Exercise and high altitude

Cardiovascular response to exercise

• Sympathetic activity in exercise raises heart rate and contractility (β1), constricts splanchnic, renal and inactive-muscle vessels (α1), mobilises glucose and fatty acids, and dilates bronchi. The muscle pump and venoconstriction increase venous return, sustaining stroke volume.
• Isotonic (dynamic) exercise mainly raises cardiac output with a fall in SVR; isometric (static) exercise raises blood pressure sharply because contracting muscle compresses its own vessels.
• Training increases stroke volume (resting bradycardia), capillary density, mitochondria and myoglobin. VO₂ max is limited mainly by maximum cardiac output.

Respiratory response to exercise

• Ventilation rises up to 15–20 times. It increases almost immediately (feedforward from the motor cortex and limb proprioceptors) and then tracks CO₂ production, so in moderate exercise arterial PO₂, PCO₂ and pH stay close to normal; the extra CO₂ load delivered to the lungs is what ventilation matches.
• Above the anaerobic (lactate) threshold, lactic acid accumulates; the acidosis drives extra ventilation, so PaCO₂ falls.
• Ventral respiratory group neurons (expiratory and accessory inspiratory) become active during forced breathing, recruiting internal intercostal and abdominal muscles for active expiration; the dorsal respiratory group sets the basic inspiratory rhythm.
• Oxygen consumption by the respiratory muscles rises steeply with ventilation.
• Pulmonary circulation: pulmonary blood flow rises several-fold while pulmonary artery pressure rises only slightly, because previously closed apical capillaries are recruited and open ones distend, lowering pulmonary vascular resistance. Flow therefore increases most in the upper zones, making perfusion more uniform and improving V/Q matching. The ratio of dead space to tidal volume falls as tidal volume rises.
• Oxygen extraction rises: the arteriovenous O₂ difference widens, and heat, CO₂, H⁺ and 2,3-BPG shift the dissociation curve to the right.

Metabolism in exercise

• Energy sources in sequence: stored ATP, creatine phosphate (about 10 s), anaerobic glycolysis, then aerobic oxidation of glucose and fat.
• Respiratory quotient: about 0.7 for fat, 1.0 for carbohydrate; it rises towards 1 in intense exercise.
• Muscle contraction moves GLUT4 to the membrane independently of insulin.
• Potassium leaves contracting muscle, so strenuous exercise is the commonest physiological cause of a shift of K⁺ into the ECF.
• Oxygen debt (excess post-exercise oxygen consumption) restores ATP and creatine phosphate, reloads myoglobin and clears lactate.

High altitude

• Barometric pressure falls, so inspired PO₂ falls: PIO₂ = 0.21 × (P_B − 47). At about 5,500 m P_B is half of sea level. At a barometric pressure of 275 mmHg (about one-third of an atmosphere, near 8,500 m), PIO₂ is about 48 mmHg; even with intense hyperventilation alveolar PO₂ is only about 25–30 mmHg and arterial saturation falls to about 50% or less.
• The hypoxia of altitude is hypoxic hypoxia (low arterial PO₂), unlike anaemic, stagnant or histotoxic hypoxia.

• Acute mountain sickness: headache, nausea, fatigue, poor sleep. Prevent with slow ascent and acetazolamide, which causes bicarbonate loss and a mild metabolic acidosis that stimulates breathing.
• High-altitude pulmonary oedema: patchy, uneven hypoxic vasoconstriction overperfuses some capillaries, which leak. Descent, oxygen, nifedipine.
• High-altitude cerebral oedema: ataxia, confusion. Descent, oxygen, dexamethasone.
• Chronic mountain sickness: excessive polycythaemia and hypoxaemia in long-term residents.

Diving

• Pressure rises by 1 atmosphere for every 10 m of seawater.
• Boyle's law: gas volume falls on descent and expands on ascent. Ascending while holding the breath over-expands the lungs, causing pulmonary barotrauma, pneumothorax and arterial gas embolism. Middle ear and sinus barotrauma occur if they do not equalise.
• Henry's law: more gas dissolves at depth. Nitrogen narcosis appears beyond about 30 m (euphoria, impaired judgement).
• Decompression sickness: on rapid ascent, dissolved nitrogen comes out as bubbles in tissues and blood, causing joint pain ("the bends"), itchy rash, breathlessness ("the chokes") and spinal or cerebral deficits. Treat with 100% oxygen and hyperbaric recompression.
• Oxygen toxicity at high partial pressures causes seizures and lung injury.
• Breath-hold diving: hyperventilation beforehand lowers PCO₂, removing the urge to breathe, so the diver can lose consciousness from hypoxia (shallow water blackout).

Microgravity

Fluid shifts towards the head, plasma volume falls by diuresis, bone mineral and muscle mass are lost, and orthostatic intolerance appears on return to gravity.

Heat stress

• At rest in a cool room most heat is lost by radiation; during exercise and whenever air is hotter than skin, evaporation of sweat is the main and finally the only route.
• High humidity reduces the vapour pressure gradient, so sweat drips without evaporating. An athlete in humid heat still depends on evaporation, but it becomes inefficient and core temperature rises, so heat illness is more likely.
• Acclimatisation over 1–2 weeks: earlier and greater sweating, lower sweat sodium (aldosterone), larger plasma volume.
• Heat exhaustion: water and salt depletion; core temperature below 40 °C; normal mental state.
• Heat stroke: core temperature above 40 °C with CNS dysfunction; multi-organ failure; rapid cooling first.

Remember Exercise is matched by cardiac output and redistribution; altitude by hyperventilation, bicarbonate loss and red cells; diving by respecting Boyle and Henry.

Exam trap At altitude the kidney excretes bicarbonate, which lets ventilation rise further.

Exam trap Pulmonary resistance falls as flow rises in exercise, through recruitment and distension.

How FCPS asks about this

• Pulmonary flow rises with little pressure rise: recruitment and distension of apical capillaries.
• Neurons active in forced breathing: ventral respiratory group.
• Acclimatisation: bicarbonate excretion, raised 2,3-BPG and erythropoietin, polycythaemia.
• Diver with joint pain and breathlessness after rapid ascent: decompression sickness from nitrogen bubbles; give oxygen and recompression.
• Pressure at depth: rises 1 atm per 10 m.
• Athlete in humid heat: evaporation is the main route but is impaired by humidity.
• Cardiac output in heavy exercise: up to 5–6 times resting, mostly to muscle.