Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

• Published in: Acta physiologica Scandinavica Vol. 166; no. 4; pp. 309 - 318
• Main Authors: Pedersen, P.K., Kiens, B., Saltin, B.
• Format: Journal Article
• Language: English
• Published: Oxford UK Blackwell Science Ltd 01.08.1999; Blackwell Science
• Subjects: Acid-Base Equilibrium - physiology; Adult; Biological and medical sciences; Blood Gas Analysis; blood pressure; Capillaries - metabolism; Energy Metabolism - physiology; Exercise - physiology; Female; Fundamental and applied biological sciences. Psychology; Hemodynamics - physiology; Humans; Hyperoxia - metabolism; Lactic Acid - blood; Male; Muscle Contraction - physiology; Muscle, Skeletal - blood supply; Muscle, Skeletal - metabolism; O2 delivery; O2 diffusion limitation; O2 tension; O2 uptake; Oxygen - blood; Oxygen Consumption - physiology; peripheral gas exchange; Potassium - blood; Pulmonary Gas Exchange - physiology; Regional Blood Flow - physiology; Space life sciences; Striated muscle. Tendons; vascular conductance; Vertebrates: osteoarticular system, musculoskeletal system; V˙O2max; Physical exercise; Extension; Knee; Human; Maximum oxygen consumption; Oxygen; Hyperoxia; Quadriceps muscle; Gas exchange; Striated muscle; Ergometry; Uptake
• ISSN: 0001-6772; 1365-201X
• DOI: 10.1046/j.1365-201x.1999.00575.x

We examined the influence of hyperoxia on peak oxygen uptake (V˙O2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single‐leg knee‐extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O2 (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O2 tension (PaO2) increased from 13.5 ± 0.3 (x ± SE) to 41.6 ± 0.3 kPa, O2 saturation (SaO2) from 98 ± 0.1 to 100 ± 0.1%, and O2 concentration (CaO2) from 177 ± 4 to 186 ± 4 mL L–1 (all P < 0.01). Peak exercise femoral venous PO2 (PvO2) was also higher in HiOX (3.68 ± 0.06 vs. 3.39 ± 0.7 kPa; P < 0.05), indicating a higher O2 diffusion driving pressure. HiOX femoral venous O2 saturation averaged 36.8 ± 2.0% as opposed to 33.4 ± 1.5% in NOX (P < 0.05) and O2 concentration 63 ± 6 vs. 55 ± 4 mL L–1 (P < 0.05). Peak exercise quadriceps blood flow (Q˙leg), measured by the thermo‐dilution technique, was lower in HiOX than in NOX, 6.4 ± 0.5 vs. 7.3 ± 0.9 L min–1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O2 delivery to the limb (Q˙leq times CaO2) was not significantly different in HiOX and NOX. V˙O2peak of the exercising limb averaged 890 mL min–1 in NOX and 801 mL min–1 in HiOX (n.s.) corresponding to 365 and 330 mL min–1 per kg active muscle, respectively. The V˙O2peak‐to‐PvO2 ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O2 conductance. We conclude that the similar V˙O2peak values despite higher O2 driving pressure in HiOX indicates a peripheral limitation for V˙O2peak. This may relate to saturation of the rate of O2 turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O2 conductance.