Exercise Physiology I: the Scope and Importance of Exercise Physiology, Cardiorespiratory Adaptations to Short-Term and Long-Term Physical Activity, Muscle Types, Characteristics and Functions, the Microscopic Structure of the Muscle Fibre, the Sliding Filament Theory, Muscle Fibre Types and Sports Performance, and Muscular Adaptations to Exercise

Cardiac output (Q) is the volume of blood the heart pumps per minute: Q = heart rate × stroke volume. At rest, 70 beats per minute × 70 mL per beat ≈ 4.9 L/min, roughly 5 L. During exercise both rise: heart rate rises almost linearly with intensity up to its maximum, and stroke volume rises to a plateau at about 40–60 per cent of VO2max in most people, so cardiac output can reach about 20 L/min in untrained adults and 35–40 L/min in elite endurance athletes. Blood is redistributed from the gut and kidneys to working muscle; systolic blood pressure rises with intensity while diastolic pressure changes little in dynamic exercise; and muscles extract more oxygen, widening the arteriovenous oxygen difference (a–vO2 diff). The Fick equation ties these together: VO2 = Q × a–vO2 diff.

Ventilation also rises. Minute ventilation (VE) = tidal volume × breathing frequency: at rest about 0.5 L × 12 breaths = 6 L/min, and in heavy exercise well over 100 L/min, first by deeper breaths and then by faster ones. At the start of exercise ventilation jumps almost immediately (a neural response), then rises more slowly (a chemical response to carbon dioxide and hydrogen ions); above the ventilatory threshold it rises out of proportion to oxygen uptake. In short, intense activity such as a 400 m run, heart rate and ventilation climb steeply and the anaerobic systems supply much of the energy; in prolonged activity such as a marathon, heart rate drifts upward at constant pace (cardiovascular drift, as plasma is lost in sweat and stroke volume falls) and oxygen uptake stays at a steady state.

Long-term endurance training produces adaptations. The heart enlarges (athlete's heart): endurance training mainly enlarges the left ventricular cavity, while heavy resistance training mainly thickens its wall. Stroke volume rises at rest and at maximum, so resting and submaximal heart rates fall (resting bradycardia; elite endurance athletes may rest in the 40s), while maximal heart rate changes little. Blood volume and plasma volume increase, capillary density in muscle rises, mitochondria multiply, and VO2max rises, typically by 15–20 per cent in previously sedentary people, within a ceiling set largely by heredity. Respiratory adaptations include greater maximal ventilation and more enduring respiratory muscles, though resting lung volumes change little. Recovery heart rate falls faster, which is the basis of step tests such as the Harvard test in Unit IX.

The body has three types of muscle: skeletal muscle (striated, voluntary, attached to bones, moving the body), cardiac muscle (striated but involuntary, branched and joined by intercalated discs, found only in the heart) and smooth muscle (non-striated, involuntary, in the walls of the gut, blood vessels and other hollow organs). Muscle tissue has four characteristics: excitability (it responds to stimuli), contractility (it shortens with force), extensibility (it can be stretched) and elasticity (it returns to its resting length). Skeletal muscle produces movement, maintains posture, stabilises joints, generates heat and protects internal organs; in movement muscles act as agonists (prime movers), antagonists (which relax or control the opposite action), synergists (which assist) and fixators or stabilisers.

A skeletal muscle is wrapped in epimysium and divided into bundles (fascicles) wrapped in perimysium; each fascicle contains muscle fibres (cells), each wrapped in endomysium. A fibre is a long, multinucleated cell whose membrane is the sarcolemma and whose cytoplasm is the sarcoplasm; it contains the sarcoplasmic reticulum, which stores calcium, and transverse (T) tubules that carry the impulse inside. The fibre is packed with myofibrils made of repeating sarcomeres, the functional units of contraction, each running from one Z line (Z disc) to the next. Thick filaments are myosin, whose heads form cross-bridges; thin filaments are actin, carrying the regulatory proteins tropomyosin and troponin. The dark A band is the length of the myosin filaments; the light I band contains only actin and is bisected by the Z line; the H zone in the centre of the A band contains only myosin, with the M line at its centre.

The sliding filament theory, proposed in 1954 by Andrew Huxley and Rolf Niedergerke and independently by Hugh Huxley and Jean Hanson, explains contraction as the sliding of thin actin filaments over thick myosin filaments towards the centre of the sarcomere; neither filament shortens. The sequence runs: a motor nerve impulse reaches the neuromuscular junction and triggers a muscle action potential; the impulse spreads along the sarcolemma and down the T tubules; the sarcoplasmic reticulum releases calcium ions; calcium binds troponin, which shifts tropomyosin off the binding sites on actin; energised myosin heads attach to actin, forming cross-bridges; the power stroke pulls actin towards the M line as ADP and phosphate are released; a new ATP binds the myosin head and detaches it; hydrolysis of that ATP re-cocks the head for the next cycle. Relaxation follows when stimulation stops, calcium is pumped back into the sarcoplasmic reticulum (which also needs ATP) and tropomyosin covers the sites again.

During contraction the I band and H zone shorten and the Z lines move closer, but the A band keeps its length, because it is the length of the myosin filaments, which do not change. This is the observation that proved the theory. The force a fibre can develop depends on the overlap of actin and myosin: at too short or too long a sarcomere length fewer cross-bridges can form (the length–tension relationship), which is one reason a muscle is strongest in the middle of its range and why pre-stretch matters in throwing and jumping.

Skeletal muscle fibres are classified by contraction speed and metabolism. Type I (slow-twitch, slow oxidative) fibres are red, rich in mitochondria, myoglobin and capillaries, contract slowly with modest force and resist fatigue. Type IIa (fast oxidative-glycolytic) fibres are intermediate: fast and fairly fatigue-resistant. Type IIx (fast glycolytic; called IIb in older texts, a type more prominent in small animals) fibres are white, rely on anaerobic glycolysis, contract fast and forcefully and fatigue quickly. Most muscles are a mosaic, and the proportion is largely inherited: elite marathon runners typically have a high percentage of type I fibres in the leg muscles and elite sprinters a high percentage of type II. The motor units of each type are recruited in order of size (Henneman's size principle): small, slow units first for gentle effort, large, fast units only as force demands rise.

Muscle adapts specifically to the training it receives. Resistance training increases strength first through neural adaptations, meaning better recruitment of motor units, higher firing rates, better synchronisation and less co-contraction of antagonists, which explains most strength gains in the first weeks; hypertrophy, the growth of fibre cross-sectional area by adding contractile protein, follows over months, and type II fibres enlarge most. Endurance training increases mitochondrial number and size, oxidative enzymes, capillary density, myoglobin and stored glycogen and fat, raising the muscle's capacity to use oxygen and delay fatigue. Training can shift fibres within the type II group, from IIx towards IIa, but conversion of type II into type I in humans is at most limited. Disuse and immobilisation reverse these gains (atrophy), which is the principle of reversibility.