Evidence of O-2 supply-dependent (V)over-dotO(2max) in the exercise-trained human quadriceps

Maximal O-2 delivery and O-2 uptake (VO2) per 100 g of active muscle mass a re far greater during knee extensor (KE) than during cycle exercise: 73 and 60 mi 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 s upply dependence in itself, it raises the following question: With such hig h O-2 delivery in KE, are the quadriceps still O-2 supply dependent at maxi mal exercise? To answer this question, seven trained subjects performed max imum KE exercise in hypoxia [0.12 inspired O-2 fraction (FIO2)], normoxia ( 0.21 FIO2), and hyperoxia (1.0 FIO2) in a balanced order. The protocol(afte r warmup) was a square wave to a previously determined maximum work rate fo llowed by incremental stages to ensure that a true maximum was achieved und er each condition. Direct measures of arterial and venous blood O-2 concent ration in combination with a thermodilution blood flow technique allowed th e determination of O-2 delivery and muscle Vet. Maximal O-2 delivery increa sed with inspired O-2: 1.3 +/- 0.1, 1.6 +/- 0.2, and 1.9 +/- 0.2 1/min at 0 .12, 0.21, and 1.0 FIO2,, respectively (P < 0.05). Maximal work rate was af fected by variations in inspired O-2 (-25 and + 14% at 0.12 and 1.0 FIO2, r espectively, compared with normoxia, P < 0.05) as was maximal VO2 (VO2max): 1.04 +/- 0.13, 1.24 +/- 0.16, and 1.45 +/- 0.19 1/min at 0.12, 0.21, and 1 .0 FIO2, respectively (P < 0.05). Calculated mean capillary Po, also varied with FIO2 (28.3 +/- 1.0, 34.8 +/- 2.0, and 40.7 +/-: 1.9 Torr at 0.12, 0.2 1, ana 1.0 FIO2, respectively,P < 0.05) and was proportionally related tb c hanges in VO2max, supporting our previous finding that a decrease in O-2 su pply will proportionately decrease muscle VO2max. AS even in the isolated q uadriceps (where normoxic O-2 delivery is the highest recorded in humans) a n increase in O-2 supply by hyperoxia allows the achievement of a greater V O2max, we conclude that, in normoxic conditions of isolated KE exercise, KE VO2max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O-2 supply.