The endocrine system is the body's network of glands that release hormones, chemical messengers carried in the blood to act on distant tissues. During exercise it works with the nervous system to coordinate the whole-body response, mobilising fuel, defending blood glucose, helping manage fluid and salt, and driving the recovery and adaptation that follow a session. For sport and exercise medicine (SEM), this physiology underpins several important areas: the hormonal disturbance of relative energy deficiency in sport (RED-S), the use of exercise to prevent and treat conditions such as type 2 diabetes, the endocrine changes of overtraining, and the anti-doping context, since many prohibited substances are hormones. This page sets out the glands and hormones involved, how they respond acutely to exercise, and how they adapt to training.
The Glands and Hormones Involved
Several glands drive the response to exercise. The hypothalamus and the pituitary gland, in the brain, act as the control centre, releasing hormones that direct other glands through signalling pathways known as axes. The adrenal glands, which sit above the kidneys, have two parts: the inner medulla releases the catecholamines adrenaline and noradrenaline, and the outer cortex releases cortisol and aldosterone. The pancreas releases insulin and glucagon, which between them govern blood glucose. The thyroid gland sets the resting metabolic rate, and the gonads, the testes and ovaries, release testosterone and oestrogen.
The main endocrine glands involved in exercise and the hormones they release: the hypothalamus and pituitary (control centre), thyroid, adrenal glands (medulla giving adrenaline and noradrenaline, cortex giving cortisol and aldosterone), pancreas (insulin and glucagon) and gonads (oestrogen and testosterone).
Hormones act by binding receptors on or inside their target cells. Water-soluble hormones, such as the catecholamines and the peptide hormones insulin and growth hormone, bind receptors on the cell surface and act within seconds to minutes. Fat-soluble steroid hormones, such as cortisol, testosterone and oestrogen, pass into the cell and change which genes are switched on, a slower but longer-lasting effect. Most of these systems are held in check by negative feedback, so that a rise in the final hormone dampens the signals that drove it. Exercise is a powerful stimulus that shifts many of them at once, and how far each one moves depends on how hard and how long the effort is.
The Acute Response to Exercise
As soon as exercise begins, sympathetic activation releases catecholamines, adrenaline from the adrenal medulla and noradrenaline mainly from nerve endings. These raise heart rate and the force of contraction and mobilise fuel, driving the breakdown of stored glycogen in the liver and muscle and of fat in adipose tissue. At the same time the pancreas lowers its output of insulin and raises glucagon. This shift promotes glucose release from the liver, by glycogenolysis and by gluconeogenesis, and the fall in insulin also releases the brake on fat mobilisation, so blood glucose is defended even as the working muscle takes up large amounts of it, which it does through a pathway driven by muscle contraction that does not depend on insulin.
The acute hormonal response to prolonged exercise: catecholamines rise early and steeply, glucagon, cortisol and growth hormone also rise, and insulin falls, with the size of the changes increasing with intensity and duration.
As exercise becomes harder or more prolonged, the slower hormones come into play. Cortisol, released from the adrenal cortex through the hypothalamic-pituitary-adrenal (HPA) axis, supports glucose production and fat mobilisation and has a catabolic action, freeing amino acids from protein. Growth hormone, from the anterior pituitary, rises during exercise, promoting fat breakdown and helping to spare glucose; it acts both directly and through insulin-like growth factor 1 (IGF-1) signalling, although the acute rise in circulating IGF-1 with exercise is variable. This overall pattern is most marked in moderate-to-hard or prolonged exercise, and its size varies with the intensity, duration and type of exercise, with feeding, and with how well trained the person is: an easy walk changes little, whereas hard or lengthy exercise produces large rises in catecholamines, cortisol and growth hormone. During the session itself the balance tips towards catabolism and fuel release; it is in the hours of recovery afterwards, once feeding resumes, that insulin and the anabolic hormones support repair and the refilling of fuel stores. Fluid balance is defended in parallel, as antidiuretic hormone and the renin-angiotensin-aldosterone system act to conserve water and sodium as sweat losses mount.
High-Yield
•In moderate-to-hard or prolonged exercise, catecholamines, glucagon, cortisol and growth hormone rise and insulin falls.
•Catecholamines and glucagon mobilise fuel and defend blood glucose; falling insulin permits fat use.
•Contracting muscle takes up glucose through an insulin-independent pathway, even as circulating insulin falls.
•Cortisol, through the hypothalamic-pituitary-adrenal axis, is catabolic and rises with harder, longer exercise.
•The size of the response varies with intensity, duration, exercise mode, feeding and training status.
•Regular training improves insulin sensitivity, a central benefit in type 2 diabetes.
Adaptation to Training
Repeated exercise reshapes the endocrine system. The clearest change is improved insulin sensitivity: trained muscle takes up glucose more readily, so less insulin is needed to control it, which is one of the main ways regular activity prevents and treats type 2 diabetes. The response to a given absolute workload also settles, with trained people often releasing less adrenaline and cortisol for the same task as it becomes relatively easier for them. The anabolic hormones, testosterone, growth hormone and insulin-like growth factor 1, contribute to the muscle's response to resistance training, although the local signalling within the loaded muscle that drives muscle protein synthesis matters more for growth than the brief hormone surges seen after a session, a point where older training lore overstated the case. Pushed too far, the same systems can be disturbed. Sustained heavy training without adequate recovery can contribute to the fatigue and underperformance of overtraining, although the endocrine findings here are inconsistent and no single hormone or ratio identifies it. Separately, problematic, prolonged or severe low energy availability can disrupt the hypothalamic-pituitary-gonadal (HPG) axis, reducing the pituitary output of luteinising hormone (LH) and follicle-stimulating hormone (FSH), with variable effects that include menstrual dysfunction or reduced oestrogen in females and altered reproductive function or lower testosterone in males.
Clinical Relevance
This physiology reaches the clinic in several ways that matter in sport. Its most important link is relative energy deficiency in sport (RED-S), in which problematic low energy availability can disrupt the reproductive and other hormonal axes, with variable and wide-ranging effects on health and performance, including weaker bone that raises the risk of bone stress injury, and it needs recognition rather than being put down to hard training. The thyroid also down-regulates as an energy-conserving response, and a fall in free triiodothyronine (free T3), with thyroid-stimulating hormone (TSH) staying normal or low rather than rising, is one of the earliest and most sensitive endocrine markers of low energy availability, a pattern distinct from primary hypothyroidism. In the other direction, exercise is a powerful endocrine treatment, since improving insulin sensitivity places regular activity at the centre of preventing and managing type 2 diabetes. Hormonal disturbance can also feature in overtraining, and the endocrine system sits behind much of anti-doping, since exogenous testosterone, growth hormone and insulin are prohibited at all times under the current World Anti-Doping Agency (WADA) list, with a therapeutic use exemption required where they are medically necessary, as for insulin-treated diabetes.
Exam Tips
•In moderate-to-hard or prolonged exercise, catecholamines, glucagon, cortisol and growth hormone rise while insulin falls.
•Catecholamines and glucagon mobilise fuel and defend blood glucose, while falling insulin allows fat use.
•Contracting muscle takes up glucose through an insulin-independent pathway, even as insulin falls.
•Cortisol acts through the hypothalamic-pituitary-adrenal axis and is catabolic.
•Training improves insulin sensitivity, central to preventing and managing type 2 diabetes.
•Problematic low energy availability can disrupt the reproductive axis, the endocrine basis of RED-S.