Gas Exchange

Plants exchange gases (CO₂ in, O₂ out during photosynthesis; O₂ in, CO₂ out during respiration) through pores called stomata in the leaf epidermis.

Stomata structure.

• Most stomata are on the LOWER epidermis of the leaf — cooler, less light, less air movement → less water loss.
• Each stoma is bounded by a pair of guard cells that are bean- or kidney-shaped.
• The INNER wall (next to the pore) is THICKER than the outer wall.

How stomata open and close:

• When guard cells are turgid (full of water — water has entered by osmosis), the thinner outer wall stretches more than the thicker inner wall → cells curve outwards → STOMA OPENS.
• When guard cells lose water and become flaccid, they straighten → STOMA CLOSES.
• Light → opening (allows CO₂ in for photosynthesis).
• Darkness or water stress → closing (reduces water loss).

Net gas exchange in a leaf:

Time	Photosynthesis	Respiration	Net exchange	Stomata
Day (bright light)	FAST	Slow	CO₂ IN, O₂ OUT	OPEN
Day (dim light)	Slow	Slow	Roughly balanced	Partly open
Night	NONE	Slow	O₂ IN, CO₂ OUT	CLOSED (usually)

Compensation point. At dawn / dusk, the rate of photosynthesis briefly equals the rate of respiration → NET gas exchange is zero. The light intensity at which this happens is called the compensation point.

Other gas-exchange surfaces in plants. Lenticels — small pores in the bark of woody stems — allow gas exchange when stomata are absent. Roots take up O₂ from spaces between soil particles (waterlogged soils starve roots of O₂).

The human respiratory system carries air from the atmosphere to the gas-exchange surface (alveoli).

Pathway of air: nose / mouth → larynx (voice box) → trachea (windpipe) → bronchi (one to each lung) → bronchioles (smaller branches) → alveoli (air sacs).

Key structural features:

Nose. Hairs and mucus trap dust and pathogens. Air is warmed to body temperature and moistened to prevent drying of the alveoli.

Trachea.

• C-shaped rings of cartilage in the wall keep the airway PERMANENTLY OPEN — the airway can't collapse during inspiration when internal pressure drops.
• C-shaped (not full rings) so the oesophagus behind can expand during swallowing.
• Lined with ciliated epithelium + goblet cells: goblet cells produce mucus that traps dust and bacteria; cilia beat upwards to move the mucus to the throat where it is swallowed (the mucociliary escalator). Smoking paralyses these cilia.

Bronchi. Two — one to each lung. Same structure as trachea (cartilage rings + ciliated mucus epithelium).

Bronchioles. Smaller branches. NO cartilage; have smooth muscle in the wall that can constrict (e.g. asthma narrows bronchioles).

Alveoli. Microscopic air sacs at the ends of the bronchioles. Where gas exchange happens.

Thorax — supporting structures:

• Ribs — bony cage protecting heart and lungs.
• Intercostal muscles — between the ribs; external (inspiration) + internal (forced expiration).
• Diaphragm — dome-shaped muscle separating thorax from abdomen.
• Pleural membranes — two thin layers (visceral on lung, parietal on chest wall) with pleural fluid between them. The fluid lubricates and 'glues' the lungs to the chest wall by surface tension.

Alveoli are the site of gas exchange — where O₂ diffuses from the air into the blood and CO₂ diffuses out. Their structure is optimised for this in several ways.

1. Vast surface area.

• There are ~300-500 million alveoli in adult human lungs.
• Total surface area ~70 m² — about half a tennis court.
• More SA → more diffusion at any moment.

2. Thin (one-cell-thick) walls.

• Alveolar wall = single layer of squamous (flattened) epithelium.
• Capillary wall = single layer of endothelium.
• Two cells separate air from blood → SHORT DIFFUSION DISTANCE → fast diffusion (Fick's Law).

3. Moist inner surface (surfactant).

• Each alveolus is lined with a thin film of fluid (containing surfactant which reduces surface tension and prevents the alveolus collapsing).
• Gases must DISSOLVE before diffusing → moisture is essential.

4. Dense capillary network.

• Every alveolus is surrounded by many capillaries with continuous blood flow.
• Constant blood flow REMOVES oxygenated blood and BRINGS deoxygenated blood → maintains a steep concentration gradient for O₂ (in) and CO₂ (out) on the BLOOD side.

5. Constant ventilation.

• Breathing constantly renews the air in the alveoli — high O₂ + low CO₂ in fresh air; the used air is exhaled.
• Maintains a steep concentration gradient on the AIR side.

Gas exchange itself.

In the alveolus the air has high O₂ (~21 %) and low CO₂ (~0.04 %). Capillaries arrive carrying blood with low O₂ (returned from body) and high CO₂. By DIFFUSION:

• O₂ moves from alveolar air → through the alveolus + capillary walls → into the plasma → into the red blood cells, where it binds to haemoglobin.
• CO₂ moves from the plasma → through the capillary + alveolus walls → into the alveolar air → exhaled.

Breathing (ventilation) moves air in and out of the lungs. The lungs themselves are passive — they have no muscle. The work is done by the diaphragm and the intercostal muscles.

INSPIRATION (active process):

1. Diaphragm CONTRACTS → FLATTENS (moves down).
2. External intercostal muscles CONTRACT → ribs move UP and OUT.
3. Thoracic volume INCREASES.
4. Pressure in the thorax (and lungs) DECREASES below atmospheric — Boyle's Law: $P \propto 1/V$ at constant T.
5. Air flows from HIGH pressure (atmosphere) → LOW pressure (lungs).

EXPIRATION (usually passive at rest):

1. Diaphragm RELAXES → returns to dome shape (moves up).
2. External intercostal muscles RELAX → ribs move DOWN and IN under gravity / elasticity.
3. Elastic recoil of lung tissue helps squeeze out air.
4. Thoracic volume DECREASES.
5. Pressure INCREASES above atmospheric.
6. Air flows OUT through the trachea.

Forced (vigorous) expiration — during exercise, coughing:

• Internal intercostal muscles CONTRACT → pull ribs DOWN actively.
• Abdominal muscles CONTRACT → push diaphragm UP forcefully.
• Forces more air out than the passive recoil alone.

Why lungs are passive. The visceral pleura (on the lung) is attached to the parietal pleura (on the chest wall) by surface tension in the thin layer of pleural fluid between them. When the chest wall moves out, it drags the lung surface out with it — like two wet glass plates that can slide past each other but not separate.

During exercise both breathing rate (breaths per minute) and breathing depth (tidal volume per breath) INCREASE. The combined effect is a several-fold increase in minute ventilation (rate × depth).

Why the increase happens — the feedback chain:

1. Exercising muscles respire faster.

   • Skeletal muscle contraction requires ATP from aerobic respiration.
   • More contractions per second → more ATP demand → more O₂ used + more CO₂ produced per minute.

2. CO₂ rises in the blood.

   • CO₂ dissolves in plasma as carbonic acid: CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻.
   • Blood pH falls slightly (becomes more acidic).

3. Chemoreceptors detect the change.

   • Chemoreceptors in the medulla (brain stem) and in the aortic + carotid bodies (in the major arteries) respond to rising CO₂ / falling pH.

4. The medulla sends nerve impulses to the breathing muscles.

   • Higher frequency of impulses to the diaphragm and intercostal muscles.
   • Muscles contract MORE OFTEN (rate ↑) and MORE STRONGLY (depth ↑).

5. Result: more O₂ delivered to muscles + more CO₂ removed at the alveoli → meets the increased demand.

After exercise. Breathing rate slowly returns to baseline. The body may also need extra O₂ to oxidise any lactic acid that built up during the exercise — this is the oxygen debt (covered in detail in the Respiration topic).

Counter-intuitive point. The trigger is CO₂ rising, NOT O₂ falling. Blood O₂ stays remarkably constant (~95-98 % saturation) during exercise; CO₂ varies much more, so it is the sensitive trigger.

Cigarette smoke contains over 4000 chemicals. Three of them are key for the IGCSE spec:

1. Tar — a black, sticky residue.

Chronic bronchitis:

• Tar paralyses the cilia in the airways → mucus + trapped dust + bacteria are no longer swept up.
• Mucus accumulates in the airways → persistent cough to clear it.
• Bacteria multiply in the trapped mucus → repeated chest infections.
• Long-term: airways inflamed and narrowed → wheezing, breathlessness.

Lung cancer:

• Tar contains many carcinogens (cancer-causing chemicals — e.g. polycyclic aromatic hydrocarbons, benzpyrene).
• Carcinogens damage DNA in lung-tissue cells → mutations → uncontrolled cell division → tumour.
• Lung cancer is the most common cancer death in smokers.

Emphysema:

• Chronic coughing + chemicals in tar break down the elastic fibres in the walls of alveoli.
• Alveoli rupture and merge → fewer, larger air sacs → massively reduced surface area for gas exchange.
• Diffusion is much slower → patients become breathless on exertion and need supplementary oxygen.

2. Carbon monoxide (CO) — toxic gas.

• CO binds to haemoglobin in red blood cells to form carboxyhaemoglobin — a STABLE complex.
• CO binds ~200× more strongly than O₂ does.
• Haemoglobin saturated with CO cannot carry O₂.
• Net effect: reduced oxygen-carrying capacity of the blood → less O₂ to tissues.
• Affects the unborn baby of a pregnant smoker — fetus may be smaller, with developmental issues.

3. Nicotine — addictive stimulant.

• The chemical responsible for addiction — smokers crave it.
• Stimulant: raises heart rate and constricts blood vessels → raises blood pressure.
• Long-term: increased risk of coronary heart disease (CHD) and stroke.
• Combined with CO's effect on O₂ delivery, smokers' cardiovascular systems are doubly stressed.

Summary of named smoking-related diseases:

• Chronic bronchitis — tar.
• Emphysema — tar (+ chronic coughing).
• Lung cancer — carcinogens in tar.
• Coronary heart disease / stroke — nicotine (raising BP) + CO (reducing O₂).

Aim: investigate how exercise changes breathing rate (or breathing depth).

Method:

1. The subject sits quietly for 5 minutes to ensure baseline.
2. Count the breaths in 30 seconds (one breath = one rise + fall of the chest). Multiply by 2 to give breaths per minute. Record as resting rate.
3. Subject performs 1 minute of light exercise (e.g. walking on the spot).
4. Immediately afterwards, count breaths for 30 s → ×2 → record.
5. Rest until breathing returns to baseline (5+ min).
6. Repeat with progressively more intense exercise: jogging on the spot, then running on the spot or sprinting, each for 1 minute.
7. Repeat the whole protocol 3 times and calculate the mean breathing rate at each intensity.
8. Plot a graph of breathing rate against exercise intensity.

Variables:

• IV: intensity of exercise (rest, walk, jog, sprint).
• DV: breathing rate (breaths per minute).
• CVs: SAME SUBJECT (controls fitness, age, lung capacity); same duration (1 min) of each exercise; same recovery time; same ambient temperature; subject has not exercised in the 2 hours before; subject does not smoke.

Expected results:

• Resting rate ~12-16 breaths/min.
• After light exercise: ~20-25 breaths/min.
• After vigorous exercise: 35-45+ breaths/min.
• Pattern: breathing rate INCREASES with exercise intensity.

Reliability vs validity:

• Reliability: repeat measurements 3 times + mean.
• Validity: ensure timing starts IMMEDIATELY after exercise (rate falls rapidly back to baseline once exercise stops); use a metronome / heart-rate monitor to standardise intensity.

Extension — also measure depth. Use a spirometer / breathing-rate sensor to record tidal volume. Both rate AND depth increase; the product (minute ventilation) shows the largest change.