amazon.co.ukA-level PE revision on applied anatomy and exercise physiology: cardiovascular and respiratory responses to exercise, neuromuscular control, the three energy systems, EPOC recovery and training adaptations for AQA 7582, OCR H555 and Edexcel 9PE0.
Every cardiovascular question is anchored in three variables: heart rate (HR), stroke volume (SV) and cardiac output (Q = SV x HR). Blood flows through the heart from the vena cava to the right atrium, through the tricuspid valve to the right ventricle, to the lungs via the pulmonary artery, back through the pulmonary vein to the left atrium, through the bicuspid (mitral) valve to the left ventricle and out through the aorta. The heart is myogenic: the impulse originates in the SA node (the pacemaker), travels to the AV node (brief delay allowing ventricular filling), down the bundle of His and through the Purkinje fibres, causing ventricular contraction. The cardiac cycle alternates systole (contraction, ~0.3 s) and diastole (relaxation and filling, ~0.5 s) at rest, shortening during exercise because heart rate rises. The exam rewards linking structure to function: thick left ventricular walls generate the pressure for systemic circulation.
Stroke volume is governed by venous return and Starling's law: the greater the venous return, the greater the end diastolic volume, the more the cardiac fibres are stretched, and the more forcefully they contract - increasing SV and ejection fraction. Five mechanisms maintain venous return during exercise and are a guaranteed 5-mark list: (1) the skeletal muscle pump (contracting muscles squeeze deep veins); (2) the respiratory pump (pressure changes during breathing assist flow in the thoracic veins); (3) pocket valves (prevent backflow); (4) smooth muscle in vein walls (venoconstriction squeezes blood centrally); (5) gravity (assists return from the upper body). Typical figures: SV around 60-80 ml at rest, rising to 110-120 ml in untrained maximal exercise but 160-200 ml in endurance-trained athletes - the key trained-versus-untrained distinction the mark scheme looks for.
Cardiac output is approximately 5 l/min at rest (70 bpm x 70 ml) and rises to 20-22 l/min in untrained maximal exercise and up to 35-40 l/min in elite endurance performers. Maximal heart rate is estimated as 220 minus age and barely changes with training; trained athletes therefore achieve higher Q through SV. Endurance training produces cardiac hypertrophy (larger left ventricular cavity, increased wall thickness), giving a bradycardia - resting HR below 60 bpm, sometimes 40-50 in elite road cyclists - because a larger SV satisfies resting demand at a lower rate. Know the trained athlete's paradox for application questions: resting Q is unchanged, but it is delivered by a big SV and low HR, sparing the myocardium.
Regulation is by the cardiac control centre (CCC) in the medulla oblongata, informed by three receptors that must be memorised: chemoreceptors (detect rising CO2, falling pH, lactate in the blood), proprioceptors (detect muscle and joint movement - the muscle pump) and baroreceptors (detect changes in blood pressure). The CCC increases heart rate via the sympathetic nervous system (cardiac accelerator nerve releasing noradrenaline, plus circulating adrenaline) and decreases it via the parasympathetic vagus nerve (acetylcholine). At exercise onset, HR shows an anticipatory rise driven by the brain and proprioceptors before chemical changes even occur - a subtlety worth a mark in regulation questions.
The vascular shunt redistributes blood: at rest only 15-20% of cardiac output goes to skeletal muscle (most to gut, liver, kidneys, brain); in maximal exercise 80-85% is diverted to working muscle. This is achieved by vasodilation of arterioles and pre-capillary sphincters supplying active muscle and vasoconstriction of those supplying inactive organs, under sympathetic control (vasomotor control centre in the medulla). Purpose: deliver O2 and nutrients, remove CO2 and lactate, and assist thermoregulation through the skin. Link it to exercise: the shunt explains why digestion is impaired during competition - a classic applied point.
Blood pressure: systolic ~120 mmHg, diastolic ~60-80 mmHg at rest. During dynamic exercise systolic pressure rises sharply (more blood ejected per beat) while diastolic pressure stays broadly stable (vasodilation offsets the increased flow) - know this pattern and why. After exercise, blood pools in dilated skeletal veins if the performer stops suddenly (venous pooling), reducing venous return and causing dizziness or fainting (post-exercise hypotension). An active cool-down maintains the skeletal muscle pump and venous return, preventing this - a standard 2-mark application.
The a-VO2 difference (difference in oxygen content between arterial and venous blood) widens from ~4-6 ml per 100 ml at rest to 16-20 ml per 100 ml in maximal exercise: muscles extract more oxygen as intensity rises, aided by training adaptations (capillarisation, mitochondria). Exam application: training increases both maximal Q and a-VO2 difference, so VO2 max improves through central (cardiac) and peripheral (muscular) mechanisms.
| Variable | Rest | Maximal exercise (untrained) | Maximal exercise (trained) |
|---|---|---|---|
| Heart rate | 60-80 bpm | ~185-200 bpm (220 - age) | ~185-200 bpm |
| Stroke volume | 60-80 ml | 110-120 ml | 160-200 ml |
| Cardiac output | ~5 l/min | 20-22 l/min | up to 35-40 l/min |
| Blood to skeletal muscle | 15-20% | 80-85% | 80-85% |
| a-VO2 difference | 4-6 ml/100 ml | 16-20 ml/100 ml | 16-20 ml/100 ml |
Cardiac cycle volumes and ejection fraction add the A* numbers: at rest the left ventricle fills to an end diastolic volume (EDV) of ~120 ml and ejects ~70 ml, leaving an end systolic volume (ESV) of ~50 ml - so the ejection fraction is roughly 60%, and rises with exercise and training because Starling's law increases contractile force. Blood composition matters for the transport half of the story: plasma (~55%, mostly water carrying nutrients, hormones and waste), red blood cells containing haemoglobin (each molecule carries four O2 molecules), white cells and platelets; haematocrit is the percentage of blood volume occupied by red cells (~45% male, ~40% female). Training expands plasma volume more than red cell volume initially, slightly lowering viscosity and aiding flow - which is why plasma volume expansion is cited in endurance adaptation answers. At exercise onset the autonomic sequence is precise and examinable: vagal (parasympathetic) withdrawal raises heart rate first (fast, within seconds), then sympathetic activation raises it further and increases contractility - state the order.
Baroreceptor reflex: baroreceptors in the aortic arch and carotid sinus normally resist rises in blood pressure, but during exercise their threshold resets upward (resetting by the CCC), allowing systolic pressure to rise to drive blood to muscle - the standard explanation for why systolic pressure is permitted to climb during exercise. Cardiovascular drift is the A* detail for prolonged exercise: in a long session (90+ minutes), heart rate slowly drifts upward while stroke volume declines, driven by rising body temperature and dehydration (falling plasma volume) - quote it in endurance fatigue answers alongside glycogen depletion. Application chains to rehearse: why does an athlete feel dizzy standing still after a hard run (venous pooling, lost muscle pump); why does digestion slow during competition (vascular shunt away from the gut); why is the trained athlete's resting heart rate low (larger SV meeting the same resting Q).
Exam logic: for any explain question, chain cause to effect - venous return rises (five mechanisms), Starling's law stretches the ventricle, SV rises, Q rises; receptors feed the CCC, which shifts the autonomic balance from vagal to sympathetic. For evaluate questions, contrast trained and untrained responses: trained = bigger SV, lower resting HR, faster recovery.
Mechanics of breathing rest on pressure-volume relationships. At rest, inspiration is active: the diaphragm contracts and flattens while the external intercostals lift the ribs and sternum, increasing thoracic volume, decreasing pressure, and air moves in down the pressure gradient. Expiration at rest is passive: the muscles relax and the lungs' elastic recoil pushes air out. During exercise, breathing becomes forced: inspiration adds sternocleidomastoid, pectoralis minor and scalenes; expiration recruits internal intercostals and rectus abdominis to pull the ribcage down faster. Exam phrasing that scores: air moves from high to low pressure; volume changes precede pressure changes.
Volumes and capacities: tidal volume (TV) ~500 ml at rest, rising to ~2-3 l in maximal exercise; breathing frequency rises from 12-15 to 40-50 breaths per minute; minute ventilation (VE = TV x f) rises from ~6 l/min to 100-120 l/min untrained and 160-200 l/min trained. Reserve values matter for A* precision: IRV ~3 l, ERV ~1.2 l, residual volume ~1.2 l (constant - it cannot be expired, protecting alveolar structure), vital capacity ~4.8 l (IRV + TV + ERV, only slightly changed by training - training improves ventilatory muscles and VE max, not lung structure; a common misconception the exam probes).
Gaseous exchange occurs at two sites: external (alveoli to pulmonary capillaries) and internal (systemic capillaries to muscle). Exchange follows partial pressure gradients (Dalton's law): alveolar PO2 is high (~104 mmHg) versus deoxygenated venous blood (~40 mmHg), so O2 diffuses into blood; alveolar PCO2 (~40 mmHg) versus venous PCO2 (~46 mmHg) drives CO2 the other way. At the muscle the gradients reverse. The alveoli provide a huge, thin, moist surface with a dense capillary network, so diffusion is fast - and even faster in trained performers through greater capillarisation and larger TV. Oxygen travels bound to haemoglobin as oxyhaemoglobin; at the muscle, higher temperature, CO2 and acidity (from H+ and lactate) reduce haemoglobin affinity - the Bohr shift - unloading O2 where it is needed most. The Bohr shift is the standard A* detail in gaseous exchange questions.
Regulation of breathing: the respiratory centre in the medulla sets the rhythm, adjusted by (1) chemical factors - central and peripheral chemoreceptors (medulla; aortic and carotid bodies) detect rising CO2 and falling pH, increasing rate and depth; (2) neural factors - proprioceptors in muscles and joints and temperature receptors feed the respiratory centre, producing the anticipatory rise at exercise onset; (3) hormonal adrenaline. During steady submaximal exercise, ventilation plateaus to match oxygen demand; in high-intensity exercise it keeps climbing as buffering of lactate produces extra CO2 - link this to the lactate threshold for top-band answers.
Neuromuscular system. A motor unit = one motor neurone plus all the fibres it innervates (small units in eyes and fingers for precision; large units in quadriceps for force). The all-or-nothing law: when the motor neurone's stimulus reaches threshold, all fibres in the unit contract maximally; below threshold, none contract. Force is therefore graded by recruitment (how many units fire - spatial summation) and frequency (repeated stimuli before full relaxation - wave summation, leading to unfused then tetanic contraction). The size principle earns A* marks: small slow-oxidative units are recruited first, fast oxidative and then fast glycolytic units join as force demand rises - which is why lifting light weights slowly barely touches the fast fibres.
| Characteristic | Type I (slow oxidative) | Type IIa (fast oxidative glycolytic) | Type IIx (fast glycolytic) |
|---|---|---|---|
| Contraction speed | Slow (~110 ms) | Fast (~50 ms) | Fastest (~50 ms) |
| Force produced | Low | High | Very high |
| Fatigue resistance | Very high | Moderate | Very low |
| Colour | Red (myoglobin-rich) | Red | White (pale) |
| Mitochondria, capillaries | Many, high blood supply | Moderate | Few |
| Motor unit size | Small (few fibres) | Large | Large |
| Dominant energy system | Aerobic | Aerobic and anaerobic | ATP-PC and glycolytic |
| Typical performers | Marathon runner, Tour cyclist | 1500 m runner, swimmer | Sprinter, javelin thrower |
Application logic: a marathon runner's leg muscles are predominantly Type I; a 100 m sprinter's predominantly Type IIx; training can shift IIx towards IIa but cannot convert Type I to Type II - a guaranteed discrimination point.
Proprioceptors sense muscle state and protect the muscle: muscle spindles (intrafusal fibres lying parallel to extrafusal fibres) detect the speed and magnitude of stretch and, when stimulated, trigger an excitatory stretch reflex (contraction to resist stretching - e.g. the knee-jerk reflex, or the spring-like reflex in sprinting). Golgi tendon organs (at the muscle-tendon junction, in series) detect tension; when tension is excessive they trigger the inverse stretch reflex (autogenic inhibition) - an inhibitory response that relaxes the muscle to prevent tearing. PNF (proprioceptive neuromuscular facilitation) exploits the GTO: the CRAC sequence - passive stretch, isometric contraction against a partner for 6-10 s (stimulating the GTO), relaxation, then contracting the antagonist to push the stretch further. Autogenic inhibition plus reciprocal inhibition allows a greater range of motion than static stretching alone, which is why PNF is the most effective flexibility method in exam answers - link spindles (must be quiet), GTO (deliberately stimulated) and the improved ROM.
Reading a spirometer trace is an examinable skill: the resting wave amplitude gives tidal volume; the rise from the top of the tidal wave to a maximal inhalation gives IRV; from the bottom of the tidal wave to maximal exhalation gives ERV; the volume that cannot be expired is the residual volume (the trace flattens at maximal expiration but never reaches zero); vital capacity is the maximum exhale after maximum inhale (IRV + TV + ERV). During exercise the trace widens (TV up) and quickens (frequency up); minute ventilation is read as TV x frequency per minute. Training effects: stronger diaphragm and intercostals raise inspiratory volume and reduce fatigue of the ventilatory muscles; VE max increases; alveolar and lung structure are essentially unchanged - repeat this distinction, it is a common misconception.
Motor neurone structure and transmission earn neuromuscular depth: the cell body with dendrites receives impulses; the axon conducts them; myelinated axons (Schwann cells) transmit faster because the impulse jumps between nodes of Ranvier (saltatory conduction); the impulse crosses the neuromuscular junction by acetylcholine release, triggering fibre contraction. Recruitment and rate coding in strength training is the applied depth: heavy loads (above ~85% 1RM) recruit high-threshold fast glycolytic units that light training never touches, and increased firing frequency (rate coding) raises force output - which is why heavy resistance work builds strength even before hypertrophy. Fatigue across fibre types: Type I fibres resist fatigue (aerobic dominant, high lactate tolerance), Type IIx fatigue fastest (H+ accumulation); in maximal sprints the fast units fail first, explaining the deceleration phase - link to the glycolytic system's fatigue mechanism. Application logic: motor unit questions reward all-or-nothing plus graded force (spatial and wave summation, recruitment order); fibre-type questions reward the table plus a training-conversion point (IIx shifts towards IIa with endurance training; Type I cannot become Type II).
Exam logic: respiratory questions reward the pressure-gradient chain and the anticipatory rise; neuromuscular questions reward all-or-nothing plus graded force (summation, recruitment) and a fibre-type table with a sporting application; PNF questions always want the proprioceptor names and the words excitatory/inhibitory.
ATP (adenosine triphosphate) is the only usable energy currency: breaking the terminal phosphate bond releases energy, leaving ADP + P. ATP is resynthesised by three systems whose dominance depends on intensity and duration - the energy continuum: the systems operate together from the start; the exam wants the dominant contributor identified for a given event, not an either/or. Frame every answer with intensity first, duration second.
ATP-PC (phosphagen) system: phosphocreatine (PC) is stored in the sarcoplasm; the enzyme creatine kinase splits PC into creatine and phosphate, and the released energy resynthesises ATP from ADP + P - a coupled reaction requiring no oxygen (alactic). Characteristics: yield ~1 ATP per PC (small), power very high, duration 0-10 seconds of maximal effort, no fatiguing by-products (PC depletion is the limiter), full resynthesis in ~2-3 minutes of rest (relevance to repeated sprints and substitutions). Examples: 100 m sprint, javelin throw, vault, netball centre pass. A* detail: sprint training and creatine supplementation increase PC stores; games players resynthesise PC during walk intervals - link to training and to intermittent sports.
Glycolytic (lactic acid) system: anaerobic glycolysis breaks down glucose or glycogen (stored as muscle glycogen) via the enzyme PFK (phosphofructokinase) into pyruvate, which - without sufficient oxygen - becomes lactic acid. Net yield: 2 ATP from glucose, 3 from glycogen; moderate power, larger capacity than ATP-PC, dominant in high-intensity exercise from ~10 seconds to ~2 minutes. Fatigue mechanism (a guaranteed mark): lactate dissociates into lactate + H+ ions; H+ accumulation lowers muscle pH, inhibiting PFK (slowing glycolysis), interfering with calcium release and cross-bridge cycling, and causing the burn and slowing in a 400 m. Examples: 400 m, 800 m closing laps, repeated high-intensity efforts in hockey.
Aerobic system - three stages, in order: (1) aerobic glycolysis: glycogen/glucose to pyruvate, then to acetyl CoA (fats enter via beta oxidation); (2) Krebs cycle: acetyl CoA oxidised, releasing CO2 and hydrogen ions; (3) electron transport chain: hydrogen ions oxidised to water, driving oxidative phosphorylation of large amounts of ATP. Yield: ~36-38 ATP per glucose (and far more per fat molecule, but fat requires more oxygen per ATP - the reason fat oxidation dominates low-intensity exercise and glycogen dominates higher intensities - glycogen sparing). Characteristics: slow power, virtually unlimited capacity, dominant in sustained submaximal exercise; measured by VO2 max. Examples: marathon, triathlon, 1500 m middle portion. A* detail: the aerobic system also fuels recovery - PC restoration and lactate removal both occur aerobically, which links the systems together on the continuum.
Energy continuum applications: 100 m = ATP-PC dominant; 400 m = glycolytic dominant (with ATP-PC start and growing aerobic contribution); 1500 m = aerobic-glycolytic mix; marathon = aerobic dominant. In games (netball, football) the systems interplay with work:rest ratio determining which resynthesises between efforts. AQA-style extended questions give an athlete and a duration - state the dominant system, justify with intensity and duration, then describe that system's stages in order.
EPOC (excess post-exercise oxygen consumption, historically oxygen debt) is the elevated O2 uptake after exercise that restores the body to pre-exercise state. Two components, in order: the fast (alactacid) component, lasting ~2-3 minutes, restores PC and ATP stores and reloads myoglobin with oxygen; the slow (lactacid) component, lasting from minutes to hours after hard sessions, removes lactate (oxidised as fuel in active muscle, or converted back to glucose/glycogen in the liver via the Cori cycle), replenishes muscle and liver glycogen, and pays for still-elevated ventilation, heart rate and body temperature (plus circulating adrenaline). The greater the anaerobic contribution (higher intensity, longer lactate production), the larger the EPOC - an 800 m produces a bigger debt than a jog. Cool-down value: light exercise keeps the skeletal muscle pump working, maintaining venous return and blood flow to muscles, which speeds lactate oxidation and removal compared with passive rest, and prevents venous pooling and dizziness - the standard two-mark application; it does not fully restore PC (that needs the fast component).
Fatigue mechanisms to cite by system: ATP-PC - PC depletion; glycolytic - H+ accumulation/acidosis (plus reduced calcium release - neuromuscular fatigue); aerobic - glycogen depletion (hitting the wall, ~90+ minutes), dehydration beyond ~2% body mass impairing thermoregulation and blood volume. Match the fatigue mechanism to the energy system in the question - the most common lost mark is quoting H+ for a marathon.
Training methods and adaptations. Aerobic training (continuous, Fartlek, long interval, HIIT) produces: cardiac hypertrophy with greater SV and bradycardia; increased blood volume and haemoglobin; capillarisation; more and larger mitochondria; increased myoglobin and oxidative enzymes; greater fat oxidation; a rightward shift of the lactate threshold (submaximal pace at lower lactate) and VO2 max improvement of roughly 5-20% (genetically capped - a top-band evaluation point). Anaerobic/sprint and plyometric training increases PC stores (~up to 10%), glycolytic enzyme activity and buffer capacity (tolerating H+ longer). Strength training (free weights, machines, body weight) produces neural adaptations first (improved recruitment, coordination and rate of force development in the first ~6-8 weeks) followed by hypertrophy (increased contractile protein - actin and myosin). Flexibility training (static, ballistic, dynamic, PNF) increases extensibility and stretch tolerance via the GTO adaptations described earlier. Periodisation organises it: macrocycle (season/year), mesocycle (4-8 week block), microcycle (week), with tapering before competition to peak - link each adaptation to the training method that produces it, and the method to the performer's event, for full marks.
Measuring the systems links the theory to data (see the Performance Data topic): the lactate threshold is measured during an incremental test (treadmill or cycle, increasing stages) with blood samples analysed for lactate; OBLA (onset of blood lactate accumulation) is the intensity at which lactate exceeds ~4 mmol/l - the conventional marker used to set training intensities. Training shifts both the threshold and OBLA to a higher percentage of VO2 max, so race pace is sustainable at lower lactate - the physiological explanation of improved endurance performance. Direct VO2 max testing (incremental test to exhaustion with a mask and gas analysis measuring O2 uptake and CO2 output) is the criterion measure; field estimates (multi-stage fitness test) trade accuracy for accessibility. Glycogen loading (carbo-loading) is the diet-application detail: in the days before a long endurance event, the performer tapers training while loading carbohydrate, super-compensating muscle glycogen stores, delaying the point of glycogen depletion (hitting the wall) - evaluate with the downside: extra glycogen binds water, adding weight and stiffness. Creatine supplementation increases PC stores, benefiting the ATP-PC system in repeated maximal efforts - evaluate with weight gain and variable individual response.
Recovery strategies beyond the cool-down - pair each to its EPOC component: nutrition - carbohydrate plus protein within ~30-60 minutes post-exercise replenishes glycogen (slow component) and repairs muscle; hydration and electrolytes - restores plasma volume, limiting cardiovascular drift; sleep - the largest single recovery window, supporting hormonal restoration; ice baths/cryotherapy - reduce inflammation and soreness, though evidence suggests they may blunt some training adaptations (a strong evaluation point); compression garments and massage - may aid venous return and perceived recovery. Exam logic for recovery questions: state the component (fast/slow), the strategy, and the mechanism it supports - nutrition targets glycogen (slow component), the cool-down targets lactate removal and venous pooling, sleep supports everything. The most common lost mark: attributing a marathon's fatigue to H+ ions - it is glycogen depletion; H+ belongs to high-intensity glycolytic fatigue.
Exam logic: state the dominant system from intensity and duration; describe stages in order with enzymes and yields; explain fatigue with the matching mechanism; for EPOC give both components with timings and functions; for training, pair method - adaptation - performance benefit in one chain per mark point.