Altitude Illness and Training in the Athlete

Air pressure falls with altitude, so although the air still holds the same proportion of oxygen, each breath delivers less of it, a state called hypobaric hypoxia. The body responds by breathing faster and deeper and by raising the heart rate to maintain oxygen delivery, and over days to weeks it acclimatises. Erythropoietin (EPO), the hormone that stimulates red cell production, rises quickly, but a meaningful increase in total red cell or haemoglobin mass generally needs sustained exposure over weeks, and any early rise in haemoglobin concentration may partly reflect a reduced plasma volume rather than new red cells.

Altitude illness arises when ascent outpaces this acclimatisation, generally above about 2500 metres, with the risk rising the higher and the faster the ascent, and with individual susceptibility. In acute mountain sickness and cerebral oedema, hypoxia is thought to lead to swelling of the brain. In pulmonary oedema, hypoxia causes uneven hypoxic pulmonary vasoconstriction, the normal tightening of lung vessels in low oxygen, which here is patchy and overperfuses some capillaries, leading to stress failure and fluid leaking into the lungs. This is a non-cardiogenic, hydrostatic oedema, which is why descent and pulmonary vasodilators, rather than treatments for a failing heart, are what help.

Acute mountain sickness needs recent ascent plus a headache and at least one of nausea or vomiting, fatigue or weakness, or dizziness, so headache alone is not enough. It is common, comes on within hours, and is usually mild to moderate and settles if no further ascent is made. High-altitude cerebral oedema is the severe end of that spectrum and is defined by ataxia, unsteadiness on the feet, or an altered mental state such as confusion or drowsiness, rather than simply a worsening headache, and if untreated it progresses to coma.

High-altitude pulmonary oedema is fluid in the lungs, presenting with breathlessness that comes to be present even at rest, a cough, reduced exercise capacity and chest tightness, and later pink frothy sputum. Examination may show rapid breathing, a fast pulse, crackles or wheeze and blueness of the lips (cyanosis), with low oxygen levels, and it is the leading cause of death from altitude illness. Both pulmonary and cerebral oedema are emergencies.

The diagnosis is largely clinical, based on the symptoms and the pattern of ascent, and acute mountain sickness is graded with the 2018 Lake Louise score. Important differentials should be considered, including dehydration or exhaustion, low blood glucose, hypothermia, low blood sodium, carbon monoxide poisoning from stoves in tents, infection, pneumonia and a clot on the lung. Oxygen saturation (SpO2) from a pulse oximeter can support the assessment but must be read against the altitude, the clinical picture and readings from fellow travellers, since there is no single normal value that excludes illness. Other tests are rarely needed in the field. In hospital a chest X-ray in pulmonary oedema shows patchy shadowing and brain imaging may be used in cerebral oedema, but management is not delayed for these.

Management depends on severity. Mild to moderate acute mountain sickness can stay at the same sleeping altitude with rest, observation and symptomatic treatment such as simple painkillers and anti-sickness medicine, descending only if symptoms worsen or fail to improve over one to three days. Severe acute mountain sickness, and any cerebral or pulmonary oedema, need urgent descent, since even a modest loss of altitude can be life-saving, with supplemental oxygen and, where available, a portable hyperbaric chamber, especially when immediate descent is not possible.

Medicines have specific roles. Acetazolamide is a carbonic anhydrase inhibitor that causes a mild loss of bicarbonate in the urine and a compensatory metabolic acidosis, which drives ventilation through the peripheral chemoreceptors and speeds acclimatisation; it is established mainly for prevention and is not routinely needed for mild acute mountain sickness. Dexamethasone relieves symptoms and treats cerebral oedema but does not promote acclimatisation. For pulmonary oedema, descent and oxygen are primary, and a pulmonary vasodilator, either nifedipine or a phosphodiesterase-5 (PDE-5) inhibitor such as sildenafil or tadalafil, is reserved mainly for when descent is delayed or impossible and oxygen is unavailable, or as selected prevention in people with previous pulmonary oedema.

Prevention is more effective than treatment. Above 3000 metres the sleeping altitude should rise by no more than about 500 metres per day, with a rest day every three to four days, and it is the sleeping altitude that matters most rather than the highest point reached during the day. Acetazolamide can be taken to reduce the risk in those who are susceptible or must ascend quickly. Recognising early symptoms, and not ascending further while symptomatic, prevents progression.

Altitude training aims to improve endurance performance by prompting the body to carry more oxygen. Living or sleeping at altitude can increase red cell mass through erythropoietin, and one of the most studied and widely used models is live high, train low (LHTL), in which the athlete lives and sleeps at altitude to gain the adaptation but trains at lower altitude to keep training quality and intensity high. Living and training high, and intermittent hypoxic exposure or altitude tents, are alternatives. Altitude is also used to acclimatise before competing at altitude, which reduces both altitude illness and the drop in performance on arrival.

The benefits are variable and not guaranteed. Physiological and sea-level performance gains depend on the hypoxic dose, iron status, training quality and individual response. Because new red cells need iron, iron deficiency should be identified and treated medically rather than every athlete simply taking supplements. The adaptation takes weeks, the timing of the return to sea level is planned, and the demands of altitude carry risks of illness, poor recovery and overtraining, so athletes are monitored. On anti-doping, hypoxic exposure and altitude tents are permitted, whereas administering erythropoietin and manipulating blood to boost oxygen transport are prohibited.

• •The 2024 Wilderness Medical Society clinical practice guideline sets out the prevention, recognition and treatment of acute altitude illness, including the central role of descent.
• •The 2018 Lake Louise score provides the criteria for diagnosing and grading acute mountain sickness.
• •Sports science literature on live high, train low and related methods informs altitude training, while acknowledging variable and individual responses.
• •Anti-doping rules distinguish permitted hypoxic exposure from prohibited erythropoietin use and blood manipulation.

• •Altitude illness ranges from acute mountain sickness to high-altitude pulmonary and cerebral oedema, generally above about 2500 metres.
• •Acute mountain sickness is recent ascent plus headache and at least one other symptom, and ataxia or altered mental state warns of cerebral oedema.
• •Breathlessness at rest suggests pulmonary oedema, driven by uneven hypoxic pulmonary vasoconstriction and the leading cause of altitude death.
• •Mild to moderate acute mountain sickness can stay put with observation; severe illness and cerebral or pulmonary oedema need urgent descent.
• •Acetazolamide, a carbonic anhydrase inhibitor, is mainly preventive; dexamethasone treats cerebral oedema; nifedipine or a phosphodiesterase-5 inhibitor is for pulmonary oedema when descent and oxygen are not enough.
• •Above 3000 metres raise sleeping altitude by no more than about 500 metres a day with regular rest days; altitude training, best known as live high train low, gives variable benefit, and erythropoietin and blood doping are prohibited.