Hormones in Short-Term Exercises: Anaerobic Events

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Strength and Conditioning Journal: Vol. 25, No. 4, pp. 31–37.

Hormones in Short-Term Exercises: Anaerobic Events
Atko Viru and Mehis Viru


Institute of Exercise Biology, University of Tartu, Estonia

Key Words: hormones, anaerobic, epinephrine, glycogenolysis



PAST REVIEWS HAVE INDICATED hormonal metabolic control as an essential mechanism for metabolic adjustments during exercise and performance (19, 20, 32, 58). Most studies have considered prolonged exercises (19, 58). However, in short-term anaerobic exercise, the actual performance may take less time compared with the triggering of the hormonal response. Therefore, a hormonal response would occur after the sprint, acyclic power, or high-resistance activity was completed because a time delay is unavoidable. However, hormonal responses such as increases of blood concentration of catecholamines, cortisol, and testosterone are evoked by sprint (15, 39), short-term power (3, 36), and strength (16, 24) exercises. A question arises whether these rapid hormonal responses influence the metabolic processes and have significance during these anaerobic exercises. This brief review explores the possibilities for hormonal metabolic control in short-term anaerobic exercises, and the following topics are discussed:

The possibility for fast-rate hormonal changes.

The time characteristics of metabolic effects of fast-rate hormones.

The exercise intensities and the hormonal response.




Fast-Rate Hormonal Responses

Exercise-induced hormonal changes are classified as fast-, moderate-, and slow-rate responses (56). The fast-rate responses are characterized by significant hormonal changes appearing within the first minute after the onset of exercise. These responses are common for activation of the sympathoadrenal system (rapid increase of blood levels of epinephrine and norepinephrine) as well as the pituitary-adrenocortical system (rapid increase of corticotropin concentration, followed by a less rapid but longer lasting cortisol response) (30, 57). Fast-rate hormonal responses are related to the effect of the central motor command. Impulsation from cortical pyramidal neurons communicates directly with the spinal motoneurons. At the same time, a collateral charge reaches the hypothalamic center and activates the sympathoadrenal system as well as neurosecretory neurons (32). The activating messages are sent to the adrenal medulla by sympathetic nerves. The pituitary hypothalamic liberins (releasing neurohormones) activate the adenohypophysis. Furthermore, hormones released from the adenohypophysis travel through circulation and act on peripherial endocrine glands. This way, highly intensive supramaximal exercises and very short muscle efforts of explosive or high resistance types are capable of triggering increased activity of several endocrine systems.

Epinephrine and norepinephrine are fast-rate response hormones that are stored in endoplasmic granules of the cells of the adrenal medulla in the definite form. Sympathetic nerve impulses from the splanchnic nerve to the adrenomedullary cells cause liberation of acetylcholine from nerve endings. Under the action of acetylcholine, epinephrine and norepinephrine release from the granules and flow into the circulating blood. As a result, epinephrine and norepinephrine levels in blood increase rapidly at the beginning of exercise. Triggering of other hormonal responses requires more time because it depends on the secretion time of neurohormones from the hypothalamus, activation of secretion of trophic hormones in the pituitary, and activation of peripheral endocrine gland.



Significance of Exercise Intensity for Hormone Responses

Exercise intensity is one of the main determinants of hormonal changes during the exercise (59). Epinephrine and norepinephrine responses are modest or nonexistent at low or moderate intensities of exercise. When a critical intensity, called intensity threshold, is surpassed, a sharp rise appears in concentrations of both epinephrine and norepinephrine (21, 38, 55). Several studies provided evidence that the threshold intensity for catecholamine response is close to the anaerobic threshold (8, 38, 40, 53).

Corticotropin (13, 48, 50), cortisol (11, 25, 46), *-endorphin (14, 48, 50), and growth hormone (8, 44, 52) also exhibit intensity thresholds during an exercise response. Similarly to catecholamines, threshold intensities for corticotropin, *-endorphin (48), and cortisol (46) are close to the anaerobic threshold as indicated by lactate dynamics. Results of Gabriel et al. (18) confirmed that exercise until volitional exhaustion increased blood levels of epinephrine, norepinephrine, cortisol, corticotropin, and *-endorphin when the intensity corresponded to 100% of the individual's anaerobic threshold. However, hormonal responses were not significant at intensities corresponding to 85% of the anaerobic threshold. Chwalbinska-Moneta et al. (8) reported a close relationship between triggering growth hormone response and the anaerobic threshold. However, others have reported that the growth hormone threshold is lower than the anaerobic threshold (25, 52). Glucagon levels appeared to increase in exercises at 100% of O2max but did not increase at lower intensities during short-term exercises (21, 45). The testosterone response to exercise for men was significant at 4.0 W·kg−1 but not at 1.5–2.5 W·kg−1 (28). Galbo et al. (22) reported a modest increase in testosterone level in their subjects after maximal, but not submaximal, treadmill exercises. Exercise intensities between 40 and 70% of O2max (21, 25, 47) were associated with a decline in the insulin concentration. Furthermore, a decrease in insulin levels appeared at very low (10% O2max) exercise intensity while consuming a high-fat diet (47). However, near- or supramaximal exercise intensities may lead to an increase in the insulin levels instead of the usual decrease (1, 27).

Unlike catecholamine responses, at overthreshold intensities the magnitude of cortisol response does not exhibit a strict dependence on futher increase of exercise intensity (46). Various studies have indicated that cortisol responses are more related to exercise duration than to the level of power output or running velocity (25, 26, 51). Supramaximal exercises may even attenuate cortisol response (2, 30, 46). It has been suggested that increased H+ ion concentration in anaerobic exercises might inhibit the cortisol response (2). The contribution of exercise intensity and duration for formation of the cortisol response is rather complicated: In some cases, the effect of the intensity may be stronger than the effect of the duration (37).

Exercise duration appears to have a strong effect on growth hormone. In fact, the exercise duration may overshadow the significance of exercise intensity (32, 51). Unlike growth hormone, exercise duration does not increase the testosterone response. As exercise duration increases, the testosterone levels decline (22) to values below the initial level (31). Wilkerson et al. (61) reported increased testosterone levels in their subjects during 20 minutes of exercise with an exercise intensity between 60 and 80% O2max. However, further increases of exercise intensity were not associated with more pronounced increases in testosterone concentrations. In women, testosterone responses are related to steroidogenesis in the adrenal cortex. Therefore, there are gender differences in testosterone patterns during exercise. In women, testosterone concentration was the highest at the end of 2 hours of exercise (60).

The determination of plasma volume showed that the increased testosterone concentrations depended on reduction of plasma volume. Thus, the actual increase in testosterone secretion was not found (61).



Effect of Anaerobic Exercise on Blood Hormone Levels

Taking into account the significance of exercise intensity for hormonal responses, there should be little doubt that anaerobic exercises activate endocrine functions. The questions remaining are what is the minimum duration of highly intensive exercise to trigger hormonal responses, and do these responses appear during or after “pure” anaerobic exercises?

Fentem et al. (15) reported increased blood epinephrine and norepinephrine concentrations during 6 seconds of cycling at maximal power output. Thus, we can conclude that anaerobic exercises lasting only a few seconds are capable of activating the sympathoadrenal system. However, blood sampling in this study took place 3 minutes after the exercise, and we cannot conclude that these hormones were released during the 6 seconds of exercise. Furthermore, a 4- to 7-fold increase in norepinephrine and epinephrine has been reported immediately after 30 seconds of maximal pedalling rate (39) or within 30–90 seconds after a 30-second dash (4). The high hormone concentrations are evidence of a high-rate catecholamine response. Consequently, it can be assumed that rapidly secreted catecholamines may contribute to the metabolic control during sprint exercises, at least during the second half of these very short-term exercises.

Fast responses have also been found in corticotropin (6, 13, 14, 17, 30), *-endorphin (4, 14, 17), and cortisol (13, 30) levels. Because corticotropin activates the secretion of cortisol, the corticotropin response is faster than that of cortisol (6, 30). Although growth hormone and glucagon responses usually appear in aerobic exercises after a lag period of 10 minutes or more (57), these responses are detectable in anaerobic exercises immediately after the end of exercise and last 1–2 minutes or even less (43, 45).

Repeated short-interval, short-term anaerobic exercise (similar to the interval training) leads to pronounced lactate accumulations in the blood and is associated with high catecholamines (45), growth hormone (1, 23, 29, 54), and testosterone (23, 28) levels. Adlercreutz et al. (1) reported that the high rate of testosterone response was associated with a parallel increase of lutropin concentration in blood. Lutropin is the endogenous stimulus for testosterone secretion.

Although short-term high-intensity exercises trigger the hormonal responses, their maximum hormonal response may not appear immediately after the end of exercise but rather 5–15 (in some cases even 30) minutes later. Obviously, the stimulus for activation of endocrine function was so strong that it created a prolonged readiness for intensive muscular activity (for fighting in phylogenetic past).

In submaximal exercise, the typical training effect is a reduced response to several hormones because of an increase of the intensity threshold measured in terms of power output (19, 58). At the same time, training increases the capacities of the endocrine system (58), leading to an exaggerated hormonal response in trained organism during supramaximal exercises. The improved functional capacities of the endocrine system are apparent by the increased concentration of blood catecholamines (5, 33, 34, 55), *-endorphine (5, 7, 14), cortisol (5, 51), and growth hormone (5, 51) responses to supramaximal exercise in a trained organism. Particularly important are exaggerated catecholamine responses after sprint training (42) and corticotropin, cortisol, and *-endorphin responses after sprint-interval training (35). In the sprint-trained person, the immediate increase of growth hormone as well as increases of cortisol and insulin concentration are, after 30 seconds of sprint, more pronounced than in endurance-trained persons (43).



Hormones in Metabolic Control During Anaerobic Exercises

Metabolic effects of hormones are based on the binding of a hormone to its specific cellular receptor. The hormone-receptor complex initiates a further chain of intracellular events, leading to a certain alteration in enzyme activity that may increase or decrease due to changes in molecules of enzyme proteins. Another possibility is induction of synthesis of an enzyme protein. Hormone receptors are located either on the cellular membrane (e.g., catecholamines), in the cytoplasm (e.g., steroid hormones), or in the cellular nucleus (e.g., thyroid hormones). Alterations in enzyme molecules are introduced by means of receptors on cellular membranes, which allow for rapid metabolic effects. Also rapid are the metabolic effects that result from hormone interference to the postreceptory processes, evoked by another hormone through its specific cellular hormone receptor. Receptors in cytoplasm or nucleus initiate protein synthesis. The cascade of these processes requires time up to a couple of hours.

The most rapid hormonal metabolic effect is that of epinephrine on glycogenolysis. In skeletal muscles, glycogen degradation is triggered by intracellular metabolic alterations associated with the initiation of the contraction of myofibrils (appearance of acetylcholine inside the cell, increased concentration of Ca2+ in sarcoplasma). However, the effects of these metabolic alterations are short-term. Epinephrine ensures prolonged and pronounced degradation of glycogen in muscle tissue (49). Because training—particularly sprint training—increases epinephrine responses, it is possible that the amount of epinephrine rapidly reaching the muscle tissue and binding with adrenoreceptors of the sarcolemma has an essential role for achieving the maximal rate of glycogenolysis. In this way, an extensive mobilization of the anaerobic working capacity is achieved.

The specific receptor for cortisol is located in the cytoplasm. Therefore, several metabolic effects of cortisol (e.g., control of glucose-alanine cycle, stimulation of gluconeogenesis and of catabolic processes) appear after an hour or more has elapsed. However, cortisol can promote processes following the binding of epinephrine to the receptor without a substantial time lag. In this case the cortisol binding by its specific cytoplasmic receptor is not necessary. Hence, cortisol is essential in creating intracellular conditions for increased action of epinephrine.

The metabolic effects of other hormones are too slow for evoking changes in cellular metabolism during short-term anaerobic exercises. However, rapid recovery of anaerobic working capacity, muscle strength, and power depends on influences of insulin, cortisol, and testosterone on glycogen resynthesis (58).

Normal intra- and extracellular balance of sodium and potassium ions must be restored with each contraction-relaxation cycle. This balance influences intracellular shifts of calcium. The relaxation process depends directly on reabsorption of cytoplasmic calcium by the sarcoplasmic reticulum. In very intensive exercises, the restoration of ionic balances between intra- and extracellular sodium and potassium contents is not complete, and this becomes a factor decreasing the performance (10, 12). Therefore, after each strong contraction, ionic shifts must happen at a high rate to restore the initial conditions. This depends on the function of the Na+/K+-pump on the cellular membrane and the Ca2+-pump in the membrane of sarcoplasmatic reticulum. The function of ionic pumps is an energy-consuming process dependent upon adenosine triphosphate by enzymes Na+, K+-ATPase, and Ca2+-ATPase. The main activator of the Na+/K+ pump is epinephrine, whereas the long-term adaptations of the pump (increased number of related molecules, particularly molecules of Na+/K+-ATPase) depend on insulin and thyroid hormones (9). Sprint training increases human skeletal muscle Na+/K+ATPase concentration and improves K+ regulation (41).



Conclusion

High intensities of anaerobic exercises elicit pronounced hormonal responses. However, most of these hormonal responses appear or reach their maximum after short-term exercises. Therefore, the existence of a certain hormonal response does not indicate that the hormone contributes to metabolic control. The rapid action of epinephrine on muscle glycogenolysis makes it essential in triggering and maintaining muscle glycogen breakdown during anaerobic exercise, mainly in those anaerobic exercises in which duration is more than 20–30 seconds. It is possible that cortisol influences the epinephrine hormone response. Contribution of other hormones in metabolic control during short-term anaerobic exercises does not seem plausible. However, the exercise-induced hormonal responses may have significance during the recovery period as well as during the preparation of the athlete for subsequent efforts, with short rest intervals. The role of hormones in long-term adaptation for anaerobic performance has not been demonstrated.



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Atko-Meeme Viru is a professor emeritus specializing in exercise physiology at the University of Tartu, Estonia. He earned a Ph.D. from the University of Tartu, and D.Sc. from the Academy of Sciences of Estonia. His investigations examine endocrine functions in muscular activity and adaptation mechanisms in training.
Mehis Viru is a senior researcher at the Institute of Exercise Biology, University of Tartu. He earned a Ph.D. from the University of Tartu. His research work is focused on specificity of training effects on skeletal muscles and endocrine functions, as well as on biochemical monitoring of training.