Cortisol and Catabolism

Cortisol is often painted as the enemy of muscle: a stress hormone that eats away at hard-earned gains. The truth is more interesting. Cortisol is essential for life and for training adaptation, and it becomes a problem mainly when it stays high for too long. Our editorial team explains how cortisol drives catabolism, when that matters and how to keep it in balance.

What cortisol is and why we need it

Cortisol is the main glucocorticoid hormone in humans, produced by the outer layer of the adrenal glands under the control of the hypothalamus and pituitary — the so-called HPA axis. Its release is triggered by adrenocorticotropic hormone (ACTH), which in turn responds to corticotropin-releasing hormone from the brain.

The hormone follows a pronounced daily rhythm. Levels rise sharply in the first 30–45 minutes after waking, a phenomenon called the cortisol awakening response, then fall gradually through the day to their lowest point around midnight.

Cortisol keeps blood glucose stable between meals, maintains blood pressure, regulates the immune response and helps the body cope with physical and psychological stress. People whose adrenal glands cannot produce it, as in Addison's disease, need lifelong replacement therapy and can become dangerously ill during illness or injury.

As Sapolsky and colleagues described in a landmark review, glucocorticoids have permissive, stimulatory, suppressive and preparative actions. In short, cortisol helps mobilise resources for a challenge and then helps switch the stress response off.

How cortisol breaks down muscle

Catabolism is the breakdown of complex molecules into simpler ones to release energy or building blocks. Cortisol promotes catabolism in several tissues, and skeletal muscle is one of the main targets because it is the body's largest reservoir of amino acids.

• Protein breakdown: cortisol activates the ubiquitin–proteasome system and genes such as atrogin-1 and MuRF1 that tag muscle proteins for degradation.
• Reduced synthesis: it dampens the mTOR pathway, which drives muscle protein synthesis, partly by interfering with insulin and IGF-1 signalling.
• Gluconeogenesis: released amino acids such as alanine travel to the liver, where they are turned into glucose.
• Fat mobilisation: cortisol supports the release of fatty acids from adipose tissue, although chronic excess favours fat storage around the abdomen.

Schakman and colleagues reviewed how high glucocorticoid exposure causes muscle atrophy, especially in fast-twitch type II fibres — the ones most important for strength and power. This is clearly seen in Cushing's syndrome and in people on long-term high-dose steroid tablets such as prednisolone.

In healthy people with a normal rhythm, however, these catabolic actions are balanced by anabolic signals from feeding, insulin, growth factors and mechanical loading. Muscle is constantly being broken down and rebuilt, and cortisol is just one of many regulators of that turnover.

Exercise, cortisol and adaptation

Intense or prolonged exercise raises cortisol. Hackney has shown that the response depends on intensity and duration: efforts above roughly 60 per cent of maximal oxygen uptake, or very long sessions, produce the largest increases, which return to baseline within a few hours.

This transient rise is not harmful. It helps maintain blood glucose, mobilises fuel and contributes to the inflammatory signalling that drives adaptation. In a large study of young men undergoing resistance training, West and Phillips found that the post-exercise cortisol response was not negatively associated with gains in muscle — if anything, a weak positive relationship was seen for lean mass.

Problems appear when stress is chronic and recovery is inadequate. The joint ECSS/ACSM consensus on overtraining describes altered HPA-axis responses as one of the features of non-functional overreaching and overtraining syndrome, alongside persistent fatigue, falling performance and mood disturbance.

Low energy availability, now discussed under the term Relative Energy Deficiency in Sport (RED-S), is another major driver. When athletes eat too little for their training load, cortisol tends to rise while anabolic hormones fall, creating a catabolic environment that affects bone, muscle and reproductive health.

What raises cortisol chronically

Several everyday factors can push cortisol above its normal pattern for long periods. They are often more important than anything that happens in the gym.

A classic study by Leproult and colleagues showed that even a single night of restricted sleep raised cortisol the following evening, when it should be falling. Repeated over weeks, this pattern can impair recovery and body composition.

It is worth stressing that prescribed steroid tablets, inhalers or injections must never be stopped suddenly without medical advice, as this can trigger an adrenal crisis.

Keeping catabolism in check

The most effective anti-catabolic strategy is not a supplement but adequate total energy and protein. Most sports nutrition bodies suggest around 1.6 g of protein per kilogram of body weight per day for those trying to gain muscle, spread across several meals.

Carbohydrate intake around hard sessions blunts the exercise-induced cortisol rise and spares muscle protein. This is one reason very low-carbohydrate diets can be challenging for athletes with high training volumes.

Supplements marketed as cortisol blockers — phosphatidylserine, ashwagandha, rhodiola and others — have only limited and inconsistent evidence in athletes. Some may modestly reduce perceived stress, but none should be relied on to override poor sleep or underfuelling.

If you have symptoms such as unexplained weight gain around the trunk, purple stretch marks, easy bruising, muscle weakness or very high blood pressure, see your GP. Testing for cortisol excess requires specific protocols, such as late-night salivary cortisol or a dexamethasone suppression test, interpreted by a specialist.

Editorial conclusions

Cortisol is a vital hormone with genuine catabolic effects on muscle, but in healthy athletes the short post-exercise rise is a normal part of adaptation rather than a threat to gains.

Catabolism becomes significant when cortisol remains high for long periods — through chronic sleep loss, persistent underfuelling, excessive training or long-term steroid medicines.

Sleep, sufficient energy and protein, sensible carbohydrate around training and planned recovery are the best tools for keeping cortisol in a healthy range.

For further reading, see our editorial articles on overtraining syndrome, on RED-S in male and female athletes and on how sleep affects muscle recovery.

References

1. Sapolsky RM, Romero LM, Munck AU. How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions. Endocr Rev. 2000;21(1):55–89.
2. Hackney AC. Stress and the neuroendocrine system: the role of exercise as a stressor and modifier of stress. Expert Rev Endocrinol Metab. 2006;1(6):783–792.
3. Schakman O, Kalista S, Barbé C, Loumaye A, Thissen JP. Glucocorticoid-induced skeletal muscle atrophy. Int J Biochem Cell Biol. 2013;45(10):2163–2172.
4. West DWD, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2012;112(7):2693–2702.
5. Meeusen R, Duclos M, Foster C, et al. Prevention, diagnosis, and treatment of the overtraining syndrome: joint consensus statement of the European College of Sport Science and the American College of Sports Medicine. Med Sci Sports Exerc. 2013;45(1):186–205.
6. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the Female Athlete Triad — Relative Energy Deficiency in Sport (RED-S). Br J Sports Med. 2014;48(7):491–497.
7. Leproult R, Copinschi G, Buxton O, Van Cauter E. Sleep loss results in an elevation of cortisol levels the next evening. Sleep. 1997;20(10):865–870.