Environmental Physiology

High Altitude and Acclimatization

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  • 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 → ⛔ ventilationSlight ↓ in ventilationafter 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 bicarbonateBicarbonate shifts from CSF to blood →
    • ↓↓ CSF bicarbonate → ↑↑ Acidity of CSF Stimulates central chemoreceptors 
      • Further ↑↑ ventilation

High Altitude Sicknesses :

  1. Acute Mountain Sickness
      • Complications
        • HAPE
        • HACE
  1. Chronic Mountain Sickness
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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 hypertensionCor 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
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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 bonesProne 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

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
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

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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)

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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

  1. Cardiac Output (CO):
      • CO ↑↑
        • CO = SV x HR.
        • due to ↑ HR.
        • Reaches a plateau.
      • 7 fold in athletes
      • 4 fold in non-athletes
  1. Anticipatory Tachycardia:
      • Even before starting exercise.
      • Cause: Joint proprioceptors → Impulse → Brain.
  1. Blood Pressure:
    1. 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
  1. Preload:
      • Sympathetic nervous system stimulation 
      • Releases Norepinephrine 
        • Venoconstriction → ↑ mean systemic filling pressure (MSFP) → ↑ preload.

Blood Flow during Rhythmic Muscle Exercise

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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
          1. Local metabolites from exercising muscles
              • Most Important
              • Vasodilation
          1. Increased arterial BP.
          1. 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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ANS
3

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.