The Endocrinology of Strongman: Hormones That Influence Mass, Strength and Recovery - Episode 5: Growth Hormone and IGF-1

Episode 5: Growth Hormone and IGF-1

In the series on Strongman endocrinology, we have reached one of the most famous hormonal axes in sport: growth hormone, GH, and insulin-like growth factor 1, IGF-1. They are often presented as a simple formula for muscle growth, but their physiology is much richer. GH participates in metabolism, fatty-acid mobilization, growth regulation, and tissue repair, while IGF-1 mediates an important part of growth and remodeling effects.

For the strength athlete, the key is to distinguish an acute hormonal response from long-term adaptation. A post-exercise GH spike is not a direct measure of hypertrophy, and the workout that produces the largest hormonal spike is not automatically the most effective workout.

1. What is growth hormone?

GH is a peptide hormone produced and released by somatotroph cells in the anterior pituitary. Its secretion is pulsatile rather than constant. The hypothalamus mainly controls it through GHRH, which stimulates GH release, and somatostatin, which inhibits it. Ghrelin can also stimulate the axis, while GH and IGF-1 contribute to negative feedback.

This organization explains why a single blood GH measurement has limited value in many situations: the concentration can change quickly even in the same person.

2. GH is not a constant hormone

In healthy adults, GH appears in pulses separated by periods of low secretion. Pulse amplitude and frequency are influenced by age, sex, body composition, sleep, energy intake, and physical exercise.

GH secretion decreases with age. Adiposity, particularly visceral fat, is associated with lower secretion. At the same time, deep sleep favors one of the most important physiological GH pulses.

3. Sleep is one of the major stages for GH

One of the most reproducible increases in adult GH occurs after sleep onset and is closely linked to slow-wave sleep. That is why sleep architecture matters, not just the number of hours spent in bed.

For a Strongman athlete, short nights before competition, altered schedules, travel, and fragmented sleep can affect the endocrine environment even when the training program stays the same.

4. What does GH do in the body?

GH has direct and indirect effects. It influences glucose and lipid metabolism, stimulates fatty-acid use, and participates in tissue growth and remodeling. A substantial part of its growth-related effects are linked to stimulation of IGF-1 production and the action of IGF-1 on target tissues.

This distinction matters: GH is not simply another name for IGF-1, and the two molecules have overlapping but non-identical roles.

5. IGF-1: systemic mediator and local growth factor

IGF-1 is produced in multiple tissues. The liver is a major source of circulating IGF-1, but muscle and other tissues can also produce IGF-1 locally. Local IGF-1 can act through autocrine and paracrine mechanisms, affecting the same cell or neighboring cells.

This creates one of the most important nuances of the axis: the blood IGF-1 concentration does not tell the whole story about what is happening inside the muscle fiber that is being trained.

6. GH, IGF-1, and muscle hypertrophy

It is tempting to say that more GH means more muscle. Human evidence is more nuanced. Resistance exercise can increase GH, and the GH/IGF-1 axis participates in growth and remodeling processes, but an acute GH rise is neither a necessary nor a sufficient condition for muscle hypertrophy.

Muscle adaptation depends primarily on mechanical loading and local muscle processes, together with amino-acid availability, energy intake, and overall recovery. Longitudinal studies show that strength and muscle mass can improve without robust and consistent increases in circulating IGF-1.

7. Why does GH spike after training?

The exercise response depends on intensity, duration, muscle mass involved, work density, and training status. Higher-volume resistance protocols with moderate to high intensity and shorter rest periods tend to produce larger acute GH responses than some very heavy, low-volume protocols with long rests.

But this observation should not be turned into a rule that says «the biggest GH response equals the best workout». The hormonal signal is only one piece of a much larger puzzle.

8. GH and energy metabolism

GH promotes fatty-acid mobilization and can reduce glucose utilization in some contexts, helping redistribute energy substrates when metabolic demand changes. During and after exercise, this contributes to the body’s response to altered energetic requirements.

This means GH has a major metabolic role, not just a «muscle-building» role.

9. GH and adipose tissue

One well-established metabolic effect of GH is stimulation of lipolysis. The relationship with body composition is bidirectional: adiposity, especially visceral adiposity, can suppress GH secretion, while changes in body composition can alter axis dynamics.

10. IGF-1 and protein synthesis

IGF-1 activates its receptor and intracellular pathways that can support processes related to cell survival, proliferation, and protein synthesis. In muscle, these signals are part of the adaptation network responding to loading.

Still, it is wrong to reduce hypertrophy to one molecular pathway. Mechanical tension, mTORC1 signaling, amino-acid availability, energy status, and local tissue responses interact continuously.

11. Circulating IGF-1 versus local IGF-1

This is one of the most important distinctions when interpreting laboratory testing. Serum IGF-1 reflects part of endocrine-axis activity, but it is not a perfect window into growth-factor concentration and activity inside a particular trained muscle.

Exercise can produce local changes in growth-factor expression that are not proportionally reflected in the blood. Therefore, a normal IGF-1 test does not mean that muscle tissue is not responding to training.

12. GH and recovery

The GH/IGF-1 axis participates in processes involved in tissue repair and remodeling. During post-exercise recovery, however, it operates together with the nervous system, metabolism, inflammation, sleep, and energy availability.

An athlete does not recover because a certain IGF-1 number is present. Recovery happens because the whole system can support repair and adaptation.

13. GH and tendons

The GH/IGF-1 axis is also relevant to connective tissues. Human research indicates links between activation of this axis, local IGF-1 expression, and collagen synthesis in muscle and tendon.

For Strongman, where tendons and ligaments tolerate enormous loads, this matters. But activating a growth pathway does not mean connective tissue can be accelerated indefinitely. Adaptation still has a time course and depends on loading.

14. GH and bone

GH and IGF-1 participate in the development and maintenance of bone. IGF-1 contributes to osteoblast activity and bone formation processes, while GH influences the growth and remodeling axis.

For an athlete moving very heavy loads, skeletal health is infrastructure, not decoration. But bone adaptation also depends on mechanical loading, nutrients, sex steroids, vitamin D, calcium, and many other factors.

15. Nutrition and the GH/IGF-1 axis

Energy availability influences the axis. Severe energy restriction, illness, and inflammation can alter GH secretion and the relationship between GH and IGF-1. A well-described paradox is that in some states of energy deficit, GH can be elevated while IGF-1 is low, reflecting a form of GH resistance and an attempt to prioritize substrate mobilization.

For Strongman, this shows why overly restrictive dieting during high training demands can affect several endocrine systems at once.

16. Why protein cannot be separated from endocrinology

GH and IGF-1 do not operate in a metabolic vacuum. Amino-acid intake, insulin, energy supply, and carbohydrate availability influence tissue responses. For muscle growth, the mechanical signal and the raw materials have to meet.

17. GH, testosterone, and estrogen are not rivals

Earlier episodes covered testosterone and estradiol and their own roles. The GH/IGF-1 axis interacts with gonadal hormones, and these systems can influence one another in growth, body composition, and metabolism.

Sports endocrinology is not a competition between hormones. It is a network.

18. Why acute GH is not an «anabolic score»

One of the most persistent myths in fitness is that a workout must create the largest possible GH spike to produce the best hypertrophy. Modern research does not support that simple equivalence.

Acute hormonal responses are real, but the relationship between one hormonal pulse and long-term structural adaptation is more complex. Muscle primarily responds to the loading it receives and to the internal environment that allows it to build.

19. GH and maximal strength

Maximal strength in Strongman depends on muscle mass, motor-unit recruitment, coordination, technique, leverage, specificity, and experience. GH can contribute to the general physiological environment, but it is not the switch that turns on a heavy lift.

20. GH and body fat

In general, greater adiposity is associated with lower GH secretion, and loss of excess fat can improve the response. But strength athletes have a particular body-composition context, and a GH value should not be used by itself to judge an athlete.

21. Age and the somatotropic axis

GH secretion declines with age, a phenomenon sometimes called somatopause. The decline is part of normal aging biology, but it does not mean that a healthy adult should try to artificially reproduce adolescent hormone levels.

22. What happens in GH deficiency?

Adult GH deficiency is a distinct medical condition. It can be associated with changes in body composition, bone density, quality of life, and exercise capacity. Benefits of GH treatment in patients with documented deficiency should not automatically be extrapolated to healthy adults.

23. Pharmacological GH is not the same as endogenous GH

Exogenous GH changes hormonal exposure differently from physiological pulsatile secretion. Outside medical indications, pharmacological use is a different situation from normal exercise physiology and can cause adverse effects.

This article describes physiology and does not recommend the use of growth hormone or IGF-1.

24. GH, IGF-1, and sleep across a recovery cycle

In an ideal scenario, an athlete moves through training stress and then into a recovery period in which sleep and adequate energy availability support restoration of the systems. GH is one of the signals involved in this transition, not the sole director.

25. What should a Strongman athlete monitor?

In practice, it makes little sense to judge every workout by how much GH it produced. Much more useful are performance, strength progression, body mass and composition, sleep, appetite, perceived recovery, and training-load history.

When there is clinical suspicion of a GH/IGF-1 disorder, evaluation should be medical and may require dynamic testing rather than a single GH measurement.

26. The central message about GH

Growth hormone is important, but it is not a magic wand for muscle mass. It participates in metabolism and tissue growth and remodeling, while IGF-1 is one of the major mediators of the axis. Yet muscle adaptation cannot be reduced to the blood level of one of these hormones.

27. Conclusion

GH and IGF-1 form a sophisticated endocrine axis influenced by sleep, age, body composition, nutrition, stress, and exercise. In Strongman, this axis contributes to metabolism, tissue remodeling, bone health, connective tissue biology, and recovery processes.

But the most important lesson is the difference between a hormonal response and an adaptation. A GH spike or a change in IGF-1 can show that the body responded to a stressor without proving that the workout automatically produced more muscle.

For the strength athlete, the real objective is not to maximize one isolated hormone. It is to build an environment in which mechanical loading, nutrition, sleep, and recovery allow the entire endocrine system to do its job.

Selected bibliography

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2. Kraemer WJ, et al. “Recovery responses of testosterone, growth hormone, and IGF-1 after resistance exercise.” Journal of Applied Physiology. 2017. DOI: 10.1152/japplphysiol.00599.2016.

3. Van Every WD, D'Souza AC, Phillips SM. “Hormones, Hypertrophy, and Hype: An Evidence-Guided Primer on Endogenous Endocrine Influences on Exercise-Induced Muscle Hypertrophy.” Exercise and Sport Sciences Reviews. 2024;52(4):117-125. DOI: 10.1249/JES.0000000000000346.

4. Jenkins PJ. “Growth hormone and exercise: physiology, use and abuse.” Growth Hormone & IGF Research. 2001;11 Suppl A:S71-S77. DOI: 10.1016/S1096-6374(01)80012-5.

5. Heinemeier KM, Mackey AL, Doessing S, et al. “GH/IGF-I axis and matrix adaptation of the musculotendinous tissue to exercise in humans.” Scandinavian Journal of Medicine & Science in Sports. 2012;22(4):e1-e7. DOI: 10.1111/j.1600-0838.2012.01459.x.

6. Gharahdaghi N, Phillips BE, Szewczyk NJ, Smith K, Wilkinson DJ, Atherton PJ. “Links Between Testosterone, Oestrogen, and the Growth Hormone/Insulin-Like Growth Factor Axis and Resistance Exercise Muscle Adaptations.” Frontiers in Physiology. 2021. DOI: 10.3389/fphys.2020.621226.

7. “Can IGF-1 Serum Levels Really be Changed by Acute Physical Exercise? A Systematic Review and Meta-Analysis.” Journal of Physical Activity and Health. 2020. DOI: 10.1123/jpah.2019-0453.

8. “Sleep and the GH/IGF-1 axis: Consequences and countermeasures of sleep loss/disorders.” Sleep Medicine Reviews. 2019.

9. “The growth hormone/insulin-like growth factor-I axis in exercise and sport.” Endocrine Reviews. DOI: 10.1210/er.2006-0052.

10. “Growth hormone: Synthesis and regulation.” Review of GH physiology, receptor signaling, metabolic regulation and the GH/IGF-1 axis. 2026.