Sec 3 Biology Respiration in Humans notes

Respiration is the release of energy from glucose in every living cell — a chemical process that never stops. Breathing (ventilation) is the muscular act that swaps the air in the lungs, simply delivering the oxygen and removing the carbon dioxide that respiration produces. Examiners punish anyone who writes "breathing releases energy"; energy release happens in the cells, not in the lungs.

With a generous oxygen supply, cells run aerobic respiration — the complete breakdown of glucose that releases a large amount of energy per glucose molecule:

glucose + oxygen → carbon dioxide + water + much energy, or in symbols: C₆H₁₂O₆ + 6O₂ → 6CO₂ + 6H₂O (+ energy). The equation is perfectly balanced: 6 carbon, 12 hydrogen and 18 oxygen atoms on each side. When oxygen supply cannot keep up, human muscle switches to anaerobic respiration, covered at the end of this chapter.

Air enters through the nose and passes down the larynx (voice box) into the trachea (windpipe). The trachea divides into two bronchi — one per lung — which branch repeatedly into ever-narrower bronchioles, ending in clusters of tiny air sacs, the alveoli, each wrapped in a net of capillaries. Rings of cartilage around the trachea and bronchi hold the airways open like the hoops of a barrel, so the tubes never collapse when chest pressure swings.

The airways clean themselves. Goblet cells secrete a sticky mucus that traps dust and microbes, and the lining is carpeted with cilia — hair-like projections that waft the mucus upward towards the throat, where it is swallowed and destroyed by stomach acid. Smoking paralyses and then destroys these cilia, which is why smokers must cough to shift the mucus their cilia can no longer move.

Inspiration (breathing in) is active — muscles must contract. The diaphragm contracts and flattens from its dome shape, while the external intercostal muscles contract to pull the ribs upward and outward (the internal intercostals relax). The chest cavity enlarges, so the volume of the thorax increases and the pressure inside falls below atmospheric pressure — and air is drawn down the trachea to equalise it.

Expiration (breathing out) at rest is largely elastic recoil: the diaphragm relaxes and domes upward, the internal intercostal muscles contract to pull the ribs down and in, the chest volume shrinks, pressure rises above atmospheric, and air is forced out. During forced expiration (coughing, blowing up a balloon, hard exercise) the internal intercostals work hard, making expiration actively powered too.

Gas exchange happens by diffusion in the millions of alveoli. Oxygen is at higher concentration inside an alveolus than in the blood arriving from the pulmonary artery, so it diffuses into the capillaries and binds to haemoglobin; carbon dioxide is more concentrated in the blood, so it diffuses the other way and is breathed out. Four adaptations keep both gradients steep and the path short:

• Count in the millions — alveoli give the lungs a total surface area estimated at tens of square metres, so the diffusion rate is enormous.
• Walls one cell thick — the barrier between air and blood is a couple of flattened cells wide, minimising the diffusion distance.
• A film of moisture lines each alveolus so oxygen dissolves first and diffuses as a solution (and it lets carbon dioxide leave the same way).
• A dense capillary network hugs every alveolus, constantly sweeping oxygenated blood away and delivering carbon-dioxide-rich blood, maintaining the steep concentration gradient.

Nicotine is the addictive drug of tobacco smoke. It speeds the heart rate, raises blood pressure and narrows blood vessels, increasing the risk of clots and of coronary heart disease (chapter 5). Carbon monoxide competes with oxygen for haemoglobin and binds it far more tightly, forming carboxyhaemoglobin — smokers carry a permanently reduced oxygen load, so the heart must work harder, especially during exercise or in pregnancy.

Tar is a sticky, carcinogenic cocktail that coats the airways and alveoli. It paralyses and destroys the cilia (so mucus and germs accumulate — chronic bronchitis), it irritates and eventually destroys alveolar walls (emphysema: less surface area, breathlessness), and it contains chemicals that trigger lung cancer. Together with mucus build-up, this is the reason for the persistent "smoker’s cough".

During vigorous exercise, muscles consume oxygen faster than breathing and circulation can deliver it. Oxygen-starved muscle cells switch to anaerobic respiration, breaking down glucose partially without oxygen:

glucose → lactic acid + little energy. Two consequences follow. First, the energy yield per glucose is much smaller than in aerobic respiration — an emergency trickle, not a bonfire. Second, lactic acid accumulates in the muscle, lowering the pH and causing fatigue, cramp and pain — the burn that ends a sprint.

After the race you keep panting hard. That extra oxygen is the oxygen debt: the amount of oxygen needed to dispose of the lactic acid — transported in the blood to the liver, where it is broken down oxidatively (and partly reconverted to glucose). The debt is repaid, the lactic acid is cleared, and only then does breathing return to resting rate.