Redox state changes in human skeletal muscle after isometric contraction.

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Abstract
Subjects maintained an isometric contraction of the quadriceps femoris muscle at two‐thirds maximal voluntary contraction (m.v.c.) force for 5 s (5.0 +/‐ 0.3 s; mean +/‐ S.E. of mean; n = 6) or until fatigue (52 +/‐ 4 s; n = 13). Muscle biopsies were obtained at rest, immediately after the contractions and also at 1 and 4 min of recovery after contraction to fatigue. In all subjects 5 s isometric contraction resulted in an increase of muscle NADH (0.084 +/‐ 0.012 at rest to 0.203 +/‐ 0.041 mmol/kg dry wt.) and a decrease of phosphocreatine (PC; change in concentration = ‐17.3 +/‐ 3.8 mmol/kg dry wt.). Glucose‐6‐phosphate concentration was more than doubled whereas lactate increased in only four of the six subjects. The two subjects who did not show any increase in lactate also had the lowest increase in NADH. At fatigue NADH increased to 0.226 +/‐ 0.032 mmol/kg dry wt. which was not significantly different from the value after 5 s contraction. Muscle PC was nearly depleted and lactate increased 12‐fold above resting levels. The major part (65%) of the NADH increase at fatigue had reverted after 1 min recovery but only a slight further decrease occurred between 1 and 4 min of recovery. In relative terms the time course of the changes in muscle NADH during the first minute of recovery was similar to that of PC resynthesis, suggesting a common regulator such as O2 availability. In contrast to the delayed return of NADH concentration, PC resynthesis continued during the later part of the recovery period and PC concentration was almost fully restored after 4 min of recovery. It is concluded that muscle NADH is already maximally increased in the first seconds of muscle contraction at two‐thirds m.v.c. Indirect evidence indicates that this increase reflects a reduction of the mitochondrial NAD‐NADH redox couple. The rapid establishment of a reduced mitochondrial redox state at the start of muscle contraction will probably lead to a reduction of the redox state in the cytoplasm also and therefore be important for enhancing lactate formation.