High Altitude and Acclimatization


- High altitude → ↓↓ barometric pressure → ↓↓ partial pressure of oxygen (PO2).
- (O2 percentage same, total pressure lower).
- Effect: Hypoxic hypoxia.
- Immediate Response upon ascent:
- Hypoxic hypoxia → Stimulates peripheral chemoreceptors → Immediate ↑ ventilation.
- ↑ Ventilation → CO2 washout → Alkalosis
- “Breaking effect”
- Alkalosis → ⛔ ventilation → Slight ↓ in ventilation → after few hours
Acclimatization Process (Over time):
Mechanism | Response |
↑ ventilation (Earliest change due to activation of peripheral chemoreceptors) | Respiratory alkalosis (CO₂ washout → ↓ PCO₂, ↓ H⁺) Hypocalcemia → Tetany (↓ free Ca²⁺ due to H⁺ & Ca²⁺ competing for albumin binding) |
↑ EPO stimulation | Polycythemia |
↑ VEGF | ↑ Vascularity (due to ↑ angiogenesis) → ↑ O₂ diffusion |
Cellular acclimatisation (↑ cytochrome oxidase activity) | ↑ O₂ utilization |
Release of oxygen → ↑ 2,3 DPG binding | Right shift on oxygen dissociation curve |
Renal Compensation:
- ↑↑ Ventilation → Respiratory alkalosis → ↑↑ HCO₃⁻ + Tetany
- Renal Compensation → HCO₃⁻ Excreted via kidney → ↓↓ HCO₃⁻
- Prevents respiratory alkalosis & tetany.
- ↓↓ blood bicarbonate → Bicarbonate shifts from CSF to blood →
- ↓↓ CSF bicarbonate → ↑↑ Acidity of CSF → Stimulates central chemoreceptors
- Further ↑↑ ventilation
High Altitude Sicknesses :
- Acute Mountain Sickness
- Complications
- HAPE
- HACE
- Chronic Mountain Sickness

1. Aka Acute Mountain Sickness (AMS)
(Insufficient acclimatization)
- Develops: First 24 hours.
- Symptoms: Headache, anorexia, nausea, sleep alteration.
- Complications
- High Altitude Cerebral Edema (HACE):
- AMS symptoms + Ataxia or mental changes.
- Edema in brain white matter
- D/t vasodilatation of cerebral arteries
- High Altitude Pulmonary Edema (HAPE):
- Develops: 2 to 4 days.
- Symptoms: Cough, dyspnea, sputum production.
Treatment:
- Most reliable/effective:
- Immediate descent to low altitude (1 km) +
- Supplemental or hyperbaric Oxygenation
- AMS & HACE:
- Dexamethasone
- Sumatriptan (5HT-agonist) & Gabapentin also used
- HAPE:
- Nifedipine (calcium channel blocker)
- Phosphodiesterase inhibitors (Sildenafil or tadalafil)
- Theophylline & Aminophylline
- Acetazolamide:
- DOC
- Used to facilitate acclimatization & as prophylaxis.
- Not primary treatment for acute disorder.
2. Chronic Mountain Sickness / Monge's Disease
- Cause
- ↑ erythrocytosis
- Clinically
- Pulmonary hypertension → Cor pulmonale
- Treatment
- Venesection
- Acetazolamide → facilitate acclimatization & as prophylaxis.
- Monks → leave in mountains → have PAH
Environmental Physiology
On Level Lands
- Atmospheric pressure: 760 mmHg
- O₂ content in atmosphere: 21%
- PO₂ atmosphere: 21% of 760 mmHg = 160 mmHg
Deep Sea Physiology
Etiology
- Divers
- Military operation
- Caisson workers
- Recreation activities
Pressure:
- At sea level: 1 atm
- For every 10 m deep: Pressure ↑ by 1 atm
- Leads to high barometric pressure (gases compressed).
- 1 km → 100 atm → 76000 mmHg
1. Barotrauma
- Pneumothorax / TM rupture

2. Caisson's Disease / Diver's Disease / Decompression Sickness
MOA:
- High barometric pressure → quick ascent → low barometric pressure
- Dissolved N₂ released as bubbles.
Features (Accumulation of N₂ bubbles):
Sites | Effects |
Crosses blood brain barrier | Euphoria (N₂ narcosis) |
In lungs | Chokes |
In joints | Bends |
In blood vessel | Obstruction → air embolism → death |
Rx:
- Hyperbaric chamber
- Slow ascent
- Slow decompression (forms less bubbles)
Note:
- Decompression sickness also affects pilots & mountaineers.
Space Physiology
Effects of Microgravity
- Loss of Ca²⁺ & PO₄³⁻ from bones → Prone to fractures
- Loss of muscle mass
- ↓ ↓ RBC count
Gravitational Forces
- Positive G:
- ↓ Cerebral perfusion → Black out
- ↓ Cardiac output
- ↓ Venous return (due to ↑ venous pooling)
- Negative G:
- ↑ Venous return
- ↑ Cardiac output
- ↑ Cerebral perfusion
- Congestion in eyes (red out)
Exercise
ㅤ | Anaerobic / Isometric Exercise intolerance | Aerobic exercises/ Isotonic exercises intolerance |
Pathway used | Anerobic glycolysis | Fatty acid oxidation |
Mechanism | Muscles cannot extract Oxygen d/t vasoconstriction d/t ↑ tension | Can extract Oxygen from circulation |
Examples | • Clenching fist • Pushing against resistance • Lifting weights | • Walking • Running • Swimming |
Heat Type | Isotonic | Isometric | ㅤ |
Resting heat | + | + | • Heat released at rest • Due to basal metabolic processes |
Initial heat | + | + | • Heat produced during contraction • Activation heat ↳ Heat produced whenever muscle contracts • Shortening heat ↳ Proportional to distance of muscle shortening |
Recovery heat | + | + | • Released during metabolic processes • Restores muscle to pre-contraction state • Equal to initial heat |
Relaxation heat | + | − | • Extra heat released after isotonic contraction • Muscle return to previous length |
- Relaxation heat occurs only in isotonic contraction
Respiration During Exercise



1. Initial rapid ↑ ventilation (Phase 1) at exercise start:
- Feedforward control system
- Anticipatory Tachypnea
- Due to psychic stimulation & proprioceptor stimulation.
2. Moderate Exercise:
- Exercise → ↑ Muscle metabolism → ↑ CO2 production, ↑ O2 consumption → Need to increase ventilation
- Primary stimuli for ↑ ventilation:
- ↑↑ in
- Potassium ion (released from muscles)
- Body temperature
- Stimulate Peripheral chemoreceptors → Results in ↑ Ventilation
- Isocapnic buffering
- Arterial PO2, PCO2, pH remains relatively normal
Why is not ↓ O2 content, ↑ CO2 content, ↑ H+ ions in Venous blood not triggering hyperventilation during exercise?
- Venous blood changes do not stimulate peripheral chemoreceptors
3. Severe Exercise:
- Significant lactic acid production → ↑ H+ and CO2.
- This acidosis and hypercapnia in arterial blood → additional stimuli for ventilation.
Increased Oxygen Consumption
- O2 consumption at rest:
- 250 ml/min → 1 MET (Metabolic equivalent)
- = 3.5 mL O2 / kg / minute
- During exercise:
- ↑ O₂ consumption → ↑ MET.
- Peak VO₂:
- O₂ consumed at the end of exercise
- VO₂ max:
- Maximum possible O₂ consumption
- (Theoretical value).
Oxygen Debt & EPOC (Excess Post-Exercise Oxygen Consumption)

Aspect | O₂ debt | EPOC (Excess Post-Exercise Oxygen Consumption) |
Timing | Onset of exercise | End of exercise |
Mechanism/ Purpose | Borrowing from O₂ storage sites (Hb & myoglobin) | • Causes ↑ RR & ↑ O₂ consumption. • Replenishes Hb & myoglobin stores |
Diffusion of Gases
- Oxygen dissociation curve: Shifts to right
- O₂ released to tissues to meet demand.
Arteriovenous (A-V O₂) Difference
- ↑ during exercise.
- Cause: Tissues extract more O₂.
- Also during stagnant hypoxia
Cardiovascular Changes in Exercise
- Cardiac Output (CO):
- CO ↑↑
- CO = SV x HR.
- due to ↑ HR.
- Reaches a plateau.
- ↑ 7 fold in athletes
- ↑ 4 fold in non-athletes
- Anticipatory Tachycardia:
- Even before starting exercise.
- Cause: Joint proprioceptors → Impulse → Brain.
- Blood Pressure:
Blood Pressure | Isotonic | Isometric |
Systolic BP | ↑ | ↑ |
Diastolic BP | ↓ | ↑ |
Cause | Local accumulation of metabolic end products → Vasodilation → ↓ TPR → ↓ DBP | Sustained muscle contraction → ↑ Tension → Compresses blood vessels (Arterioles) → ↑ TPR → ↑ DBP |
- Preload:
- Sympathetic nervous system stimulation
- Releases Norepinephrine
- Venoconstriction → ↑ mean systemic filling pressure (MSFP) → ↑ preload.
Blood Flow during Rhythmic Muscle Exercise











General Blood Flow:
- Rest: 3 ml/100g/min
- During exercise: 80 ml/100g/min
- (↑ by 20 times).
Blood Flow during Rhythmic Muscle Exercise:
- Fluctuates rhythmically:
- ↓ during contraction.
- ↑ during relaxation
- Causes
- Local metabolites from exercising muscles
- Most Important
- Vasodilation
- Increased arterial BP.
- Sympathetic-mediated vasodilation
- Beta-2 receptors on muscle arterioles
- Exercise Hyperemia:
- ↑ metabolism
- Local accumulation of H+, K+, lactate (metabolic end products)
- Vasodilation → ↑ blood flow → Hyperemia
- Organ-Level Redistribution:
- ↓ blood flow in Renal & Splanchnic (GIT) circulation.
- ↑ blood flow to Heart and skeletal muscles.
- Cerebral Circulation:
- Always maintained constant due to autoregulation.
- Skin Blood Flow:
- Initial ↓
- Later ↑ for heat dissipation.


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Effects of Smoking
- ↓ exercise capacity
- ↓ work capacity
- Mechanism:
- Toxic chemicals in smoke → Constriction of airways
- ↑ air flow resistance.
- Also causes:
- Ciliary paralysis
- Swelling of epithelial cells.
- ↑ fluid secretion into bronchial tree.