The O2 cost of the tension-time integral in isolated single myocytes during fatigue.

One proposed explanation for the Vo(2) slow component is that lower-threshold motor units may fatigue and develop little or no tension but continue to use O(2), thereby resulting in a dissociation of cellular respiration from force generation. The present study used intact isolated single myocytes with differing fatigue resistance profiles to investigate the relationship between fatigue, tension development, and aerobic metabolism. Single Xenopus skeletal muscle myofibers were allocated to a fast-fatiguing (FF) or a slow-fatiguing (SF) group, based on the contraction frequency required to elicit a fall in tension to 60% of peak. Phosphorescence quenching of a porphyrin compound was used to determine Delta intracellular Po(2) (Pi(O(2)); a proxy for Vo(2)), and developed isometric tension was monitored to allow calculation of the time-integrated tension (TxT). Although peak DeltaPi(O(2)) was not different between groups (P = 0.36), peak tension was lower (P < 0.05) in SF vs. FF (1.97 +/- 0. 17 V vs. 2. 73 +/- 0.30 V, respectively) and time to 60% of peak tension was significantly longer in SF vs. FF (242 +/- 10 s vs. 203 +/- 10 s, respectively). Before fatigue, both DeltaPi(O(2)) and TxT rose proportionally with contraction frequency in SF and FF, resulting in DeltaPi(O(2))/TxT being identical between groups. At fatigue, TxT fell dramatically in both groups, but DeltaPi(O(2)) decreased proportionately only in the FF group, resulting in an increase in DeltaPi(O(2))/TxT in the SF group relative to the prefatigue condition. These data show that more fatigue-resistant fibers maintain aerobic metabolism as they fatigue, resulting in an increased O(2) cost of contractions that could contribute to the Vo(2) slow component seen in whole body exercise.