The purpose of this study was to examine the development of fatigue in isolated, single skeletal muscle fibers when O₂ availability was reduced but not to levels considered rate limiting to mitochondrial respiration. Tetanic force was measured in single living muscle fibers (n = 6) from Xenopus laevis while being stimulated at increasing contraction rates (0.25, 0.33, 0.5, and 1 Hz) in a sequential manner, with each stimulation frequency lasting 2 min. Muscle fatigue (determined as 75% of initial maximum force) was measured during three separate work bouts (with 45 min of rest between) as the perfusate PO₂ was switched between values of 30 ± 1.9, 76 ± 3.0, or 159 Torr in a blocked-order design. No significant differences were found in the initial peak tensions between the high-, intermediate-, and low-PO₂ treatments (323 ± 22, 298 ± 27, and 331 ± 24 kPa, respectively). The time to fatigue was reached significantly sooner (P < 0.05) during the 30-Torr treatment (233 ± 39 s) compared with the 76- (385 ± 62 s) or 159-Torr (416 ± 65 s) treatments. The calculated critical extracellular PO₂ necessary to develop an anoxic core within these fibers was 13 ± 1 Torr, indicating that the extracellular PO₂ of 30 Torr should not have been rate limiting to mitochondrial respiration. The magnitude of an unstirred layer (243 ± 64 µm) or an intracellular O₂ diffusion coefficient (0.45 ± 0.04 × 10⁵ cm²/s) necessary to develop an anoxic core under the conditions of the study was unlikely. The earlier initiation of fatigue during the lowest extracellular PO₂ condition, at physiologically high intracellular PO₂ levels, suggests that muscle performance may be O₂ dependent even when mitochondrial respiration is not necessarily compromised.

mitochondria; respiration; oxidative phosphorylation; fatigue; oxygen consumption

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