Exercise Physiology at Altitude

Key Terminology

• Hypobaria – low atmospheric (barometric) pressure.
• Hypoxia – low oxygen availability in tissues or environment.
• Hypoxemia – low PO2 (partial pressure of O$2$) in arterial blood.
• Altitude (for this lecture) – any elevation > 1{,}500\text{ m} above sea level.
• Barometric pressure (P\text{bar}) vs. PO_2
  • P\text{bar} falls with elevation; %O$_2$ in the air (~21 %) remains constant.
  • Lower P\text{bar} ⇒ lower PO2 ⇒ less O$2$ available to load onto Hb.

Atmospheric & Environmental Conditions at Altitude

• Sea-level P\text{bar} \approx 760\text{ mmHg}; Mt. Everest summit \approx 260\text{ mmHg} (varies with weather, season & locale).
• Temperature lapse rate: air temp ↓ ≈ 10^{\circ}\text{C}\;(1.8^{\circ}\text{F}) every 150\text{ m} gained.
• High winds common ⇒ ↑ convective & evaporative heat loss; ↑ risk of cold injuries.
• Low absolute water-vapor pressure; cold air holds minimal moisture:
  • Skin: steep H$_2$O gradient ⇒ rapid evaporation ⇒ dehydration.
  • Lungs: ↑ respiratory water loss (further amplified by altitude-induced hyperventilation).
• Solar radiation ↑ markedly:
  • Thinner air + ↓ water vapor ⇒ less absorption ≈ more UV/short-wave radiation reaching surface.
  • Snow/ice reflectivity amplifies exposure ("albedo effect").

Acute Physiological Responses (Minutes → Days)

Pulmonary Ventilation

• Immediate chemoreceptor drive (carotid & aortic bodies) to low PO_2 ⇒ ventilation ↑ within seconds.
  • ↑ tidal volume + ↑ respiratory rate.
• Respiratory alkalosis develops (↓ P\text{a}CO2) ⇒ kidneys excrete HCO$3^- to restore pH; this renal compensation stabilises ventilation after several days.
• Hb–O$2$ dissociation curve shifts left (↑ Hb affinity) because of alkalosis; partially counterbalances low ambient PO2.

Pulmonary Diffusion

• At altitude the alveolar–arterial O$2$ gradient is already depressed; diffusion capacity itself is unchanged, so arterial hypoxemia directly mirrors low alveolar PO2.

O$_2$ Transport (Blood)

• Fewer Hb binding sites reach saturation:
  • Sea level: \text{Sa}O_2 \approx 96–97\%.
  • Moderate altitude: \text{Sa}O_2 \approx 80–89\% (depends on height).
• Diffusion gradient muscle ↔︎ blood shrinks:
  • Sea level: P\text{a}O2 \approx 100\text{ mmHg} to tissue P\text{O}2 \approx 40\text{ mmHg} (∆ ≈ 60\text{ mmHg}).
  • High altitude: P\text{a}O2 \approx 42\text{ mmHg} to tissue \approx 27\text{ mmHg} (∆ ≈ 15\text{ mmHg}) ⇒ impaired O$2$ unloading and aerobic performance.

Cardiovascular Adjustments

• Plasma volume ↓ up to 25 % (days–weeks): respiratory H$_2$O loss + altitude diuresis.
• Acute hemoconcentration ↑ hematocrit ⇒ more O$_2$ per unit blood but ↑ viscosity.
• Kidneys release erythropoietin (EPO) ⇒ RBC production ↑ (slower, unfolding over weeks).
• Cardiac output (CO)
  • Rest & sub-max exercise: CO ↑ via sympathetic surge (↑ HR, modest ↓ SV) for first 6–10 days.
  • Max exercise: ↓ SV (from ↓ plasma volume) + slightly ↓ maximal HR ⇒ max CO ↓.

Metabolic Effects

• Basal metabolic rate (BMR) ↑ from ↑ thyroxine and catecholamines ⇒ ↑ caloric need; appetite usually ↓.
• Reliance on carbohydrate ↑ (CHO yields more ATP per O$_2$).
• At first: blood lactate during sub-max ↑ (greater anaerobic glycolysis). After extended stay: lactate response ↓ (“lactate paradox”).
• Nutrition priorities: ample water (>3 L · day$^{-1}$), energy balance, and dietary iron (support erythropoiesis).

Impact on Exercise / Sport Performance

• \dot{V}O2\,\text{max} falls once ambient PO2 < 131\text{ mmHg} (~1 500 m). Drop is roughly linear from 1 500–5 000 m due to arterial PO_2 reduction; above 5 000 m, lower max CO adds further limitation.
• Anaerobic or brief, glycolytic tasks largely preserved or may improve slightly (↓ air density ⇒ ↓ aerodynamic drag) at moderate altitude.

Chronic Exposure & Acclimatization (Weeks → Months)

Ventilatory Adaptation

• Resting ventilation plateaus ≈ 40 % above sea level after 3–4 days at 4 000 m.
• Sub-max exercise ventilation climbs ≈ 50 % above baseline and remains elevated long-term.

Hematological Adaptations

• First 2 weeks: EPO peaks ⇒ RBC count & Hb mass rise.
• By 6 weeks: total blood volume ↑ ≈ 10 % (plasma partially restored; RBC mass stays high).
• Sea-level hematocrit 45–48 %; Peruvian Andean residents 60–65 %; 6 weeks of exposure in Peru produced ≈ 59 % Hct in study subjects.
• ↑ Hb content ⇒ ↑ O$_2$-carrying capacity, but sea-level values are not fully restored.

Muscle Adaptations

• After 4–6 weeks of >2 500 m exposure (mountain-climber data):
  • Muscle fiber CSA ↓ (atrophy from negative energy balance + hypoxia).
  • Capillary density ↑ (angiogenesis) ⇒ improved O$_2$ diffusion distance.
  • Mitochondrial function & glycolytic enzyme activity ↓ ⇒ reduced oxidative & glycolytic potential; impaired ATP resynthesis capacity.

Long-Term Cardiovascular Performance

• Athletes training chronically at altitude struggle to hit sea-level intensity targets because their absolute \dot{V}O_2\,\text{max}$$ remains depressed.

Genetic / Epigenetic High-Altitude Adaptations

• Tibetans (high-altitude natives):
  • Larger chest circumference; ↑ total lung capacity (TLC), vital capacity (VC), residual volume (RV), tidal volume (TV).
  • Blunted hypoxic pulmonary vasoconstriction → lower pulmonary arterial pressures.
  • Normal Hb concentration (vs. Andean polycythemia) yet higher O$_2$ saturation via more efficient ventilatory pattern.
  • Stronger myocardium & enhanced cardiac efficiency.
  • Skeletal muscle: ↑ capillary density, smaller fibers, preference for glucose oxidation, low lactate accumulation.

Practical / Ethical Implications

• Hydration & iron supplementation are critical to mitigate dehydration & support EPO-mediated erythropoiesis.
• Cold injury & UV exposure risk require protective clothing & eye-wear.
• Athletes may exploit “Live High – Train Low” strategy: reside at ~2 000–2 500 m to gain hematological benefits yet train near sea level to preserve high-intensity capability.
• Doping concern: exogenous EPO or blood transfusion mimics altitude-induced polycythemia.