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Human Physiology · Endocrine and reproduction

The Adrenal Glands and the Stress Response

The adrenal glands make the hormones of salt balance, stress and emergency. This page explains cortisol, aldosterone and adrenaline, how the stress response works, what long-term steroid medicines do to bone and muscle, and how to tell hard training from overtraining.

12Sections
5Figures
3Tables
10Questions

Part 8 · Endocrine and Reproduction · Chapter 36 of 47

Learning objectives

By the end of this page you should be able to:

  • Describe the zones of the adrenal gland and their hormones.
  • Explain the fast and slow arms of the stress response.
  • Describe the actions and daily rhythm of cortisol.
  • Describe the effects of excess and deficient adrenal hormones.
  • Explain how glucocorticoid medicines affect bone and muscle.
  • Distinguish overreaching from overtraining syndrome.

Why it matters

Many patients take steroid tablets for asthma, COPD, arthritis or inflammatory disease. These drugs weaken bone and muscle, so physiotherapists need to protect against fractures and weakness.

Stress hormones also shape pain, sleep, recovery and athletic performance. Understanding them helps distinguish productive training from harmful overload.

The adrenal glands

Figure 1 · Layers of the adrenal gland

Adrenal cortex zones and medulla with their main hormones A cross-section with three outer cortical zones and an inner medulla. The zona glomerulosa makes aldosterone, the zona fasciculata cortisol, the zona reticularis adrenal androgens, and the medulla adrenaline and noradrenaline. medullaZona glomerulosaaldosteronesalt and water, potassiumZona fasciculatacortisolstress, glucose, inflammationZona reticularisadrenal androgensDHEAMedullaadrenaline, noradrenalinefight or flight in secondsCortex: outer three layers (steroids)
Two glands in one. The cortex makes steroid hormones; the medulla is a modified sympathetic ganglion releasing catecholamines.

The stress response

Figure 2 · The two arms of the stress response

Fast sympathetic-adrenal medulla response and slower hypothalamic-pituitary-adrenal response A stressor triggers two pathways. Fast: sympathetic nerves and the adrenal medulla release adrenaline within seconds, raising heart rate, blood pressure and glucose. Slow: the hypothalamus releases CRH, the pituitary ACTH, and the adrenal cortex cortisol over minutes to hours. Stressorpain, injury, fear, exerciseFast: secondsSympathetic nervesAdrenal medullaAdrenalineheart rate, BP, glucose upSlow: minutes to hoursHypothalamus: CRHPituitary: ACTHAdrenal cortexCortisolglucose, anti-inflammatory
Short bursts help; prolonged activation harms. Chronic stress keeps cortisol raised, affecting sleep, muscle, bone and immunity.

Within seconds of a threat, sympathetic nerves and adrenaline raise heart rate, blood pressure and blood glucose and redirect blood to muscle. Over minutes, the hypothalamic–pituitary–adrenal axis raises cortisol, which mobilises fuel and limits inflammation.

Cortisol

TargetAction of cortisolEffect of long-term excess
GlucoseRaises blood glucose; opposes insulinDiabetes
MuscleBreaks down protein for fuelProximal muscle wasting and weakness
BoneReduces bone formation and calcium absorptionOsteoporosis and fractures [1]
Immune systemSuppresses inflammation and immunityInfections; slow wound healing
FatRedistributes fat to trunk and faceCentral obesity
BrainAlertness; moodSleep and mood disturbance

Figure 3 · Cortisol follows the clock

Daily rhythm of plasma cortisol Cortisol is lowest around midnight, rises in the early morning, peaks shortly after waking and falls through the day. sleeppeak soon after wakinglowest around midnight06121824Time of day (hours)Plasma cortisol
Timing matters for tests and treatment. Steroid tablets are usually taken in the morning to mimic this rhythm. Schematic.
ConditionCauseKey features
Cushing syndromeExcess cortisol, often from steroid medicinesCentral weight gain, thin skin, bruising, proximal weakness, fractures
Addison diseaseAdrenal cortex failureFatigue, weight loss, low blood pressure, dark skin, salt craving
Adrenal crisisSudden cortisol lack, e.g. stopping steroids abruptlyShock, vomiting, collapse: emergency

Aldosterone and adrenaline

Aldosterone acts on the collecting duct to retain sodium and excrete potassium (Chapter 22). It is controlled mainly by the renin–angiotensin system and by plasma potassium. Excess aldosterone causes high blood pressure and low potassium.

Adrenaline from the medulla acts on alpha and beta receptors throughout the body. In exercise, it helps release glucose and fatty acids, increases heart rate and contractility, and dilates airways.

Steroid medicines, bone and muscle

Van Staa and colleagues pooled 66 studies of bone density and 23 of fractures in people taking oral corticosteroids [1]. Bone loss tracked cumulative dose, and fracture risk tracked daily dose [1].

Figure 4 · Steroid tablets and fracture risk

Fracture risk before, during and after oral glucocorticoid therapy Fracture risk rises within three to six months of starting oral glucocorticoids above 5 milligrams of prednisolone a day, stays raised during treatment and falls after stopping. on oral glucocorticoid (over 5 mg prednisolone daily)rises within 3–6 monthsfalls after stopping061218241.01.5MonthsRelative fracture risk
Act early. The meta-analysis recommends early prevention of steroid-induced bone loss [1]. Schematic of the reported time course.

Fracture risk rose within 3–6 months of starting doses above about 5 mg prednisolone daily and fell after stopping, regardless of the underlying disease, age or sex [1]. Steroids also cause proximal muscle weakness, which, together with fragile bone, raises the risk of falls and fractures.

Practical skill · patients on long-term steroids

Start weight-bearing and progressive resistance exercise early, including hip and thigh strengthening, and add balance training [1]. Ask whether bone protection has been considered. Never advise stopping steroids suddenly.

Overreaching and overtraining

Training works by overload followed by recovery. The joint consensus of the European College of Sport Science and the American College of Sports Medicine describes a continuum from planned overreaching to overtraining syndrome [2].

Figure 5 · From hard training to overtraining

Continuum from functional overreaching to overtraining syndrome Three stages: functional overreaching with a short dip and later improvement, non-functional overreaching with falling performance and slow recovery, and overtraining syndrome with prolonged maladaptation lasting months. Other causes must be excluded first. Functional overreachingshort dip, then improvementrecovery: days to weeksNon-functional overreachingperformance falls; slow recoveryrecovery: weeks to monthsOvertraining syndromeprolonged maladaptationrecovery: months or longerBefore diagnosing overtraining, exclude:infection, low energy intake, low carbohydrate or protein, iron deficiency, other illness [2]No single blood marker reliably diagnoses it; monitor performance, mood and fatigue
Balance load with recovery. The consensus stresses prevention, because diagnosis is difficult and recovery from the syndrome is slow [2].

Overtraining syndrome involves prolonged maladaptation of hormonal and other systems, with fatigue, falling performance and mood change [2]. It is a diagnosis of exclusion: infection, low energy intake, iron deficiency and other illness must be ruled out first [2]. No hormone or blood marker meets all criteria for diagnosis [2].

Clinical relevance for the physiotherapist

  • Steroid users. Protect bone and muscle early; fracture risk rises within months [1].
  • Steroid withdrawal. Never advise stopping suddenly; adrenal crisis is a risk.
  • Athletes. Plan recovery; investigate persistent underperformance broadly [2].
  • Chronic pain and stress. Sleep, activity and graded exposure help regulate stress responses.
  • Addison disease. Patients may need extra steroid during illness or intense exertion; liaise with their team.

Assessment and application

SituationInterpretationAction
COPD patient on prednisolone 10 mg for 6 monthsHigh fracture risk [1]Strength and balance training; ask about bone protection
Runner with falling times, poor sleep, low mood for 2 monthsPossible non-functional overreaching or OTS [2]Reduce load; medical screen for other causes
Patient stopped steroids last week, now vomiting and faintPossible adrenal crisisEmergency medical care
Rounded face, thin skin, difficulty rising from chairCushingoid features, proximal myopathyHip and thigh strengthening; inform team

Common mistakes

  • Waiting for fractures before addressing steroid bone loss [1].
  • Diagnosing overtraining from a single blood test [2].
  • Advising abrupt steroid withdrawal.
  • Ignoring energy intake in tired athletes [2].
  • Confusing aldosterone and cortisol actions.

Exam preparation

Long answer

Describe the physiological actions of glucocorticoids. Add a note on Cushing syndrome.

  • Adrenal zones (Figure 1).
  • HPA axis and stress response (Figure 2).
  • Actions on metabolism, muscle, bone, immunity (table).
  • Daily rhythm (Figure 3).
  • Clinical: steroid osteoporosis [1]; Cushing and Addison.

Short notes

  • Aldosterone.
  • Adrenaline in exercise.
  • Glucocorticoid-induced osteoporosis [1].
  • Overtraining syndrome [2].

Viva and practical

  • “Which zone makes cortisol?” — zona fasciculata.
  • “When does fracture risk rise on steroids?” — within 3–6 months [1].
  • “How is overtraining diagnosed?” — by exclusion and monitoring [2].
  • OSCE: plan exercise for a patient on long-term prednisolone.

Current evidence

Exam and traditional teaching

Steroid bone loss is a long-term problem; cortisol or testosterone ratios diagnose overtraining.

What the evidence adds

Fracture risk rises within months of starting steroids and falls after stopping [1].

No single hormonal marker diagnoses overtraining; exclusion and monitoring are key [2].

What the student should understand

Stress hormones are essential in bursts and harmful in excess. Protect bone and muscle early in steroid users, and protect recovery in athletes.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. In the meta-analysis of oral corticosteroids, fracture risk rose:
  1. (A) Only after 10 years
  2. (B) Within 3–6 months of starting
  3. (C) Never
  4. (D) Only in men

Answer: (B) Fracture risk increased rapidly within 3–6 months [1].

Q2. Above what daily dose of prednisolone did bone density fall and fracture risk rise?
  1. (A) 0.5 mg
  2. (B) 5 mg
  3. (C) 50 mg
  4. (D) 500 mg

Answer: (B) Doses over 5 mg daily led to bone loss and fracture risk [1].

Q3. After stopping oral corticosteroids, fracture risk:
  1. (A) Keeps rising
  2. (B) Decreases
  3. (C) Doubles
  4. (D) Is unchanged forever

Answer: (B) Risk decreased after stopping therapy [1].

Q4. Bone density loss with corticosteroids correlated most strongly with:
  1. (A) Patient height
  2. (B) Cumulative dose
  3. (C) Blood group
  4. (D) Time of day

Answer: (B) Strong correlation with cumulative dose [1].

Q5. Functional overreaching is best described as:
  1. (A) A disease
  2. (B) A short performance dip followed by improvement after recovery
  3. (C) Permanent decline
  4. (D) Infection

Answer: (B) Functional overreaching leads to improvement after recovery [2].

Q6. A key word in recognising overtraining syndrome is:
  1. (A) Brief fatigue
  2. (B) Prolonged maladaptation
  3. (C) Muscle soreness
  4. (D) Dehydration

Answer: (B) The consensus highlights prolonged maladaptation [2].

Q7. Before diagnosing overtraining syndrome, clinicians should exclude:
  1. (A) Nothing
  2. (B) Organic disease, infection, low energy intake and iron deficiency
  3. (C) Only injuries
  4. (D) Only sleep

Answer: (B) OTS is a diagnosis of exclusion [2].

Q8. Is there a single accepted blood marker for overtraining syndrome?
  1. (A) Yes, cortisol
  2. (B) Yes, testosterone
  3. (C) No; none meets all criteria
  4. (D) Yes, CRP

Answer: (C) No marker meets all criteria for general use [2].

Q9. Which risk factor is listed as relevant to overtraining?
  1. (A) Negative energy balance
  2. (B) Too much sleep
  3. (C) High iron
  4. (D) Low training

Answer: (A) Caloric restriction and inadequate carbohydrate or protein are relevant [2].

Q10. For a patient starting long-term steroids, physiotherapy should include:
  1. (A) Avoiding all exercise
  2. (B) Early bone-protective loading and fall prevention
  3. (C) Only stretching
  4. (D) Nothing until fractures occur

Answer: (B) Early preventive measures are recommended because risk rises quickly [1].

Quick review

Key takeaways

  • Cortex: aldosterone, cortisol, androgens; medulla: adrenaline.
  • Stress: fast sympathetic–adrenal, slow HPA axis.
  • Cortisol peaks after waking; lowest at midnight.
  • Steroids over 5 mg/day raise fracture risk within 3–6 months [1].
  • Never stop long-term steroids suddenly.
  • Overtraining: prolonged maladaptation; diagnosis of exclusion [2].

Further reading

SourceWhy it earns its place
van Staa TP et al. — Osteoporos Int, 2002Steroids and fracture risk [1]
Meeusen R et al. — Med Sci Sports Exerc, 2013Overtraining consensus [2]
Greenspan’s Basic and Clinical EndocrinologyAdrenal physiology

References

  1. van Staa TP, Leufkens HGM, Cooper C. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporosis International. 2002;13(10):777–787. doi:10.1007/s001980200108 PMID 12378366 Meta-analysis
  2. 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. Medicine and Science in Sports and Exercise. 2013;45(1):186–205. doi:10.1249/MSS.0b013e318279a10a PMID 23247672 Consensus statement

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Reviewed by the Physiotherapist India Team. · Human Physiology contents