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

Abstract

Maximal O2 delivery and O2 uptake (VO2) 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 O2 supply dependence in itself, it raises the following question: With such high O2 delivery in KE, are the quadriceps still O2 supply dependent at maximal exercise? To answer this question, seven trained subjects performed maximum KE exercise in hypoxia [0.12 inspired O2 fraction (FIO2)], normoxia (0.21 FIO2), and hyperoxia (1.0 FIO2) 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 O2 concentration in combination with a thermodilution blood flow technique allowed the determination of O2 delivery and muscle VO2. Maximal O2 delivery increased with inspired O2: 1.3 +/- 0.1, 1.6 +/- 0.2, and 1.9 +/- 0.2 l/min at 0.12, 0.21, and 1.0 FIO2, respectively (P < 0.05). Maximal work rate was affected by variations in inspired O2 (-25 and +14% at 0.12 and 1.0 FIO2, respectively, compared with normoxia, P < 0.05) as was maximal VO2 (VO2 max): 1.04 +/- 0.13, 1. 24 +/- 0.16, and 1.45 +/- 0.19 l/min at 0.12, 0.21, and 1.0 FIO2, respectively (P < 0.05). Calculated mean capillary PO2 also varied with FIO2 (28.3 +/- 1.0, 34.8 +/- 2.0, and 40.7 +/- 1.9 Torr at 0.12, 0.21, and 1.0 FIO2, respectively, P < 0.05) and was proportionally related to changes in VO2 max, supporting our previous finding that a decrease in O2 supply will proportionately decrease muscle VO2 max. As even in the isolated quadriceps (where normoxic O2 delivery is the highest recorded in humans) an increase in O2 supply by hyperoxia allows the achievement of a greater VO2 max, we conclude that, in normoxic conditions of isolated KE exercise, KE VO2 max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O2 supply.

Is the balance between skeletal muscular metabolic capacity and oxygen supply capacity the same in endurance trained and untrained subjects?

“…Previous studies have found the 1-KE mass-specific O 2 uptake, measured by invasive methods, to range from 350 to 602 ml·kg -1 ·min -1 (Andersen & Saltin, 1985i;Rowell et al, 1986;Richardson et al, 1993a;Radegran et al, 1999a;Richardson et al, 1999a;Mourtzakis et al, 2004). The mass specific O 2 uptake found in the present study of 386 and 570 ml·kg -1 ·min -1 for controls and ET, closely agree with this range.…”

“…The highest mass-specific bloodflow and VO 2 in humans is probably achieved during 1-KE (Andersen et al, 1985a;Richardson et al, 1995b). Due to overperfusion, and therefore a short capillary mean transit time of the blood cells, the muscles would probably not reach higher mass-specific VO 2 without increasing the arterial PO 2 (Richardson et al, 1995a;Richardson et al, 1999b;Richardson et al, 1993c). 1-KE exercise is therefore a widely accepted method of quantifying the muscular metabolic capacity in vivo in healthy subjects.…”

“…This again may be caused by the fact that the adaptive range is larger in the skeletal muscles than in the heart. During one-legged knee-extension when only about 2 kg of muscle is working, neither trained nor untrained individuals are O 2 -supply limited since end capillary PO 2 is high compared with whole body exercise (Andersen & Saltin, 1985g;Richardson et al, 1993d;Magnusson et al, 1997;Richardson et al, 1999c). During bicycling, O 2 supply may be limiting because end capillary PO 2 is low and training tends to reduce it (Saltin, 1977).…”

Skeletal muscle oxidative metabolism in sedentary humans: 31P-MRS assessment of O2 supply and demand limitations

“…There is prior evidence in subjects performing small-muscle-mass submaximal exercise that suggests the effect of varying FI O 2 on O 2 delivery is dampened by an alteration in muscle blood flow (28). Specifically, it has been shown that across a range of submaximal work intensities muscle blood flow is elevated to compensate for the reduced arterial O 2 content in hypoxia and decreased in hyperoxia, thus either partially or totally compensating, in terms of O 2 delivery, for changes in arterial O 2 content (20,24 In our laboratory's previous study (7), the increase in the PCr recovery rate constant in hyperoxia and decrease in hypoxia for the physically active group is also suggestive of this scenario because the most significant effect of hyperoxia is to raise blood PO 2 because hemoglobin saturation is already close to its ceiling in normoxia (and muscle blood flow tends to fall in hyperoxia). Hence, it is suggested that in hyperoxia the driving gradient from blood to muscle was enhanced, resulting in an elevated intracellular PO 2 , facilitating increased oxidative metabolism, and ultimately increased PCr recovery rate constants.…”

Dietary nitrate supplementation enhances high-intensity running performance in moderate normobaric hypoxia, independent of aerobic fitness

“…Conversely, the Larginine NOS pathway becomes dysfunctional with low O2 tensions and pH [33]. Such cellular conditions are likely to be especially prevalent during exercise in a hypoxic environment [8,34], such as experienced on ascent to terrestrial altitude. This suggests that nitrate supplementation may be more likely to enhance NO generation and therefore improve performance in hypoxia relative to normoxia.…”