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Respiration vs Breathing — Definitions
Key Definitions
- Breathing (Pulmonary respiration / External respiration) — the physical process of exchange of gases between the organism and the environment (inhaling O₂, exhaling CO₂)
- Cellular Respiration (Internal respiration) — oxidation of food (glucose) inside cells to produce ATP energy; involves O₂ and produces CO₂
- Combustion — oxidation of food outside the body; uncontrolled release of energy as heat
- In absence of specialized respiratory organ — gas exchange occurs through body surface (e.g. Cnidarians, flatworms)
Respiratory Organs in Different Animals
| Respiratory Organ | Type | Animals |
|---|
| Body surface (Cutaneous) | No specialized organ | Earthworm, Cnidarians (Hydra), flatworms (Planaria) |
| Gills (Branchial) | Aquatic | Fish, prawn, tadpole |
| Book gills | Aquatic | King Crab (Limulus) |
| Book lungs | Terrestrial/semi-aquatic | Spiders, Scorpions (Arachnids) |
| Tracheal system | Terrestrial | Insects (Cockroach), Arthropods |
| Lungs (Pulmonary) | Terrestrial | All vertebrates (Reptiles, Birds, Mammals) |
| Moist skin + Buccal cavity + Lungs | Both | Frog (3 respiratory organs — on land: lungs + moist skin; in water: only skin; hibernation: only skin) |
Q. How does a frog breathe in water vs on land?
✅ Answer: In water — cutaneous respiration (moist skin only); On land — lungs + moist skin + buccal cavity (3 organs)
Explanation
Frog is unique in having three respiratory organs. On land, frogs use lungs (primary), moist skin (cutaneous — through dissolved O₂), and buccal cavity for breathing. In water, frogs breathe only through moist skin since lungs would fill with water. During hibernation (winter sleep), frogs are completely submerged and breathe entirely through their moist skin. This is why frogs must keep their skin moist — dry skin would stop cutaneous respiration and the frog would suffocate even on land. This is a classic example of how a single animal can use multiple respiratory strategies.
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Human Respiratory System
Parts of Human Respiratory System (Conducting Zone)
- Nostrils → Nasal passage (vestibule) → Nasopharynx → Pharynx → Larynx → Trachea
- → Primary Bronchi (2) → Secondary Bronchi (Right: 3 branches, Left: 2 branches) → Tertiary Bronchi
- → Bronchioles → Terminal Bronchioles (conducting zone ends here)
- → Respiratory Bronchioles → Alveolar ducts → Alveolar sacs → Alveoli (exchange zone)
- This entire branching = Respiratory/Bronchial tree
Nasal Cavity Functions
- Filtration — nasal hair cells trap dust, particles, pathogens
- Humidification — blood vessels warm and moisten incoming air
- Olfaction — bipolar olfactory neurons detect smell → signals go to olfactory lobe (limbic system)
- Temperature regulation — raises cold air temperature to body temperature
- Also has pressure receptors (high systolic BP detected here)
Lungs — Structure
Lobes of Lungs
- Right lung — 3 lobes (Superior, Middle, Inferior) — divided by Horizontal fissure (between superior and middle) and Oblique fissure
- Left lung — 2 lobes (Superior, Inferior) — divided by Oblique fissure only; has Cardiac notch (indentation where heart sits)
- Left lung is slightly smaller than right due to cardiac notch
Coverings of Lungs — Pleura
- Pleura = double-layered membrane around each lung
- Parietal pleura — outer layer (lines thoracic wall)
- Visceral pleura — inner layer (directly covers lung)
- Pleural cavity — space between the two layers; filled with pleural fluid — reduces friction during breathing
- Pleuritis / Pleurisy — inflammation of pleural membranes → painful breathing
Alveoli — Functional Units of Lungs
- Site of actual gas exchange — ~300–400 million alveoli per lung
- Total surface area: ~70–80 m² (size of a tennis court)
- Membrane thickness: <1 mm (extremely thin for rapid diffusion)
- Wall cells: Type I Pneumocytes — simple squamous (thin, for diffusion); Type II Pneumocytes — secrete Surfactant (lecithin/phospholipid) — prevents alveoli from collapsing
- Also contain Alveolar Macrophages — phagocytose dust particles
- Diffusion membrane: alveolar epithelium + basement membrane + capillary endothelium (all together <1 mm thick)
Thoracic Chamber — Formed By
- Vertebral column (dorsal)
- Sternum (ventral)
- Ribs (lateral)
- Diaphragm (floor)
Lungs are situated in the thoracic chamber. Volume of lungs is always equal to volume of thoracic chamber (because of pleural fluid — negative intrapleural pressure keeps lungs expanded against thoracic wall).
| Process | Muscles Used | Volume Change | Pressure Change | Air Movement |
|---|
| Inspiration (Inhalation) | Diaphragm contracts (↓ in D-V axis) + External intercostal muscles contract (ribs move up & out = ↑ in A-P axis) | Thoracic volume ↑ | Intra-pulmonary pressure ↓ (below atmospheric) | Air rushes IN (pressure gradient) |
| Normal Expiration (Passive) | Diaphragm relaxes + External intercostals relax → ribs fall back | Thoracic volume ↓ | Intra-pulmonary pressure ↑ (above atmospheric) | Air pushed OUT |
| Forced/Active Expiration | Internal intercostal muscles contract + Abdominal muscles contract → force ribs down further | Thoracic volume ↓↓ | Pressure ↑↑ | Air forcibly expelled |
Types of Breathing
- Abdominal breathing (75%) — mainly by diaphragm; used during normal quiet breathing; more common
- Thoracic breathing (2.5%) — by intercostal muscles; used when more effort needed
- Normal breathing rate: 12–16 breaths/minute
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Respiratory Volumes & Capacities
| Term | Abbreviation | Value | Definition |
|---|
| Tidal Volume | TV | ~500 ml | Volume inhaled/exhaled during normal quiet breathing |
| Inspiratory Reserve Volume | IRV | 2500–3000 ml | Extra volume that can be inhaled forcibly after normal inspiration |
| Expiratory Reserve Volume | ERV | 1000–1100 ml | Extra volume that can be exhaled forcibly after normal expiration |
| Residual Volume | RV | 1100–1200 ml | Volume remaining in lungs after maximum forcible expiration; CANNOT be measured by spirometer |
| Capacity | Formula | Value |
|---|
| Inspiratory Capacity (IC) | TV + IRV | ~3500 ml |
| Expiratory Capacity (EC) | TV + ERV | ~1500 ml |
| Functional Residual Capacity (FRC) | ERV + RV | ~2300 ml |
| Vital Capacity (VC) | TV + IRV + ERV = IC + ERV | ~4600 ml (4.6 L) |
| Total Lung Capacity (TLC) | TV + IRV + ERV + RV = VC + RV = IC + FRC | ~5800 ml (5.8 L) |
Dead Space Volume
Dead Space = volume of conducting zone (trachea, bronchi, bronchioles) where no gas exchange occurs = ~150 ml. This volume does NOT participate in gas exchange — it just transports air.
Alveolar Ventilation = (TV − Dead space) × Breathing rate = (500 − 150) × 12 = ~4200 ml/min
Note: Spirometer cannot measure Residual Volume, FRC, or TLC (any capacity including RV) because you cannot expel residual volume from lungs.
Q. What is Vital Capacity and what is its normal value?
✅ Answer: VC = TV + IRV + ERV = ~4600 ml; it is the maximum volume of air that can be expelled after a maximum inhalation
Explanation
Vital Capacity represents the maximum usable lung volume — it is the total amount of air you can move in and out of the lungs with maximum effort. It equals Tidal Volume (500 ml) + Inspiratory Reserve Volume (2500–3000 ml) + Expiratory Reserve Volume (1000–1100 ml) = approximately 4600 ml. It does NOT include Residual Volume (1100–1200 ml) because that air can never be expelled no matter how hard you try. Vital Capacity is reduced in conditions like asthma, emphysema, fibrosis (obstructive/restrictive lung diseases). It is a clinically important measure of lung function. Total Lung Capacity = VC + RV.
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Exchange of Gases — Partial Pressures
Partial Pressure of Gases (in mmHg)
Gas exchange occurs by simple diffusion down partial pressure gradients. Rate of diffusion ∝ partial pressure difference, solubility; inversely ∝ membrane thickness.
CO₂ is 20–25 times more soluble than O₂ in plasma — diffuses much faster despite lower partial pressure gradient.
| Location | pO₂ (mmHg) | pCO₂ (mmHg) |
|---|
| Atmospheric air | 159 | 0.3 |
| Alveolar air | 104 | 40 |
| Deoxygenated blood (pulmonary artery) | 40 | 45 |
| Oxygenated blood (pulmonary vein) | 95 | 40 |
| Oxygenated blood entering tissues | 95 | 40 |
| Tissue cells | 40 (or less) | 45 |
| Deoxygenated blood leaving tissues | 40 | 45 |
Direction of Gas Exchange (by diffusion)
- At alveoli (External respiration): O₂ moves from alveolar air (pO₂ 104) → blood (pO₂ 40) = O₂ enters blood; CO₂ moves from blood (pCO₂ 45) → alveoli (pCO₂ 40) = CO₂ leaves blood
- At tissues (Internal respiration): O₂ moves from blood (pO₂ 95) → tissues (pO₂ 40) = O₂ enters cells; CO₂ moves from tissues (pCO₂ 45) → blood (pCO₂ 40) = CO₂ enters blood
How O₂ is Transported in Blood
- 97–98% as Oxyhaemoglobin (Hb-O₂) — bound to haemoglobin in RBCs
- 2–3% dissolved in plasma (O₂ not very soluble in water)
- 1 Hb molecule carries 4 O₂ molecules (1 per haem group)
- 1 gram of Hb carries 1.34 ml O₂
- Normal Hb = 15 g/100 ml blood → carries 1.34 × 15 = ~20 ml O₂ per 100 ml blood
- At rest: only 5 ml O₂/100 ml blood is delivered to tissues (25% dissociation)
- During exercise: up to 15 ml O₂/100 ml blood (75% dissociation)
Oxygen-Haemoglobin Dissociation Curve
Sigmoid (S-shaped) curve. Shows % saturation of Hb vs pO₂.
- Left Shift — Hb has MORE affinity for O₂ → loads O₂ easily at lungs → less O₂ released to tissues; caused by: ↑ pH, ↓ PCO₂, ↓ temperature, ↓ H⁺
- Right Shift (Bohr's Effect) — Hb has LESS affinity for O₂ → more O₂ released to tissues; caused by: ↓ pH, ↑ PCO₂, ↑ temperature, ↑ H⁺ — conditions found in metabolically active tissues
- P50 = pO₂ at which Hb is 50% saturated (~26 mmHg for normal Hb)
Carbon Monoxide Poisoning (CO)
- CO has 200–250 times more affinity for Hb than O₂
- Forms Carboxyhaemoglobin (Hb-CO) — irreversible binding → Hb cannot carry O₂
- Causes: headache, dizziness, coma, death (even small amounts are dangerous)
- Also: Methaemoglobin — when Fe²⁺ in Hb is oxidized to Fe³⁺ → cannot bind O₂
Q. What is Bohr's Effect and why is it important at the tissue level?
✅ Answer: Bohr's Effect = decrease in O₂ affinity of Hb due to ↑CO₂, ↑H⁺, ↑temperature; this promotes O₂ release at metabolically active tissues
Explanation
In metabolically active tissues, CO₂ is produced rapidly, H⁺ ions accumulate (acidic pH), and temperature rises. These three conditions together cause the oxygen-haemoglobin dissociation curve to shift RIGHT — meaning Hb's affinity for O₂ decreases. As a result, Hb releases more O₂ to the tissues that need it most. This self-regulating mechanism is called Bohr's Effect. Conversely, at the lungs where CO₂ is expelled and pH is higher, Hb's affinity for O₂ increases (left shift) — allowing efficient O₂ loading. This beautifully matches O₂ supply to O₂ demand in the body.
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Transport of Carbon Dioxide
3 Forms of CO₂ Transport
- 70–77% as Bicarbonate ions (HCO₃⁻) — most important form; formed in RBCs and plasma
- 23% as Carbaminohaemoglobin (Hb-CO₂) — CO₂ binds to globin portion (amino groups) of Hb; NOT to haem; different binding site from O₂
- 7% dissolved in plasma
Bicarbonate Transport — Chloride Shift (Hamburger Phenomenon)
- CO₂ from tissues enters RBC
- Carbonic Anhydrase Enzyme (CAE) catalyzes: CO₂ + H₂O → H₂CO₃ (carbonic acid) → H⁺ + HCO₃⁻
- HCO₃⁻ moves out of RBC into plasma (in exchange for Cl⁻ moving in) → this is the Chloride Shift / Hamburger Phenomenon
- H⁺ remains in RBC → binds to Hb (forming HHb) → Bohr's effect → O₂ released
- At lungs: reverse happens — HCO₃⁻ re-enters RBC, CAE converts H₂CO₃ → CO₂ + H₂O → CO₂ expelled in expired air
- NaHCO₃ in plasma serves as blood buffer (prevents pH changes)
Q. What is the role of Carbonic Anhydrase Enzyme (CAE) in CO₂ transport?
✅ Answer: CAE catalyzes the reversible reaction CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻ — making 70–77% of CO₂ transport possible as bicarbonate
Explanation
Without Carbonic Anhydrase (present in RBCs), the conversion of CO₂ to bicarbonate would be far too slow to be physiologically useful. CAE speeds up this reaction about 10,000 times. At tissues, CO₂ enters RBCs → CAE converts it to H₂CO₃ → dissociates to H⁺ + HCO₃⁻. HCO₃⁻ moves into plasma (Chloride Shift maintains electrical neutrality). At lungs, the reverse: HCO₃⁻ + H⁺ → H₂CO₃ → CAE converts back to CO₂ + H₂O → CO₂ diffuses into alveoli and is exhaled. This elegant reversible system handles the majority of CO₂ transport in the body.
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Neural Regulation of Breathing
Respiratory Centres in Medulla Oblongata & Pons
- Dorsal Respiratory Group (DRG) — in Medulla oblongata; controls normal rhythmic breathing; sends signals to diaphragm (via phrenic nerve) and external intercostals → inspiration; also called Respiratory Rhythm Centre
- Ventral Respiratory Group (VRG) — in Medulla oblongata; inactive during quiet breathing; activated during forceful breathing → controls both forced inspiration and forced expiration (internal intercostals + abdominals)
- Pneumotaxic Centre — in Pons; switches OFF inspiration — limits duration of inspiration (1–5 sec); prevents over-inflation of lungs; when pneumotaxic centre is active → shorter, faster breaths
Chemical Regulation — Chemoreceptors
- Central Chemoreceptors — in medulla oblongata; sensitive to CO₂ and H⁺ in cerebrospinal fluid (CSF)
- Peripheral Chemoreceptors — in Carotid body (carotid artery) and Aortic body (aortic arch); sensitive to ↑CO₂, ↑H⁺ in blood; also sense ↓O₂ (severe hypoxia)
- Primary stimulus for breathing = CO₂ / H⁺ (NOT O₂ directly in normal conditions)
- If CO₂ or H⁺ ↑ in blood/CSF → chemoreceptors send signals to DRG → rate and depth of breathing increase → more CO₂ is expelled → levels normalize (negative feedback)
Voluntary vs Involuntary Control
- Involuntary (automatic) — controlled by Medulla oblongata (DRG); normal resting breathing
- Voluntary — controlled by Cerebral cortex; can consciously increase/decrease rate, hold breath; overrides automatic control temporarily
| Disorder | Cause | Features |
|---|
| Asthma | Inflammation of bronchi and bronchioles (often allergic/immune-mediated); bronchospasm | Wheezing, difficulty breathing (especially expiration), episodes of breathlessness; managed with bronchodilators & steroids |
| Emphysema | Destruction of alveolar walls (mainly due to cigarette smoking); irreversible | Reduced surface area for gas exchange → chronic breathlessness; barrel-shaped chest; major cause = cigarette smoking |
| Occupational Respiratory Disorders (Pneumoconiosis) | Inhalation of dust/toxic fibres at workplace over years → inflammation → fibrosis of lung tissue | Types: Silicosis (silica dust), Asbestosis (asbestos fibres), Byssinosis (cotton dust); leads to reduced lung function |
| Altitude Sickness (Hypoxia) | At high altitude — low partial pressure of O₂ → less O₂ in blood | Dizziness, breathlessness, headache, nausea, vomiting; ↑ breathing rate, ↑ heart rate; body compensates by increasing RBC count (Polycythaemia) via erythropoietin |
Altitude Sickness — Body's Compensation
- At high altitude: pO₂ ↓ → less O₂ loading in Hb → Hypoxia
- Kidneys & JG cells detect low O₂ → release Erythropoietin
- Erythropoietin → stimulates bone marrow → ↑ RBC production (Polycythaemia)
- Also: ↑ breathing rate + ↑ heart rate (immediate compensation)
- Hb-O₂ dissociation curve shifts right → more O₂ released to tissues per unit Hb
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Quick Revision — Must-Know Points
Frog in hibernation breathes via → Moist Skin only
Right lung lobes → 3 (Superior, Middle, Inferior)
Left lung lobes → 2 (Superior, Inferior)
Surfactant secreted by → Type II Pneumocytes
Tidal Volume → ~500 ml
Vital Capacity → ~4600 ml
Total Lung Capacity → ~5800 ml
Residual Volume → 1100–1200 ml
Dead space volume → ~150 ml
O₂ carried as HbO₂ → 97–98%
CO₂ as HCO₃⁻ → 70–77%
CO₂ as Hb-CO₂ → 23%
Bohr's Effect → ↑CO₂/↑H⁺ = right shift = more O₂ released
CO affinity vs O₂ → 200–250 times more
Pacemaker of breathing → DRG in Medulla oblongata
Pneumotaxic centre → Pons; switches off inspiration
Primary stimulus for breathing → CO₂ / H⁺ (not O₂)
Major cause of Emphysema → Cigarette smoking