Evidence of O2 supply-dependentV˙o 2 max in the exercise-trained human quadriceps

Abstract

Maximal O 2 delivery and O 2 uptake (V˙o 2) per 100 g of active muscle mass are far greater during knee extensor (KE) than during cycle exercise: 73 and 60 ml ⋅ min−1 ⋅ 100 g−1 (2.4 kg of muscle) (R. S. Richardson, D. R. Knight, D. C. Poole, S. S. Kurdak, M. C. Hogan, B. Grassi, and P. D. Wagner. Am. J. Physiol. 268 ( Heart Circ. Physiol. 37): H1453–H1461, 1995) and 28 and 25 ml ⋅ min−1 ⋅ 100 g−1 (7.5 kg of muscle) (D. R. Knight, W. Schaffartzik, H. J. Guy, R. Predilleto, M. C. Hogan, and P. D. Wagner. J. Appl. Physiol. 75: 2586–2593, 1993), respectively. Although this is evidence of muscle O 2 supply dependence in itself, it raises the following question: With such high O 2 delivery in KE, are the quadriceps still O 2 supply dependent at maximal exercise? To answer this question, seven trained subjects performed maximum KE exercise in hypoxia [0.12 inspired O 2 fraction ([Formula: see text])], normoxia (0.21 [Formula: see text]), and hyperoxia (1.0 [Formula: see text]) in a balanced order. The protocol (after warm-up) was a square wave to a previously determined maximum work rate followed by incremental stages to ensure that a true maximum was achieved under each condition. Direct measures of arterial and venous blood O 2 concentration in combination with a thermodilution blood flow technique allowed the determination of O 2 delivery and muscleV˙o 2. Maximal O 2 delivery increased with inspired O 2: 1.3 ± 0.1, 1.6 ± 0.2, and 1.9 ± 0.2 l/min at 0.12, 0.21, and 1.0 [Formula: see text], respectively ( P < 0.05). Maximal work rate was affected by variations in inspired O 2 (−25 and +14% at 0.12 and 1.0 [Formula: see text], respectively, compared with normoxia, P < 0.05) as was maximal V˙o 2(V˙o 2 max): 1.04 ± 0.13, 1.24 ± 0.16, and 1.45 ± 0.19 l/min at 0.12, 0.21, and 1.0[Formula: see text], respectively ( P < 0.05). Calculated mean capillary [Formula: see text] also varied with[Formula: see text] (28.3 ± 1.0, 34.8 ± 2.0, and 40.7 ± 1.9 Torr at 0.12, 0.21, and 1.0 [Formula: see text], respectively, P < 0.05) and was proportionally related to changes inV˙o 2 max, supporting our previous finding that a decrease in O 2 supply will proportionately decrease muscleV˙o 2 max. As even in the isolated quadriceps (where normoxic O 2 delivery is the highest recorded in humans) an increase in O 2 supply by hyperoxia allows the achievement of a greater V˙o 2 max, we conclude that, in normoxic conditions of isolated KE exercise, KEV˙o 2 max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O 2 supply.