The Endocrinology of Strongman: Hormones That Influence Mass, Strength and Recovery - Episode 8: Insulin and Insulin Sensitivity

1. Insulin is not just the blood-glucose hormone

Insulin is one of the main hormones coordinating how the body handles nutrients after a meal. It is secreted by pancreatic beta cells when energy availability and, in particular, blood glucose rise. Its role is not limited to lowering glucose: insulin changes glucose transport, glycogen synthesis, protein turnover, lipolysis, and energy storage.

In strength sports, insulin matters because skeletal muscle is one of the major tissues responsible for glucose disposal and use. For a Strongman, the useful question is not whether insulin is “good” or “bad,” but how well the body responds to it and how insulin signaling interacts with training, carbohydrates, protein, sleep, and energy availability.

2. How insulin is produced

Insulin is produced in the pancreas, in the islets of Langerhans, by beta cells. After being synthesized as preproinsulin and processed into mature insulin, it is stored in granules and released according to the body's needs.

The insulin response to a meal depends on several factors, including how much and how quickly glucose appears in the circulation, amino acids, and gut-derived signals. Therefore, the same amount of carbohydrate does not always create exactly the same insulin dynamics.

3. The insulin receptor: where the signal begins

Insulin binds to its cell-surface receptor. This receptor is a tyrosine kinase, and its activation triggers a signaling cascade that prominently includes IRS, PI3K, and Akt. These pathways influence glucose transport, glycogen synthesis, and other metabolic processes.

In muscle, one of the clearest consequences is the translocation of the GLUT4 glucose transporter to the cell membrane. This allows glucose to enter the muscle fiber more effectively and be used or stored as glycogen.

4. GLUT4 is central to muscle glucose handling

GLUT4 is a glucose transporter expressed especially in skeletal muscle and adipose tissue. When insulin signals, or when muscle fibers are activated by contraction, GLUT4 can be mobilized to the membrane.

An important detail for athletes is that exercise can increase glucose uptake through pathways that do not depend entirely on insulin. This is one reason a training session can improve insulin sensitivity even when body mass does not immediately change.

5. What insulin sensitivity means

Insulin sensitivity describes how strongly a tissue responds to a given amount of insulin. Better sensitivity means that the same insulin signal can produce a more effective metabolic response.

Insulin resistance is a state in which the response to insulin is reduced. To keep blood glucose within a normal range, the body can compensate for some time by secreting more insulin.

6. Muscle is a major glucose sink

The large amount of muscle mass a Strongman may carry means skeletal muscle represents a major metabolic compartment. Greater muscle mass and regular physical activity can substantially influence how the body handles glucose.

That does not mean more muscle automatically guarantees perfect insulin sensitivity. Sleep, body fat, metabolic inflammation, stress, activity levels, and diet also matter.

7. What happens after resistance training

Muscle contractions and the metabolic changes of exercise increase the availability of mechanisms that allow muscle to take up glucose. After training, insulin sensitivity can remain elevated for a period of time, depending on exercise intensity and volume, the muscles trained, and the starting metabolic state.

This is one physiological reason carbohydrate intake around training can be practical, but it should not become a religion built around an “anabolic window.” Total intake and the whole-day context matter more than a perfect minute for insulin.

8. Insulin and muscle glycogen

Insulin stimulates processes that favor storage of glucose as glycogen. For a Strongman, muscle glycogen matters because it contributes to repeated effort, work volume, and recovery between sessions.

Glycogen restoration is not exclusively an insulin phenomenon. Muscle contraction, carbohydrate intake, and the increased insulin sensitivity after exercise work together.

9. Insulin and muscle protein metabolism

Insulin has anabolic effects on protein metabolism, including reducing protein breakdown under some conditions. However, in healthy humans, simply forcing insulin higher after every meal does not automatically create a large increase in muscle protein synthesis.

For hypertrophy, mechanical loading and adequate amino acid availability are central. Insulin provides important metabolic and anti-catabolic context, but it does not replace mechanical stimulus or sufficient protein intake.

10. Insulin is not a universal muscle-growth switch

The idea that a large insulin rise automatically produces more hypertrophy is an oversimplification. A meal containing adequate amino acids, energy, and carbohydrate can generate a physiological insulin response without an athlete trying to create extreme insulin excursions.

In practice, repeatedly trying to maximize insulin secretion through refined sugars does not guarantee a hypertrophy advantage and can make energy intake harder to control.

11. Why insulin should not be demonized in nutrition

Insulin lowers blood glucose by facilitating glucose uptake and storage and changes substrate use. That is physiologically necessary. The metabolic problem is not the existence of insulin, but chronic dysregulation between energy intake, metabolic tissues, and insulin responsiveness.

12. Insulin and fat storage

Insulin inhibits lipolysis and, under appropriate conditions, supports energy storage. This is where its reputation as a “fat-storage hormone” comes from. But regulating energy storage does not mean that insulin alone causes fat gain regardless of energy balance.

Increasing adipose tissue reflects sustained positive energy balance over time, while insulin is one of the regulators controlling nutrient flux in that context.

13. Insulin sensitivity versus compensatory hyperinsulinemia

With insulin resistance, the pancreas can compensate for a period by producing more insulin. Blood glucose may therefore remain apparently normal while the metabolic system is already working with a greater hormonal demand.

This is why a single fasting glucose value does not always provide the full picture. Markers should be interpreted within clinical and metabolic context.

14. What can reduce insulin sensitivity

Sedentary behavior, excess adiposity, insufficient sleep, some metabolic diseases, chronic stress, and certain pharmacological contexts can be associated with insulin resistance. Effects differ between people and cannot be reduced to a single cause.

15. Exercise is a powerful metabolic tool

Both acute exercise and repeated training can improve insulin action in skeletal muscle. Chronic adaptations involve multiple changes, including glucose transport, oxidative capacity, and muscle tissue composition.

A recent umbrella review of resistance training in adults with type 2 diabetes found improvements in fasting insulin, HOMA-IR, glucose, and HbA1c, along with increases in muscle mass and strength. Certainty was more modest for some metabolic markers than for strength outcomes.

16. Why resistance training matters for Strongman

A Strongman does not just need an abstractly “healthy” metabolism. He needs to ingest, store, and use substantial amounts of fuel around repeated high-output efforts. Trained muscle is a critical part of that system.

Good insulin sensitivity can therefore be viewed as metabolic infrastructure: it helps the body handle nutrients efficiently without turning every meal into an endocrine experiment.

17. Carbohydrates do not automatically damage insulin sensitivity

A high carbohydrate intake can create repeated insulin responses, but repeated responses are not automatically equivalent to insulin resistance. Total energy intake, activity level, body composition, diet quality, and training demands all matter.

During heavy training phases, carbohydrates can be essential for performance and recovery. Demonizing carbohydrates simply because they stimulate insulin ignores the physiology of active muscle.

18. Carbohydrate timing: useful, not magical

Placing carbohydrates before and after training can be useful for fueling exercise and replenishing glycogen. For most athletes, however, total daily energy and nutrient intake matter more than a strict several-minute “window.”

19. Insulin and energy availability

Insulin is part of the network of energy signals that change when energy availability is reduced. Under low energy availability, insulin can change along with leptin, IGF-1, T3, and reproductive hormones.

For athletes, the important point is that severe energy deficiency is not only a calorie problem. It can alter endocrine physiology that supports recovery, tissue synthesis, and performance.

20. Severe restriction can change metabolic signals

Recent athlete literature shows that very low energy availability can be associated with lower insulin, IGF-1, T3, and leptin and with changes in protein turnover. These are signals of adaptation to deficiency, not proof that the body has suddenly become “metabolically efficient.”

21. Sleep and insulin sensitivity

Insufficient or fragmented sleep can impair glucose regulation and insulin action. For a Strongman combining high workloads, mechanical stress, and substantial energy demands, sleep is not a metabolic luxury but a core component of recovery.

22. Stress and cortisol meet insulin

Cortisol and other stress hormones influence substrate availability and carbohydrate metabolism. During chronic stress, poor sleep, and incomplete recovery, glucose regulation can become more difficult. The relationship is dynamic and context-dependent, not simply “cortisol blocks insulin.”

23. Insulin sensitivity and body composition

Excess adipose tissue, especially when associated with metabolic dysfunction, can contribute to insulin resistance. But classifying someone by weight or BMI alone does not tell you their insulin sensitivity.

A very large athlete may have an excellent metabolic profile or a problematic one. Body composition, activity, family history, diet, and relevant laboratory testing are more informative than a weight-based label alone.

24. Insulin and muscle mass: the relationship is bidirectional

Insulin affects muscle metabolism, but muscle mass also affects glucose handling. More active muscle tissue generally means a larger compartment where glucose can be taken up and used.

This is one reason resistance training has metabolic effects that go beyond simply increasing strength.

25. Hyperinsulinemia does not automatically mean “bad fuel”

A transient rise in insulin after a meal is physiological. Chronic compensatory hyperinsulinemia is something else and should be interpreted together with glucose, insulin sensitivity, and other markers.

26. HOMA-IR and its limits

HOMA-IR is an index calculated from fasting glucose and insulin and can be useful in research or clinical orientation. It should not, however, be treated as a universal score that by itself diagnoses every insulin-sensitivity problem.

Thresholds vary by population, assay, and context. Proper interpretation belongs within clinical assessment, especially when symptoms, family history, or other metabolic abnormalities are present.

27. Why normal glucose does not tell the whole story

The body can maintain glucose within a normal range by increasing insulin secretion as sensitivity declines. Therefore, metabolic assessment may need several variables rather than a single fasting glucose value.

28. What does “high insulin” mean in an athlete?

Without context, a single insulin measurement does not tell you whether an athlete is healthy, insulin resistant, in energy surplus, or simply responding to the previous meal. Sampling time, fasting status, carbohydrate intake, physical activity, and biological conditions matter.

29. Fasting is not required for good insulin sensitivity

Periods without food can temporarily change insulin and substrate use, but fasting is not synonymous with metabolic health. For a Strongman, an eating strategy must fit energy needs, training volume, and competition objectives.

30. Carbohydrates before training

Pre-exercise carbohydrate can support glucose and glycogen availability and may be particularly useful before long or high-volume sessions. A rise in insulin after eating does not make carbohydrate useless for sport.

31. Carbohydrates after training

Post-training carbohydrate can contribute to glycogen restoration, and increased insulin sensitivity after exercise can facilitate that process. The exact importance depends on how soon the next session occurs and on total daily intake.

32. Why a Strongman should not eat like a patient with diabetes

Nutrition strategies for metabolic disease and performance are not identical. A healthy athlete with high energy expenditure may need substantial carbohydrate intake to support training. The goal is adequate fuel and nutrients, not eliminating every post-meal insulin rise.

33. What can support insulin sensitivity

Regular physical activity, maintaining body composition compatible with metabolic health, sufficient sleep, and a well-structured diet are foundational. There is no single “insulin hack” that replaces these basics.

34. When it becomes a medical issue

Repeatedly abnormal glucose, HbA1c, insulin, or other clinical findings deserve medical evaluation. The exact testing set and interpretation depend on the situation. An athlete should not attempt to treat suspected insulin resistance alone through extreme dieting or supplements.

35. Insulin and pharmacology are a different discussion

Pharmacological insulin use outside medical indications is not equivalent to normal physiology and can cause severe hypoglycemia, loss of consciousness, and other complications. The fact that insulin is anabolic in some processes does not make it a safe muscle-building tool.

36. Insulin, GH, IGF-1, cortisol, and thyroid hormones

Athlete endocrinology does not operate through isolated hormones. Insulin interacts with the GH/IGF-1 axis, energy signals such as leptin, thyroid hormones, and the stress response. A change that looks favorable in one system may be unfavorable in another if the body is under-fueled, ill, or overloaded.

37. The myth that lower insulin is always better

Very low insulin is not an end goal. During prolonged fasting or energy restriction, lower insulin can be a normal adaptation. Around meals and after training, insulin secretion is physiological and useful.

38. The myth of the “maximal insulin spike” for anabolism

You do not need to deliberately create a huge insulin spike after training. When carbohydrate and protein are present in a normal meal, the resulting endocrine response is generally sufficient for the physiological recovery processes involved.

39. What matters in practice for a Strongman

For a healthy Strongman, priorities remain adequate energy intake, sufficient protein, carbohydrate matched to training volume, progressive training, sleep, and recovery. Insulin sensitivity is one component of the system, not the entire puzzle.

During a gaining phase, the goal is not to avoid insulin but to manage the energy surplus in a controlled way. During contest preparation or a deficit, the challenge is to avoid letting restriction destroy recovery and performance.

40. Conclusion

Insulin is a central metabolic hormone, and insulin sensitivity is one of the properties determining how efficiently the body can handle glucose and other nutrients. In muscle, the relationship between insulin, GLUT4, and contraction creates a direct link between endocrinology and resistance training.

For Strongman, the key message is simple: do not demonize insulin and do not obsess over it. You need a metabolic system that responds well, supported by training, adequate energy, appropriate carbohydrate intake, sleep, and recovery. Insulin is infrastructure, not magic.

Selected references

1. DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care. 2009.

2. Richter EA, Sylow L, Kiens B. Acute and chronic exercise effects on insulin sensitivity and glucose metabolism. Endocrine Reviews. Literature on skeletal muscle glucose transport and exercise adaptation.

3. Holten MK et al. Strength training increases insulin-mediated glucose uptake in skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism. 2004.

4. Sylow L et al. Exercise-stimulated glucose uptake in skeletal muscle is mediated by multiple signaling pathways. Literature on contraction-mediated GLUT4 trafficking.

5. Colberg SR et al. Exercise and Type 2 Diabetes: American College of Sports Medicine and American Diabetes Association joint position statement. Diabetes Care. 2010.

6. Resistance training and diabetes mellitus type 2: an umbrella review of systematic reviews and meta-analyses on glycemic and cardiometabolic outcomes. 2026.

7. Resistance training, skeletal muscle hypertrophy, and glucose homeostasis: a systematic review and meta-analysis. 2024.

8. Unraveling skeletal muscle insulin resistance: molecular mechanisms and the restorative role of exercise. 2025/2026 review literature.

9. Short-Term Severe Low Energy Availability in Athletes: Molecular Mechanisms, Endocrine Responses, and Performance Outcomes. Scandinavian Journal of Medicine & Science in Sports. 2025;35(6):e70089.

10. Biochemical Responses to Experimentally Induced Short-Term Low Energy Availability in Athletes: A Systematic Review. 2025/2026.