9.3 Exercise and Sports Physiology

Exercise as an integrated systems stress test

Exercise and Sports Physiology is 10% of the Physiology domain. The official page again lists no sub-bullets. The usable syllabus is still concrete: VO2 and VO2max, anaerobic (lactate/ventilatory) threshold, oxygen debt/EPOC, cardiovascular and respiratory responses, muscle metabolism during work, training adaptations, and thermoregulation. Part I wants mechanisms you can apply to a cyclist, a deadlift, or a heat-acclimatized worker — not a training-plan app.

Quick Answer: VO2 = CO × (CaO2 − CvO2). VO2max is a plateau, not a slogan. Threshold is accumulating lactate plus extra VE, not mitochondria switching off. EPOC pays back the onset O2 deficit and then some. Dynamic exercise: CO up, muscle TPR down, MAP only modestly up. Sweat glands are sympathetic cholinergic. Training raises SV and extraction; heat acclimatization sweats earlier and more dilute.

VO2, the Fick equation, and VO2max

Oxygen consumption (VO2) is the amount of O2 used per unit time. The Fick principle applied to the whole body is:

VO2 = cardiac output × arteriovenous O2 content difference

CaO2 is set by Hb concentration, PaO2/saturation, and a small dissolved term. CvO2 falls as working muscle extracts more O2. Raising VO2 therefore requires some mix of more flow and more extraction.

VO2max is the highest VO2 reached despite further increases in external work — a plateau, not 'the VO2 at exhaustion if the subject quit early.' Typical resting VO2 is about 3.5 mL/kg/min, which is 1 MET. Relative VO2max (mL/kg/min) lets you compare people of different size; absolute VO2 (L/min) matters for non-weight-bearing work.

Those bands are teaching ranges, not NBCE-published cut scores. Do not invent a Part I 'passing VO2max.'

Central versus peripheral limit. In healthy people, maximal cardiac output is usually the largest ceiling on VO2max. Extraction (capillary density, mitochondrial volume, myoglobin, local flow matching) still matters and is what endurance training grows in muscle. Anemia, hypoxia, and carbon monoxide cut CaO2 and cut VO2max without any change in mitochondrial enzymes. That is why the Fick equation is the organizing sentence.

Respiratory exchange ratio (RER) = VCO2/VO2. Fat oxidation sits near 0.70; carbohydrate near 1.00. RER > 1.00 in heavy exercise reflects extra CO2 from bicarbonate buffering of lactic acid plus hyperventilation, not a new fuel with an RER of 1.2.

Anaerobic threshold is a threshold, not a cliff

Muscle does not flip from 'aerobic' to 'anaerobic' at a whistle. As intensity rises, type II fiber recruitment and glycolytic flux increase, lactate appearance exceeds disposal, and arterial lactate rises. The lactate threshold (and the related onset of blood lactate accumulation, often taught near 4 mmol/L) is that inflection.

The ventilatory threshold is the intensity where minute ventilation (VE) rises out of proportion to VO2 (V-slope: VCO2 versus VO2). Buffering of H+ by HCO3− generates extra CO2; later, carotid-body drive from falling pH adds more VE. PaO2 usually stays near normal in moderate exercise; above threshold, PaCO2 often falls slightly because VE overshoots VCO2.

Exam trap: 'Anaerobic threshold' does not mean oxidative phosphorylation has stopped. Mitochondria are running hard. The label is historical. What you must recognize is lactate accumulation + disproportionate ventilation.

Oxygen deficit and EPOC (oxygen debt)

At exercise onset, ATP demand jumps in milliseconds. VO2, limited by cardiorespiratory inertia, rises over minutes. The gap is the oxygen deficit, filled by:

1. ATP stores (tiny).
2. Phosphocreatine (creatine kinase: PCr + ADP ⇌ ATP + Cr).
3. Myokinase (2 ADP → ATP + AMP); AMP feeds AMPK and also uric-acid production if flux is huge.
4. Anaerobic glycolysis → lactate.

After exercise, VO2 stays above rest: excess post-exercise oxygen consumption (EPOC), the modern name for classic oxygen debt. Classic teaching splits:

EPOC is not equal, molecule for molecule, to the O2 that 'should have' been used to burn all lactate. Some lactate is oxidized as fuel; some is glycogen. Do not treat the 1920s oxygen-debt ledger as stoichiometric truth. Do know that a deficit exists at the start and an elevated VO2 exists after.

Muscle metabolism by duration and intensity

The crossover concept: as intensity rises, the percentage of ATP from carbohydrate rises even if some fat oxidation continues. Training shifts the crossover to the right: a trained person oxidizes more fat at the same absolute work rate, sparing glycogen. Protein is a minor fuel except in very prolonged work or low carbohydrate availability.

Fiber types (detail in muscle physiology): type I slow oxidative, fatigue-resistant, high mitochondria and capillaries; type IIa fast oxidative-glycolytic; type IIx fast glycolytic. Recruitment is size principle: light work is mostly type I; sprint and heavy resistance add II.

Local functional hyperemia uses K+, adenosine, phosphate, CO2/H+, osmolarity, and endothelial NO — metabolites that couple flow to metabolism without waiting for a sympathetic memo. Sympathetic norepinephrine still constricts inactive beds.

Cardiovascular responses

Central command (parallel activation of motor cortex and brainstem autonomic circuits) raises HR before the first full stride — the anticipatory response. Exercise pressor reflex from mechanically and metabolically sensitive muscle afferents (groups III and IV) adds sympathetic drive, especially when perfusion is inadequate (ischemic isometric holds).

Heart rate. Resting HR is vagally dominated. Early exercise: parasympathetic withdrawal. Further increases: sympathetic activation. Estimated maximal HR of 220 minus age is a population sketch with a large standard deviation, not a Part I constant of nature.

Stroke volume. Rises because of:

• Increased preload: muscle pump, respiratory pump, sympathetic venoconstriction.
• Increased contractility: catecholamines, Frank-Starling from the extra venous return.
• Decreased afterload in the exercising muscle circuit (arteriolar dilation).

SV plateaus in many untrained people around moderate work; further CO increase is mostly HR. Endurance athletes start with a larger end-diastolic volume and can raise SV more.

Distribution. At rest, skeletal muscle may receive ~15–20% of CO. In heavy dynamic exercise it can receive ~80–85%. Splanchnic and renal flow fall (sympathetic α1). Skin flow falls at onset then rises as core temperature climbs — a competition between pressure regulation and heat loss. Coronary flow rises with myocardial work; remember that coronary perfusion is mainly diastolic, so very high HR shortens the filling window.

Blood pressure. In dynamic (rhythmic) exercise, systolic pressure rises, diastolic is flat or slightly down, and mean arterial pressure rises only modestly because TPR falls. In static (isometric) exercise, intramuscular pressure limits vasodilation, TPR stays higher, and both systolic and diastolic pressures climb more. A prolonged Valsalva during a maximal lift is an extreme version of that afterload spike. Chiropractic relevance is mechanistic, not a technique cue: isometric spinal stabilization work is a pressure load; gait and cycling are flow loads.

Respiratory responses

VE = VT × frequency. Moderate exercise first deepens tidal volume; very heavy exercise then raises frequency. Dead-space fraction falls as VT rises. Pulmonary blood flow increases, more West-zone lung is recruited, V/Q becomes more uniform, and DLCO rises.

Arterial blood gases in moderate exercise: PaO2 nearly unchanged, PaCO2 nearly unchanged, pH nearly unchanged. Above ventilatory threshold: lactate acidosis, VE/VO2 rise, possible PaCO2 decrease. Elite athletes can show a widened A-a gradient at VO2max (diffusion limitation plus very short RBC transit) — a gas-exchange footnote, not a reason to diagnose lung disease in a healthy racer. Mechanics of compliance and surfactant stay in 8.1 Respiratory Physiology; here you need the exercise pattern.

Training adaptations

Specificity, overload, progression, reversibility are the rules. Biochemical detail differs by stimulus.

Detraining drops plasma volume and SV quickly; mitochondrial enzymes fade over weeks. The first fitness lost is often the last gained: short-term 'detraining fatigue' on a Monday is volume and autonomic, not a vanished mitochondrion.

Hormonal mix during an acute bout (do not steal the chemistry chapter): insulin tends to fall, glucagon and catecholamines rise, GH and cortisol rise with intensity and duration — a fuel-mobilization set. Trained people often show smaller endocrine swings at the same absolute work because the work is a smaller fraction of VO2max.

Thermoregulation in exercise

Core temperature is defended by balancing metabolic heat against radiation, conduction, convection, and evaporation. When air temperature exceeds skin temperature, only evaporation can dump heat. High humidity lowers the vapor-pressure gradient and caps evaporative cooling — the wet-bulb problem.

Eccrine sweat glands are innervated by sympathetic cholinergic fibers (acetylcholine on muscarinic receptors). That innervation is the classic autonomic exception and a reliable item. Cutaneous vasodilation for heat loss is a mix of sympathetic withdrawal and active vasodilator pathways.

Heat acclimatization over about 7–14 days of work in the heat:

• Plasma volume expands (better SV, lower HR at a given work rate).
• Sweating starts earlier (lower core-temperature threshold).
• Sweat rate increases.
• Sweat [Na+] and [Cl−] fall (aldosterone effect on ducts) — more cooling per liter of water, less electrolyte loss.
• Core temperature and HR at a given load decrease.

Exam trap: acclimatization is not 'sweat less to conserve water.' It is usually sweat more, but more dilute, and sooner.

Cold: cutaneous vasoconstriction, behavioral bundling, shivering (involuntary muscle heat), and in infants nonshivering thermogenesis (brown-fat UCP1). Exercising in cold still produces metabolic heat; the risk is often wet clothing destroying insulation when you stop.

Worked scenario — preseason two-a-days. Day 1 in humid heat: high HR, high core temperature, salty heavy sweat, early fatigue. Day 12: lower HR at the same drill, earlier sweat onset, more volume of hypotonic sweat, better plasma volume. That is acclimatization physiology, not a personality change.

Heat exhaustion is cardiovascular/volume limited; heat stroke adds CNS dysfunction and a failed heat-loss system. Part I wants the dissipation mechanisms more than the emergency-medicine staging, but you should know evaporation can fail.

/practice/nbce-part1Practice questions with detailed explanations