amazon.co.ukA-Level Biology revision on exchange and transport: surface area to volume ratio, gas exchange in lungs, insects, fish and plants, digestion and absorption, the heart and mass transport in animals and plants, with required practicals (AQA RP5, OCR PAG8) and multi-board exam practice.
As organisms get larger, surface area increases more slowly than volume, so the SA:V ratio falls. Small organisms exchange everything across their body surface by diffusion alone; larger organisms cannot - the diffusion distance is too great and the surface too small, so they need specialised exchange surfaces plus mass transport systems to carry substances between the exchange surface and cells. Heat loss shows the same pattern: small organisms (high SA:V) lose heat faster and need high metabolic rates; large organisms conserve heat. Fick's law gives the three features examiners want in every exchange-surface answer: rate of diffusion ∝ (surface area × concentration difference) ÷ thickness - so efficient exchange surfaces have (1) a large surface area (folds, villi, lamellae, alveoli); (2) a thin barrier (often one-cell thick squamous epithelium); and (3) a steep concentration/diffusion gradient maintained (ventilation, blood flow, counter-current flow). Quote Fick's law explicitly and link each structure to one of its three terms - that structure-function pairing is what the mark scheme awards.
Mammalian lungs: the trachea divides into bronchi, then bronchioles, ending in alveoli - the exchange surface. Adaptations to quote: ~300 million alveoli give a huge surface area; walls are one cell thick (squamous epithelium) plus one-cell-thick capillary endothelium, so the diffusion barrier is ~two cells; a dense capillary network maintains the gradient by rapidly removing oxygenated blood; ventilation maintains a high O₂/low CO₂ gradient; alveoli are moist so gases dissolve. Ventilation (inspiration): diaphragm contracts and flattens, external intercostal muscles contract, ribs move up and out - thoracic volume increases, pressure falls below atmospheric, air flows in. Expiration: diaphragm relaxes, internal intercostals contract, volume decreases, pressure rises, air flows out (passive at rest). Tidal volume ~0.5 dm³; ventilation rate = tidal volume × breaths per minute; spirometer traces and calculations appear on OCR (3.1.1) and WJEC papers. Emphysema (destroyed alveolar walls, reduced surface area, less elastic recoil) and fibrosis (thickened walls) are stock application questions linking structure to reduced gas exchange.
Insects: air enters through spiracles (open/close to limit water loss) into tracheae reinforced with chitin, branching into tracheoles ending in fluid-filled tips in contact with cells; gases diffuse directly to tissues - no blood transport of O₂. Water loss is minimised by spiracle closure, hairs and a waterproof cuticle. Fish: water flows unidirectionally over gill filaments and lamellae (large surface area, thin, rich capillary supply); counter-current exchange - water and blood flow in opposite directions, so a diffusion gradient is maintained along the whole lamella and ~80% of water's O₂ is extracted (vs ~50% with parallel flow) - explain this as maintaining the gradient at every point, the classic A* point. Plants: gases diffuse through stomata (guard cells open/close) into air spaces in the spongy mesophyll; the flat, thin leaf gives a large SA:V; stomatal closure balances gas exchange against water loss - link to xerophytes (rolled leaves, hairs, sunken stomata) in dry habitats. Required practical: AQA RP5 (dissection of lungs/gills/insect to show exchange structures); OCR PAG9 (dissection).
Spirometer traces and lung-volume terms earn regular marks on OCR and WJEC: tidal volume (air per breath at rest, ~0.5 dm³), inspiratory/expiratory reserve volumes (extra air above/below tidal), vital capacity (max in + max out) and residual volume (air that cannot be exhaled); ventilation rate = tidal volume × breaths per minute - calculate, don't just define. Disease application questions link structure to reduced gas exchange: emphysema (smoking/alveolar macrophage damage destroys alveolar walls - less surface area and less elastic recoil, so ventilation becomes laboured), fibrosis (scar tissue thickens the exchange barrier - longer diffusion distance), asthma (bronchiole constriction and mucus narrow the airways, reducing airflow). Quote Fick's law terms in each answer: which term (area, thickness, gradient) the disease changes.
Digestion hydrolyses polymers to monomers: amylase (saliva, pancreas) hydrolyses starch to maltose, maltase (membrane-bound in ileum epithelium) to glucose; lipase (pancreas) hydrolyses lipids to fatty acids + monoglycerides, aided by bile salts emulsifying lipids into micelles (large surface area for lipase); endopeptidases/exopeptidases and dipeptidases hydrolyse proteins to amino acids. Absorption in the ileum uses the villi/microvilli (folded membrane - large surface area, thin epithelium, dense capillary and lacteal supply): amino acids and monosaccharides enter by specific transport; monoglycerides/fatty acids re-form triglycerides in the epithelium and enter the lacteal as chylomicrons.
The co-transport of glucose is the classic mechanism question (from the existing site content, AQA 3.3.3): (1) Na⁺/K⁺ pump (ATPase) actively transports Na⁺ out of the epithelial cell into the blood, lowering intracellular Na⁺; (2) Na⁺ diffuses down its gradient from the lumen into the cell via sodium-glucose co-transporter proteins, dragging glucose against its gradient; (3) glucose exits into the blood by facilitated diffusion. Cystic fibrosis (defective Cl⁻ channel, thick mucus, impaired absorption) is the stock application on Edexcel T2. Water absorption follows osmosis down the water potential gradient created by solute uptake.
The heart is a double pump: right side sends deoxygenated blood to the lungs, left side (thicker myocardium) sends oxygenated blood to the body. The cardiac cycle: (1) diastole - atria and ventricles relax; atrioventricular valves open, semilunar valves close; blood fills the atria and ventricles; (2) atrial systole - the SAN (sinoatrial node, the pacemaker) initiates contraction, atria contract, pushing remaining blood into ventricles; (3) ventricular systole - impulse reaches the AVN, passes down the bundle of His and Purkyne fibres (delay at AVN allows atria to empty; Purkyne fibres ensure contraction from the apex upwards); ventricles contract, AV valves close (first sound), semilunar valves open, blood ejected into aorta/pulmonary artery. Valves prevent backflow. Cardiac output = heart rate × stroke volume - calculations guaranteed. Pressure graphs (aorta, ventricle, atrium) and valve-state interpretation are standard six-markers. Control of heart rate: medulla receives signals from baroreceptors (pressure) and chemoreceptors (CO₂/pH) - sympathetic nerves increase rate, vagus (parasympathetic) decreases it; adrenaline increases rate (link to homeostasis topic).
Blood vessels: arteries - thick muscular/elastic walls, high pressure, elastic recoil maintains pulse flow; arterioles - muscle controls flow to organs; capillaries - one-cell-thick endothelium, narrow, for exchange; veins - thin walls, low pressure, valves preventing backflow. Tissue fluid formation: at the arterial end, hydrostatic pressure (higher than the water potential of the plasma) forces fluid and small solutes out through capillary gaps - plasma proteins stay in, making the plasma water potential more negative; at the venous end, hydrostatic pressure has fallen and oncotic (water-potential) pressure pulls fluid back in; the lymphatic system drains the excess, returning it to the blood near the heart. Oedema questions follow from this balance.
Pressure-change graphs are the standard interpretation question: the aortic pressure lags behind ventricular pressure (the valve must open first), the atrial pressure stays low, and valve closure sounds mark the boundaries of systole - read which valve is open/closed from which pressure is higher, not from memory of the order. Cardiac output = heart rate × stroke volume; during exercise heart rate and stroke volume both rise (venous return increases, more blood fills the ventricles, stretching the myocardium - the Starling mechanism gives a stronger contraction), so cardiac output can rise fourfold to deliver more oxygen to respiring muscle; after exercise, parasympathetic control restores the resting rate. Arterial blood pressure is maintained by elastic recoil between beats; hypertension damages arteries and increases heart workload - the link to cardiovascular disease questions on Edexcel T1 and WJEC.
Xylem carries water and mineral ions from roots to leaves - one-way, dead, hollow, lignified cells forming continuous tubes. Movement is explained by the cohesion-tension theory: water evaporates from mesophyll cells into air spaces and diffuses out of stomata (transpiration), lowering the water potential of leaf cells; water moves from xylem into mesophyll by osmosis, creating transpiration pull (tension) in the xylem column; cohesion between water molecules (hydrogen bonding) and adhesion to xylem walls keep the column unbroken and under tension, pulling water up from the roots; root pressure contributes at the base. Transpiration rate factors: light (stomata open), temperature (more evaporation, more kinetic energy, lower water potential of air), humidity (smaller gradient), air movement (removes humid layer). Potometer (OCR PAG8) measures water uptake as an estimate of transpiration: cut shoot underwater, seal airtight, measure bubble movement; quote controls (same shoot, still air, constant temperature) and limitations (uptake ≠ transpiration exactly, cut surfaces). Xerophytic adaptations (marram grass, cacti): rolled leaves, sunken stomata, hairs, thick waxy cuticle - all reduce the water-potential gradient and air movement at the stomata.
Phloem translocates sucrose and amino acids from sources (leaves, storage organs releasing sugars) to sinks (roots, growing tips, fruits) by mass flow, in both directions over time. Mechanism: sucrose is actively loaded into companion cells/seive tube elements at the source (H⁺ gradient from ATP-driven H⁺ pumping, sucrose co-transport), lowering the water potential of the phloem; water enters by osmosis from the xylem, raising hydrostatic pressure at the source; at the sink, sucrose is unloaded (actively or by diffusion), water potential rises, water leaves, pressure falls; sap then flows en masse from high to low pressure. Evidence: ringing experiments (ringed bark accumulates sugar above the ring, swelling below is absent), aphid stylets (sap exudes under pressure), radioactively labelled CO₂ traced to sinks. Compare xylem vs phloem in a table if asked: direction, contents, living/dead cells, driving force, evidence.