensity greater than 40% IIO2 max is required to change plasma osmolality and thus stimulate significant AVP release. Boening and Skipka (1979) investigating renal blood volume regulation in trained and untrained subjects during immersion, pointed to a poor or even absent inhibition of antidiuretic hormone secretion in trained male athletes. Landgraf et al. (1982), during a prolonged day/night exercise cycle, found a marked increase in plasma AVP, peaking at exhaustion, and that changes in osmolality play a dominant role in the

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secretion of AVP. Within 1 hr after exercise, AVP levels return to basal level. Convertino et al. (1980) report that plasma hypervolemia during training was associated with two major factors: a 9-fold elevation in plasma rennin activity (PRA) and AVP during exercise that facilitated Na ÷ and H20 retention, and a progressive chronic increase in plasma albumin content that provided increased H20-binding capacity for the blood. Convertino et al. (1983) report that a similar relative exercise intensity produces similar changes in plasma volume, osmolality and vasopressin changes independent of training. Gaebelein and Senay (1980), investigating the influence of exercise type, hydration and heat on plasma volume shifts in men found that AVP may be responsible for osmodilation. The pre-exercise osmolality and rate at which the threshold for VP release is attained may determine whether osmodilution, osmoconcentration or both occur during exercise. Maresh et al. (1985) report no differences between male/female AVP increases on maximal exercise. However, water retention in oedema may mask increased levels of AVP e.g. Williams et al. (1979) found that levels of AVP and serum electrolyte concentration were not affected by seven days strenuous hillwalking. They suggest, however, that continuous exercise may cause oedema and may be a factor in the etiology of high altitude oedema which seems related to a defect in fluid homeostasis. 3. THE AMINE HORMONES

The amine hormones include acetyl choline (effective in the synapses of the autonomic nervous system), the thyroid hormones thyroxin and triiodothyronine, and the adrenomedullary hormones epinephrine and norepinephrine. These hormones play a vital role in homeostasis and in the body's responses to exercise and stress. 3.1. The catecholamines, epinephrine

epinephrine

and

nor-

Since the adrenal medulla and the sympathetic nervous system function in concert in response to situations of stress and fright, these two components are together known as the sympatho-adrenal system. Among the potent stimuli activating the sympathoadrenal system are exercise, cold exposure, fright and hypoglycaemia, all of which create a need for an increased fuel supply. The catecholamines have a profound lipid-mobilizing activity, increasing the blood level of free fatty acids (FFA) by stimulating their release from adipose tissue by increased lipolysis. A carbohydrate-poor diet increases the relative contribution of fat to oxidative metabolism and during exercise the sympatho-adrenal response in the carbohydrate poor diet is increased (Jansson et al., 1982). It is well-documented that in diabetes mellitus the unavailability of glucose in the absence of (or low levels of) insulin is compensated for by the increased secretion of adreno-medullary hormones, making the body's fat stores (and later, protein stores) available as substrates. The integrated metabolic response to

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catecholamines is due not only to the direct action of these hormones but to their influence on levels of other hormones, in particular the pancreatic hormones: insulin secretion is suppressed and glucagon secretion stimulated, thus reinforcing the tendency to glycogenolysis and lipolysis. 3.1.1.

Response

of

catecholamines

to

exercise.

Levels of blood glucose play a decisive role in the hormonal response to various types and levels of exercise. Luyckx et al. (1978) note that glucose availability reduces exercise-induced glucagon secretion and possibly, consequently, F F A mobilization, and Galbo et al. (1977a) state that decreased glucose concentrations may significantly enhance the secretion of glucagon and epinephrine during prolonged exercise, although they add that increased glucagon secretion does not seem to be a major determinant of lipolysis during exercise. The documented blunting of hormonal response to exercise after training is partly due to higher circulating blood glucose concentrations. In trained rats, adipose tissue sensitivity to catecholamines is increased and changes in glucagon and insulin concentrations are not necessary for increased lipolysis (Galbo et al., 1977a). Levels of glucagon and catecholamines increase during exercise but the magnitude of the increase is significantly less in endurance-trained individuals than untrained (Winder et al., 1979). Rats show the same blunted catecholamine response on training. Winder et al. (1982) found that differences in stress hormone response to exercise between trained and untrained animals persist in the fasted state, and appear to be a consequence of the capacity of trained animals to maintain higher blood glucose levels. Blood levels of epinephrine and norepinephrine and other stress markers (lactate, prolactin, etc.) are significantly correlated to ratings of perceived exertion (Skrinar et al., 1983). The greater the stress e.g. fasting (Galbo et al., 1981a), low carbohydrate diet (Jansson et al., 1982), exhaustive continuous exercise without sleep (Opstad et al., 1980) and anaerobic exercise (Kindermann et al., 1982), the greater the adrenal response, but this response is always blunted in the exercise-trained subject. Sinyor et al. (1983) found that trained subjects showed higher levels of norepinephrine and prolactin early in the stress period, more rapid heartrate recovery following the stressors and lower levels of anxiety at conclusion of the exercise session. They suggest that aerobically trained individuals may be capable of faster recovery in both physiological and subjective dimensions of emotionality. The integrated response of plasma levels of insulin, glucagon, epinephrine and norepinephrine during exercise, a response which functions more efficiently in exercise trained subjects, has been investigated by several workers using rats. In running rats, epinephrine exerts an acute enhancing effect on muscle glycogenolysis and glucagon secretion, elevates heart rate and has an acute depressing effect on insulin secretion (Richter et al., 1981b). Demedullated rats do not show this normal exercise induced increase in blood glucose, lactate, etc. and decline in plasma insulin levels (Carlson et al., 1985). Richter et al. (1980) report that in adrenodemedullated rats, the concentration of norepinephrine in plasma was markedly reduced during

exercise. In contrast to man, a major part of the circulating norepinephrine in the rat is of adrenomedullary origin during exercise. Richter (1984) reports that hormones from rat adrenal medulla, probably epinephrine, enhance glycogenolysis in the liver during the first two hours of exercise of moderate intensity. It was unclear, however, the extent to which such an effect is directly or indirectly due to epinephrine-induced suppression and enhancement, respectively, of insulin and glucagon secretion during exercise. Henriksson et al. (1985) suggest that the training induced decline in resting plasma insulin and glucagon levels in rats may be mediated by adrenomedullary hormones. Carlson et al. (1985) maintain that during submaximal exercise in rats, the principal targets for epinephrine release from the adrenal medulla appear to be pancreatic fl-cells and skeletal muscle and not the liver. Gorski (1978) showed that the glycogenolytic effect of epinephrine in the skeletal muscle of resting rats is greatest in the intermediate muscle, and least in white muscle. Bukouwiecki et al. (1980) noted an enhanced lipolysis in the adipose tissue of exercise-trained rats, seemingly demonstrating the markedly increased adipocyte capacity for lipolytic response to epinephrine brought about by exercise training. This increased response was regarded to occur at a metabolic step distal to the stimulus recognised by the adreno-receptors, possibly at the level of the protein kinases or lipases. Terblanche et al. (1981) observed that the livers of trained rats displayed a significant increase in glycerol kinase activity, in fact 50% higher than in untrained animals, and, as mentioned above, Taskinen et al. (1980) and Walberg et al. (1983) found increased lipoprotein lipase activity in adipose and muscle tissue, related to the blunting of the insulin response to exercise in trained subjects. Izawa et al. (1984) found that the response of rat epididymal adipose tissue to exercise training is mediated not only by the /:~-effect of catecholamines but also by various other hormonal factors. In man, Schnabel et al. (1984). investigating the rise in insulin levels after cessation of exhaustive supramaximal running, maintain that the strong sympatho-adrenal response to exercise of this nature is a major determinant in the increase of glucose at cessation of exercise. The hyperglycemia in concert with fl-adrenergic stimulation leads to elevation of insulin secretion. Many workers report the enhanced mobilization of F F A s into the blood stream brought about by exercise training. Aroa and Ikuyama (1984) report that exercise training increases the capacity of epinephrine-stimulated lipolysis and decreases sensitivity to insulin's anti-lipolytic action in fat cells. Kita et al. (1984) found that the dissolution of triacylglycerols in fat cells is accelerated during exercise in athletes, and the resynthesis of F F A s into triacylglycerols may be relatively slowed down. This may be due, they propose, to a weakened insulin action in lipolysis suppression, accelerated action of catecholamines and glucagon in lipolysis and a decrease in glucose uptake due to a weakened insulin action. The availability of glucose via carbohydrate intake affects levels of circulating hormones on exercise. Jansson et al. (1982) found that although plasma

Hormonal response to exercise levels of epinephrine and norepinephrine were similar on both a carbohydrate-poor diet and a carbohydrate-rich diet, exercise-induced increases in epinephrine and norepinephrine were more pronounced after the carbohydrate-poor diet. A carbohydrate-poor diet apparently increases the relative contribution of fat to oxidative metabolism and increases the sympatho-adrenal response to exercise. 3.2. The thyroid hormones

The thyroid gland is characterized by its very large supply of hormones and the very slow turnover of its products. It secretes a mixture of two hormones, thyroxine and triidothyronine, which accelerate cellular reactions in most organs and tissues of the body, increasing basal metabolic rate, accelerating growth and augmenting oxygen consumption. 3.2.1. Response o f the thyroid hormones to exercise.

The response of the thyroid gland and its two amine hormones, triidothyronine and thyroxine, to exerciseinduced metabolic changes is much slower and longer than that of the pancreas and the adrenomedulla, and occurs in response to changed levels of the anterior pituitary thyroid stimulating hormone. Refsum and Stromme (1979) found that serum thyroxine and triidothyronine increased after prolonged heavy exercise but fell below starting levels on the following day and were only restored four days after the exercise. Thyroid-stimulating hormone (TSH) rose after the exercise and continued to 175% of starting level by the next day and was only restored to the initial level four days after exercise. They suggest that the prolonged rise of TSH is probably due to an exercise-induced increased peripheral need for thyroid hormone. Sawhney et al. (1984) found that hormone secretion by the thyroid and its responsiveness to endogenous TSH are maintained after exercise. The observed decrease in circulatory thyroxine and triidothyronine after exercise could be due to increased degradation of the hormones or may reflect a generalised adaptation phenomenon, they suggest. Burkashov et al. (1981) report that thyroxine and TSH plasma content increased whereas triiodothyronine concentration decreased with exercise. They maintain that a rise in cell metabolism and changes in the internal medium of the organism influence the alteration of the blood thyroid hormone and TSH levels. Thyroid and hypophyseal thyrotropic functions depend to a certain degree on the exercise intensity and functional preparedness of the sportsmen. Schmid et al. (1982) report a decrease in TSH levels during maximal physical exercise and a rise during submaximal long-term physical exercise. They suggest these changes in TSH might reflect similar changes in levels of pituitary secretion. The triiodothyronine level rises significantly in maximal physical exercise whereas during submaximal long-term exercise it remains unchanged. The rise during maximal exercise might be related to hemoconcentration. The reverse triiodothyronine level does not change during the exercise. The free tetraiodothyronine level continually decreases which may be due to an elevated cellular utilization. Krotkiewski et al. (1984) report that TSH concentration increased during acute work and decreased

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immediately thereafter. Galbo et al. (1977b) found that serum concentrations of TSH increased with increasing intensity and duration of exercise. However, Smallridge et al. (1985) and Hooper et al. (1980) found that serum TSH levels were unaltered by exercise. Licata et al. (1984), however, report a decrease in TSH levels during exercise which is in agreement with the finding of Schmid et al. (1982). In the case of thyroxine and triiodothyronine levels, most workers report no alteration with exercise (Hooper et al., 1980; Smallridge et al., 1985; Galbo et al., 1977b) although as stated above, Burkashov et al. (1981) report an increase in thyroxine levels with a decrease in triiodothyronine levels. Schmid et al. (1982), as stated above, found a significant rise in triiodothyronine levels during maximal physical exercise, but no change during submaximal prolonged exercise. Krotkiewski et al. (1984) found a negative correlation between changes in fasting insulin and thyroxine levels, but a positive correlation between changes in blood pressure and triiodothyronine levels after exercise training. Hooper et al. (1980), found that both exercising humans and rats had significantly lower iodine uptake values than sedentary controls meaning that exercise significantly alters thyroid iodine economy. Licata et al. (1984) suggest that there may be a real rise in thyroid excretion during exercise. 4. THE STEROID HORMONES

The steroid hormones have two sources: the gonads and the adrenal cortex. The gonads produce the male and female sex hormones, the androgens and the oestrogens. The adrenal cortex produces at least fifty different steroids. Those with hormonal activity are of several different classes: the glucocorticoids are important in carbohydrate metabolism and have a wide variety of other activities involved in maintaining homeostasis particularly during stress; the mineralocorticoids are important in regulating the balance of Na ÷ and K ÷ ions; the adrenal cortex is also an important source of androgens and a minor source of oestrogens and progestins. 4. I. The adrenal cortex

The three major steroid hormones of the adrenal cortex are the glucocorticoids, cortisol and corticosterone and the mineralocorticoid, aldosterone. 4.1.1. The glucocorticoids cortisol and corticosterone. Cortisol is the most important of the gluco-

corticoids (cortisol, cortisone, corticosterone and 1 l-deoxycorticosterone). Its effects on carbohydrate metabolism are as follows: it increases glucose release from the liver, increases glycogenesis and decreases peripheral uptake and utilization of glucose. In lipid metabolism, glucocorticoids promote lipolysis thus facilitating the action of epinephrine and glucagon. The anti-inflammatory effects of cortisol and related compounds relate to their effects on leukocyte function and their limiting effect on formation of the inflammatory prostaglandins. 4.1.1.1. Response o f glucocorticoids to exercise.

Glucocorticoids such as cortisol are required for the organism to cope with a wide variety of stresses, thus plasma levels tend to rise according to the intensity

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of the exercise. The pituitary adrenocorticotropic hormone (ACTH) levels rise on stress, including exercise (Gambert et al., 1981) thus raising cortisol levels, depending on the intensity of the exercise (Farrell et al., 1983; Kuoppasalmi et al., 1980). Farrell et al. (1983) suggest that plasma lactic acid may influence ACTH release during exercise. Tabata et al. (1984) propose that serum ACTH and cortisol concentration during low intensity prolonged exercise may be dependent on blood glucose concentration. Pagano et al. (1979) report that cortisol levels rise higher in exercising obese subjects than non-obese. Sutton (1977) reports that cortisol levels increase more during hypoxic exercise than normoxic exercise. Francesconi et al. (1984) report that acclimation had no effect on plasma cortisol levels in the euhydrated condition but that there was an attenuation of plasma cortisol response when hypohydrated. Some workers find that cortisol levels rise on exercise but only when intense and prolonged (Kindermann et al., 1982; N~iveri, 1985) whereas Kuoppasalmi et al. (1980) report an increased mean plasma cortisol of 27% on short-term running and an increase of 43% in intense long-term running. Vanhelder et al. (1985) found that plasma cortisol levels increased significantly during anaerobic intermittent exercise but not during continuous aerobic exercise. Marniemi et al. (1984) report that on combined fasting and exercise, levels of cortisol increased significantly, greater than for exercise alone. Reports on the effect of exercise training on the cortisol response to stress vary. Bopp et al. (1978) report greater rises in untrained subjects whereas Bloom et al. (1976) reported greater cortisol values in exercise-trained cyclists than in their untrained group at higher workloads. Hakkinen et al. (1985) investigating testosterone and cortisol levels during neuromuscular performance training, found that the testosterone/cortisol ratio increased during training, correlating with changes in maximal strength. 4.1.2. The mineralocorticoids. The main hormones with mineralocorticoid activity in humans are aldosterone and deoxycortisone as well as cortisol. They promote increased reabsorption of Na + and the secretion of K ÷ and protons as ammonium ions, thus affecting fluid as well as electrolyte balance. 4.1.2.1. The effect o f exercise on aldosterone levels.

Most workers report an increase in aldosterone levels on exercise. Melin et al. (1980) found that aldosterone and vasopressin displayed highly significant increases after exercise to exhaustion in untrained, trained and well-trained groups. This type of exercise produces a highly significant increase in plasma levels of hormones involved in electrolyte and water balance. Geyssant et al. (1981) report that aldosterone and vasopressin levels displayed significant increases on exercise before and after training. Thus far there seems to be little difference reported in aldosterone levels between trained and non-trained subjects. Maresh et al. (1985) report that maximal exercise in females produced significant increases in plasma vasopressin and aldosterone levels comparable to those reported previously for male subjects. Although the adrenal cortex produces androgens and oestrogens, these will be considered under the steroid hormones.

4.2. The androgens 4.2.1. Testosterone. The androgens are produced in the testes, ovaries, the adrenal cortex and the placenta. However, it is testosterone, the main male androgen produced in the testes, that has been most investigated in response to exercise. 4.2.1.1. Testosterone response to exercise. Most workers report a drop in testosterone levels as a result of exercise, although Galbo et al. (1977b) report an increase after 40 minutes of prolonged exercise which then declined on further exercise. Kuoppasalmi et al. (1980) report no real changes in testosterone during short-term running, although there was a small increase of 19% in adrostenedione of the adrenal cortex. However, intense long-term running caused a drop in testosterone which was not apparent immediately after the exercise but 30 min later dropped and remained depressed for up to 3 hours after the end of exercise. The increase in androstenedione rose to 53% on intense long-term running. Dobrzanski et al. (1981) report a significant decrease of testosterone under work load which had not returned to normal 45 minutes after exercise. Kuusi et al. (1984) found that testosterone levels, as well as steroid hormone binding globulin levels, decreased during a 42.2 km marathon. Marniemi et al. (1984) report decreased levels of testosterone in men (not women) caused by combined fasting and several days exercise, thus indicating the involvement of the LH-testis pathway. However, Vogel et al. (1985) report a significant increase in free and total testosterone during submaximal exercise in normal males, and Kindermann et al. (1982) report that intense exercise does not affect testosterone secretion. 4.2.1.2. The effect o f exercise training. Hakkinen et al. (1985) report an increase in the testosterone/cortisol ratio during training and an increase in the testosterone/sex hormone binding globulin (SHBG) ratio. This confirms an earlier report by Remes et al. (1979) claiming highly significant increases in plasma testosterone and aldrosteredione during a training period, with an increase of the testosterone/SHBG ratio of 32%. 4.3. The estrogens

The estrogens are secreted mainly by the ovaries, although estrogens are also produced by the testes. Estrogen secretion is determined by the two pituitary gonadotropins: Luteinizing hormone ( L H - a polypeptide) and follicle stimulating hormone (FSH--also a polypeptide). During the menstrual cycle, the levels of estrogens and progesterone fluctuate (progesterone is secreted mainly by the corpus luteum and also by the adrenals). Changes in circulating levels of ovarian hormones may exert an effect on the normal menstrual cyclical fluctuations. The phenomenon of amenorrhea in many young female athletes has led to increased interest in the effects of exercise and stress on levels of ovarian hormones and other related hormones e.g. the pituitary polypeptide hormone prolactin. In 1980, Warren suggested that it seemed evident that energy drain could have an important modulatory effect on the hypothalamic pituitary set point

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Hormonal response to exercise at puberty, and in combination with low body weight, may prolong the pre-pubertal state and induce amenorrhea. Brisson et al. (1980) suggest that marked increments in prolactin in post-pubescent girls with a past and present sports history could probably furnish an explanation to findings of a significantly delayed menarche in athletic adolescents. Repeated heavy exercise could create a prolactin impregnation on the maturing ovary sufficient to delay any follitropin folli-stimulating action, a transient amenorrhic condition similar to that of the nursing mother. De Meirleir et al. (1985) report that augmented levels of prolactin during or after exercise are caused by increased pituitary secretion rather than decreased elimination. However, Chang et al. (1984) found a normal 24 hour prolactin secretion in women runners with menstrual dysfunction. Schwartz et al. (1981) comparing amenorrheic long-distance runners with regularly menstruating runners and non-running controls found that although basal steroid levels did not differ among the different groups of female runners, the ratio of estrone to estradiol was significantly higher in all amenorrhea. All amenorrheic runners tested had significantly higher LH and dehydroepiandrosterone sulphate and lower TSH levels. These findings, they claim, suggest that exercise associated amenorrhea is an entity distinct from hypothalamic amenorrhea. Ronkainen et al. (1985) seem to support this view. In their investigation of exercise-induced changes in pituitary-ovarian function of runners and joggers during autumn and spring they found that a high training activity and a dark photoperiod appeared to independently suppress ovarian activity, and were not associated with chronic changes in anterior pituitary hormones or sex hormone binding globulin concentrations. Bonen et al. (1979) reported that although heavy exercise provokes significant increases in ovarian hormones in untrained subjects, no such increments are observed in trained subjects exercising at the same absolute workload. Bullen et al. (1984) noted that within acute bouts of exercise, plasma concentrations of all stress markers and antireproductive hormones rose significantly, and that ovarian function was disturbed in four out of seven subjects as evidenced by a decreased excretion of oestriol, free progesterone or both. Cumming et al. (1985) found that exercise induces an increment in circulating LH levels greater than the change in haematocrit. They suggest that acute exercise has an inhibitory effect on LH pulsatile release at the hypothalamic level in eumenorrheic runners that is in addition to training induced effects. Hoshi et al. (1984) report that exercise produced increases in the levels of ovarian hormones such as progesterone and estradiol but that the pituitary control system for usual menstrual fluctuations does not seem to contribute to these increases. Jurbowski et al. (1978) also found that increases in estradiol and progesterone are related to the intensity of exercise and appear to be independent of pituitary control. Although advances in the important field of hormonal response to exercise have been quite spectacular during the past decade, there still remain very important unanswered questions. From the above brief literature survey it is obvious that the

polypeptide hormones have received most attention. However, this attitude is not unexpected as many metabolic abnormalities and common diseases are associated with polypeptide hormone disturbances. The amine hormones, especially the catecholamines, have also received extensive attention. It is wellknown that the catecholamines are very closely associated with very important metabolic adaptations as a result of exercise and training. However, there exist numerous avenues for research in this field to elucidate many questions, still unanswered, associated with the adaptation of the biological system to exercise and training. From this brief literature survey it would seem as if the steroid hormones did not receive the attention that they deserve during the past decade. The use and abuse of steroid hormones by sport participants should receive serious attention. The possible detrimental effects associated with the use and abuse of steroid hormones (as well as the numerous synthetic derivatives available) by sport participants should be intensively investigated. As most of these derivatives contain testosterone as the active substance it is considered of prime importance that the detrimental effects associated with the use and abuse of anabolic steroids by female sport participants should receive special attention. literature survey was made possible by financial assistance from the University of Zululand, the Chamber of Mines of South Africa and the South African Sugar Association. Acknowledgements--This

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