Secretion of Somatotropin and Human Age

It has been established that the changes in somatotropin secretion in response to intense physical exercise are somewhat limited in elderly individuals (Craig et al., 1989; Ruka et al., 1992; Kraemer et al., 1999). Growth hormone and somatotropin (STH) are synonyms. The main reason for this limited increase in STH levels could be lower physical load, due to the inability to perform the same overall volume of work during training sessions. It has been reported that a lower level of lactate in the blood of older individuals during resistance exercises is a confirmation of the hypothesis that the effort exerted during strength exercises may affect subsequent changes in STH levels (Ruka et al., 1992). The negative impact of aging on blood buffering capacity and the ability to tolerate acidosis are factors that may help explain the reduced increase in growth hormone levels induced by intense resistance training (Godfrey et al., 2003). Short-term training programs (10–12 weeks) do not lead to changes in this pattern (Craig et al., 1989; Kraemer et al., 1999). After completing a periodized resistance training program lasting 10 weeks, no significant changes in STH levels were found in both young and older individuals, either at rest or after physical exercise (Kraemer et al., 1999). Using the same relative load, the change in blood lactate levels after intense resistance training was lower in older individuals than in younger ones, and the increase in lactic acid was not accompanied by disturbances in acid-base balance (Rogers et al., 2004), which may indicate a reduction in metabolic demands and maintenance of acid-base balance. This partially explains the less pronounced changes in growth hormone levels in older individuals. The decrease in resting STH concentration and the less noticeable increase in STH levels after physical exercise remains unchanged after a short training program.

The understanding of the effects of physical exercise and the aging process on the physiological mechanisms underlying the phenomenon of somatopause (i.e., reduced activity of the STH-IGF-1 system) is still in its early stages. Since this endocrine regulation system is believed to play a crucial role in maintaining the normal condition of the musculoskeletal system, it is reasonable to suggest that attempts should be made to influence it through resistance training programs. Given the significant molecular heterogeneity of STH and the fact that the standard radioimmunoassay (RIA) is designed to detect the hormone isoform with a molecular weight of 22 kDa, this issue is an important direction for future research. It should also be noted that isoforms of STH with higher molecular mass may have higher biological activity, and the absence of changes or a decrease in immunoreactive STH may not fully reflect the adaptive changes in all forms of growth hormone in response to physical exercise. In other words, determining only the isoform of somatotropin with a molecular weight of 22 kDa may not provide a complete understanding of the adaptive changes in STH secretion by the pituitary gland in response to physical exercise.

Training Adaptations

According to available data, strength training does not affect the concentration of the 22 kDa isoform of growth hormone (GH) in the blood at rest. Surprisingly, no changes in the concentration of GH in the blood at rest were detected in men and women of various ages after strength exercise (Kraemer et al., 1999; McCall et al., 1999; Hakkinen et al., 2000; Marx et al., 2001). There were no differences in the response of the 22 kDa isoform of GH to physical activity, nor in the secretion of GH at rest, even when comparing individuals with lower physical fitness levels, including professional weightlifters and bodybuilders who have trained consistently for extended periods (Hakkinen et al., 1998; Ahtiainen et al., 2003). These results align with the existence of dynamic feedback mechanisms and the wave-like nature of GH secretion, as well as the variety of functions that this hormone may perform in the homeostatic control of several metabolic and recovery processes.

A correlation was found between the resting GH levels and the degree of hypertrophy of type I and II muscle fibers (r = 0.62 and 0.74, respectively) (McCall et al., 1999). These relationships may indicate the role of the repeated increase in GH secretion, induced by regular strength training, in cellular adaptation in trained muscles. Changes in GH receptor sensitivity, differences in feedback chain functioning mechanisms, IGF-1-mediated stimulation, interaction with binding proteins, stimulation of the formation of other molecular isoforms of the hormone in somatotropic cells of the pituitary, and diurnal fluctuations in hormone concentration—all may play a role in mediating the response of the 22 kDa isoform of GH.

Induced growth hormone secretion in women in response to physical exercise is comparable in absolute magnitude to that in men; however, the relative increase in STH levels compared to the resting state tends to be slightly lower in women (Kraemer et al., 1991). This also applies to the response to intense physical activity. Specific training programs (e.g., using 5-rep max loads, 3-minute rest intervals, or small overall volume of work) that cause a slight increase in STH levels in men may not cause significant changes in women, due to their higher baseline hormone levels at rest (Kraemer et al., 1991, 1993). How these relatively minor changes in STH levels in response to intense physical activity lead to adaptive changes in the trained tissues remains unclear.

Gender differences

It is suggested that the higher concentration of growth hormone at rest in women may compensate for the lower levels of other anabolic hormones, which could minimize the role of a sharp increase in secretion during physical activity. These observations were made during the early follicular phase of the menstrual cycle. Recent data suggest that estrogen, when taken as an oral contraceptive, has a minimal impact on the change in STH secretion in response to strength training (unpublished data). Alongside the influence of the menstrual cycle on changes in growth hormone levels in the blood, another possible explanation for the observed sex differences may be variations in STH secretion by the pituitary gland, as the regulation of the volume and character of STH secretion in men and women could also have distinct features (Pincus et al., 1996).

Specificity of the exercises

One of the fundamental principles of biology, as well as strength training, is the principle of specificity. This principle also manifests in the response of somatotropin to strength exercises. In a study conducted by Kraemer and colleagues (Kraemer et al., 2001), four different groups participated. For 19 weeks, the first group performed exercises with concentric contractions, the second group performed the same exercises but with double the volume, the third group followed a standard strength training program that included both concentric and eccentric contractions, and the fourth group did not participate in any training programs (control group). After completing the training programs, the participants were asked to perform two physical load tests, one of which included 3 sets of 30 isokinetic concentric contractions, and the other included 3 sets of 30 isokinetic eccentric contractions during knee extension. The tests were conducted with a 48-hour break. The immediate response to concentric contractions was the same across all groups, but during eccentric contractions, the group following the standard strength training program (with both eccentric and concentric contractions) showed the greatest increase in somatotropin levels. This result may indicate that their bodies were particularly sensitive to the specific eccentric stimuli that had been included in their training program. After detraining, the response to both tests returned to the same level across all four groups. These data show that STH secretion can be sensitive to specific muscle contractions used in strength training. This assumption is supported by relatively recent data suggesting that the adenohypophysis may have its own direct innervation through nerve fibers with synapses on corticotropic and somatotropic cells (Ju, 1999). Furthermore, it is suggested that the neurohormonal regulation of growth hormone secretion occurs in the following manner: initially, there is a quick response from the nervous system to stress, followed by the gradual development of the humoral phase (Ju, 1999). If this is indeed the case, it is possible that centers in the brain (such as the motor cortex) actively participate in regulating STH secretion during strength training, and this regulatory mechanism is sensitive to the specific muscle contractions used in strength exercises.

Physiological effect

Due to the diverse biological activities and the complexity of growth hormone (GH) as a biological effector, its role in skeletal muscle hypertrophy and anabolic processes in other tissues is just beginning to be explained between simplified hypotheses of direct and indirect effects. It is believed that several interacting factors contribute to the hypertrophy of skeletal muscles induced by strength training, and some researchers do not exclude the possibility that a pronounced increase in STH (somatotropin) levels in the blood after strength exercises could also be one of those factors. This assumption is supported by the fact that in conditions of optimal physical load of strength orientation, rats with removed pituitary glands exhibit impaired skeletal muscle hypertrophy processes, which can be restored by introducing synthetic or pituitary-extracted somatotropin (Goldberg, Goodman, 1969; Grindeland et al., 1994). However, in direct contradiction to this hypothesis is the fact that intensive aerobic exercise also leads to a significant increase in STH concentration in the blood, which, however, has almost no effect on skeletal muscles (Kraemer et al., 1995). Therefore, while an important role of increased GH levels in blood for muscle hypertrophy and anabolic processes in other tissues is possible, it can be suggested that intensive strength and aerobic training differ not in the level of immunoreactive STH in the serum, but in the amount of biologically active hormone. This hypothesis has recently received significant attention (Humer et al., 2001). Moreover, these differences may be due to the activation of different groups of motor neurons and the specific sequence of events that are partially stimulated by the electromechanical activation of contracting muscle fibers. However, immunoreactive STH may stimulate the secretion of high-molecular-weight binding proteins by the pituitary and form complexes with them in the blood. Each of these hypotheses requires confirmation through direct experimental data (Nindl et al., 2003).

The wave-like nature of STH secretion is also of great importance for linear growth. Measurements taken over a day or longer have shown that the growth process is episodic and discrete. For example, in rodents, the highest rate of linear growth occurs when the secretory bursts of growth hormone are separated by intervals of about 3 hours, characterized by very low levels of STH, as seen in males. The rate of linear growth is significantly lower if the deviations in hormone levels from some baseline level are small, as seen in female rats. Thus, the mechanisms regulating the wave-like nature of STH secretion are sexually dimorphic (bursts that lead to significant increases in STH levels, followed by low hormone levels in the intervals between them in males, and more irregular bursts with a higher baseline hormone level in females) and may partially account for the differences in the growth rates of male and female rats (Slob, Van der Werff Ten Bosch, 1975; Jaffe et al., 1998). Moreover, the dynamics of STH secretion is also associated with changes in key enzymes responsible for the longitudinal growth of bones, and perhaps more importantly, it is necessary to analyze the nature of the wave-like changes in STH levels in the blood rather than just assessing single static values. This point is clearly demonstrated by the example of sexual dimorphism caused by different temporal characteristics of the STH secretion process.

At the same time, there are experimental data obtained from animal models that show the importance of exercise-induced GH secretion for somatic growth and muscle hypertrophy. In particular, it has been shown that in golden hamsters (an animal model for continuous growth) subjected to physical exercise, there was an increased basal wave-like level of STH, increased skeletal element length, continuous body mass gain, and reduced fat mass compared to control animals that led a passive lifestyle (Borer, 1989, 1995). Since the wave-like nature of STH secretion is an integral component of the hormone’s function, it would seem that this parameter, as well as the heterogeneity of the superfamily of isoforms and complexes of the hormone, should not be neglected when studying similar processes in humans. However, it should be noted that these experiments were conducted on female hamsters and growth occurred only during a specific developmental age period, namely during puberty.

Conclusions

Intensive strength training may be a potential stimulus for the secretion of the 22 kDa isoform of growth hormone. The degree of increase in secretion depends on the specifics of the training program used. Strength exercises do not have a significant impact on the resting level of the 22 kDa growth hormone in individuals of different sexes and ages. However, wave-like changes in the secretion of STH may be one manifestation of the effects of intensive strength training, and these changes apparently differ between men and women. The presence of feedback loops and interactions with other hormonal systems (such as IGF, GH-binding proteins, stimulation of aggregate formation) adds significant complexity to understanding the biological effects of STH and requires further research on the processes occurring at the target tissue level. Clearly, a deeper understanding of the physiological conditions under which STH functions and its role will contribute to a better understanding of changes and adaptive responses.

Warning

Anabolic drugs should only be used as prescribed by a doctor and are contraindicated for children. The provided information does not encourage the use or distribution of potent substances and is aimed solely at reducing the risk of complications and side effects.

Sources

1. Ahtiainen, J.P., Pakarinen, A., Kraemer, W.J. & Hakkinen, К. (2003) Muscle hypertrophy, hormonal adaptations and strength develop* ment during strength training in strength-trained and untrained men. European Journal of Applied Physiology 89, 555*563.
2. Bikle, D.D., Harris, J., Halloran, B.P. et al. (1995) The molecular response of bone to growth hormone during skeletal unloading: regional differences. Endocrinology 136, 2099*2109.
3. Scanlon, MI’., Isa, B.C. & Dicgucz, C. (1996) Regulation of growth hormone secretion. Hormone Research 46, 149-154.
4. Slob, A.K. & Van der Werff Ten Bosch, JJ. (1975) Sex differences in body growth in the rat. Physiology and Behavior 14, 353-361.
5. Snyder, G., Hymer, W.C. & Snyder, D.J. (1977) Functional heterogeneity somatotrophs isolated from the rat anterior pituitary. Endocrinology 101(3), 788-799.
6. Sutton, J.R. (1983) The hormonal responses to exercise at sea level and at altitude. Progress in Clinical and Biological Research 136, 325-341.
7. Takarada. Y . Nakamura, Y., Aruga, S. et al. (2000) Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion. Journal of Applied Physiology 88(1). 61-65.
8. Turner. J.D.. Rotwein. P., Novakofoki, J. 4 Bechtel. P.J. (1988) Induction at mRNA for IGF-I and -II during growth hormone-stimulated muscle hypertrophy. American Journal of Physiology 255, E5I3-E5I7.
9. Ullman, M. & Oldfors, A. (1989) Effects of growth hormone on skeletal muscle. I. Studies on normal adult rats. Acta Physiologica Scandinavica 135, 531-536.
10. Vanhelder, W.P., Radomski, M.W. & Goode, R.C. (1984) Growth hormone responses during intermittent weight lifting exercise in men. European Journal of Applied Physiology and Occupational Physiology 53(1), 31-34.
11. van der Veen, E.A. & Netelenbos, J.C. (1990) Growth hormone (replacement) therapy in adults: bone and calcium metabolism. Hormone Research 33 (suppl. 4), 65-68.
12. Veldhuis, J.D., Patrie, J., Wideman, L. et al. (2004) Contrasting negative-feedback control of endogenously driven and exercise-stimulated pulsatile growth hormone secretion in women and men. Journal of Clinical Endocrinology and Metabolism 89(2), 840-846
13. Weiss, R.E. & Refetoff, S. (1996) Effect of thyroid hormone on growth: lessons from the syndrome of resistance to thyroid hormone. Endocrinology and Metabolism Clinics of North America 25(3), 719-730.