Exercise Physiology and Energy Systems
Domain 2: Exercise Physiology and Energy Systems
This domain tests bioenergetics, cardiorespiratory control, fatigue, and training adaptation. Questions often ask which system dominates at a given duration, or why an athlete’s performance improves without a large VO2max change.
Core rules
- ATP-PCr system: immediate, ~0–10 s, uses creatine kinase; no oxygen and no lactate.
- Fast glycolysis: ~10 s–2 min, net 2 ATP per glucose; lactate and H+ accumulate, contributing to acidosis and fatigue.
- Oxidative system: >2 min; Krebs cycle and electron transport chain; yields far more ATP and uses carbohydrate and fat. Fat oxidation is high at low intensity but rate-limited.
- Fick equation: VO2 = cardiac output × arterial–venous O2 difference. Cardiac output = heart rate × stroke volume.
- Endurance training raises plasma volume, stroke volume, capillarity, and mitochondrial density. Early strength gains are largely neural; hypertrophy follows.
- Lactate threshold and ventilatory threshold mark the intensity above which lactate and ventilation rise disproportionately.
Worked example
A 400 m sprint lasting about 55 s is not “aerobic.” ATP-PCr supplies the start, fast glycolysis dominates the middle and finish, and oxidative metabolism contributes a small but useful fraction. The athlete’s high lactate and H+ concentration constrain later performance, so pacing and tolerance matter. A 5 km race, by contrast, is overwhelmingly oxidative; training should target threshold and VO2max, not repeated maximal 10 s efforts.
Traps
Lactate is not the sole cause of acidosis, and it does not cause delayed-onset muscle soreness. RER above 1.0 suggests hyperventilation, not fat use. VO2max is not always the limiter; economy and threshold matter. Also, “fat burning” does not mean fat is the main fuel at sprint intensity.