Effect of decreased oxygen availability on NADH and lactate contents in human skeletal muscle during exercise

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Abstract
Eight men cycled for 5 min at 120±6 W (x± SE) at which O2 uptake was 50% of its maximal normoxic value, breathing room air (21 % O2; normoxia) on one occasion and 11 % O2 in N2 (respiratory hypoxia/hypoxic — Resp. Hx.) on the other. Biopsies were taken from the quadriceps femoris muscle. Oxygen uptake during exercise was not significantly different between Resp. Hx (1.59±0.08 l min‐1) and normoxia (1.55±0.08 l min‐1). At rest, muscle lactate was the same under both conditions but was four times higher after Resp. Hx (33.2±5.2 mmol kg‐1 dry wt) than normoxic cycling (8.6±1.0 mmol kg‐1 dry wt; P < 0.01). The muscle lactate/pyruvate (which is proportional to cytosolic NADH/NAD) was significantly higher after Resp. Hx. (76±19) than after normoxic cycling (26±2; P < 0.05). At rest, analytically determined NADH averaged 0.14±0.02 mmol kg‐1 dry wt under both conditions. However, exercise during Resp. Hx. resulted in a significantly higher NADH content (0.17±0.01) than exercise during normoxia (0.12±0.01; P < 0.01). Indirect evidence indicates that the difference in muscle NADH reflects a difference in the mitochondrial redox state (Sahlin & Katz 1986). The increased muscle NADH during Resp. Hx. therefore indicates a relative lack of O2 at the cellular level (muscle hypoxia). It is suggested that the increased lactate production during Resp. Hx. is a consequence of the cellular adaptation to muscle hypoxia (i.e. increases in cytosolic ADP, AMP, Pi and NADH).

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