Part 4 · Chapter 4.5

Muscle Metabolism

Muscle contraction consumes ATP at rates up to 1 000× resting — more than any other tissue. Three ATP-regenerating systems operate on different timescales: the phosphocreatine (PCr) buffer for <10 s sprints, anaerobic glycolysis for ~1–2 min, and oxidative phosphorylation for endurance work. This chapter covers the metabolic hierarchy, fatigue, and the training adaptations that shift which pathway dominates.

1. Phosphocreatine Buffer

Creatine kinase catalyses instantaneous ATP regeneration from PCr:

\[ \text{PCr} + \text{ADP} + \text{H}^+ \rightleftharpoons \text{Cr} + \text{ATP},\qquad K_{eq} \gg 1 \]

Resting [PCr] ~15 mM, enough to sustain ~10 s of maximal contraction. PCr depletion correlates with the fatigue threshold in 100 m sprints and Olympic lifting. Recovery requires oxidative PCr resynthesis over ~3–5 min.

2. Anaerobic Glycolysis

Muscle glycogen is broken down to lactate through 10 glycolytic steps yielding 2 ATP per glucose-1-P (net). Lactate accumulation produces acidification (not lactate itself, but the accompanying H+ from ATP hydrolysis imbalance); acidosis inhibits PFK1 and myosin ATPase, contributing to fatigue. Muscle contains ~100 mmol glycogen ATP-equivalents per kg — enough for ~2 minutes of maximal work.

Simulation: Three ATP Sources

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3. Oxidative Phosphorylation

For endurance work, muscle oxidises glucose and fatty acids to CO2 + H2O through glycolysis + TCA cycle + ETC, yielding ~30 ATP per glucose. VO2max — maximal aerobic oxygen consumption — is the integrative cardiovascular + mitochondrial capacity measure; typical untrained young males ~45 mL kg-1 min-1, elite marathoners ~85, cross-country skiers up to 95. Training increases mitochondrial density, capillary supply, and oxidative enzymes (Holloszy 1967).

4. Fatigue

Muscle fatigue is multifactorial: PCr depletion, glycogen depletion, H+acidosis, Pi accumulation inhibiting cross-bridge cycling, reduced SR Ca2+release (Ca2+-handling fatigue). Central fatigue (reduced motor-cortex drive) adds a CNS component, measurable via twitch interpolation. Recovery is a composite: PCr 3–5 min, glycogen 24 h, inflammation/damage repair 72–96 h.

Key References

• Holloszy, J. O. (1967). “Biochemical adaptations in muscle.” J. Biol. Chem., 242, 2278–2282.

• Allen, D. G., Lamb, G. D. & Westerblad, H. (2008). “Skeletal muscle fatigue.” Physiol. Rev., 88, 287–332.

• Sahlin, K., Tonkonogi, M. & Söderlund, K. (1998). “Energy supply and muscle fatigue in humans.” Acta Physiol. Scand., 162, 261–266.

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