Effect of altered arterial O2 tensions on muscle metabolism in dog skeletal muscle during fatiguing work.

These experiments were conducted to determine whether changes in arterial O2 tension are related to changes in muscle metabolism during fatiguing contractions. Arterial and venous circulation to the gastrocnemius muscle (n = 8) was isolated, and the Achilles tendon was attached to a force transducer. Each muscle was electrically stimulated through the sciatic nerve for three 2-min periods of fatiguing contractions separated by 8 min of rest. The arterial O2 tensions were altered for each work period (mean PO2 = 44, 72, 391 Torr). Arterial and venous samples were drawn to measure lactate, O2 and CO2 concentrations (Van Slyke analysis), and [H+]. Muscle biopsies were taken to measure muscle [H+] (homogenate method) and lactate. Fatigue was evaluated as the decline in tension from peak initial tension. At the end of the contraction periods, values were significantly different (P less than 0.05) between the low arterial O2 tension and the high for flow [84 +/- 6 (mean +/- SE) vs. 70 +/- 8 ml X 100 g-1 X min-1], muscle lactate contraction (44 +/- 10 vs. 26 +/- 4 mmol/kg dry wt), and lactate release (122 +/- 12 vs. 57 +/- 14 mumol X 100 g-1 X min-1). O2 uptake and the rate of fatigue were not different among treatments during contractions. Muscle [H+] increased (work [H+] minus rest [H+]) to a significantly greater extent during low arterial O2 tensions compared with high (P less than 0.05). We conclude that alterations in arterial O2 tension during fatiguing contractions induce changes in blood and muscle acid-base status and in muscle metabolism that are independent of O2 uptake.