title: Hemodynamics and O2 uptake during maximal knee extensor exercise in untrained and trained human quadriceps muscle: effects of hyperoxia.
abstract: To elucidate the potential limitations on maximal human quadriceps O2 capacity, six subjects trained (T) one quadriceps on the single-legged knee extensor ergometer (1 h/day at 70% maximum workload for 5 days/wk), while their contralateral quadriceps remained untrained (UT). Following 5 wk of training, subjects underwent incremental knee extensor tests under normoxic (inspired O2 fraction = 21%) and hyperoxic (inspired O2 fraction = 60%) conditions with the T and UT quadriceps. Training increased quadriceps muscle mass (2.9 +/- 0.2 to 3.1 +/- 0.2 kg), but did not change fiber-type composition or capillary density. The T quadriceps performed at a greater peak power output than UT, under both normoxia (101 +/- 10 vs. 80 +/- 7 W; P < 0.05) and hyperoxia (97 +/- 11 vs. 81 +/- 7 W; P < 0.05) without further increases with hyperoxia. Similarly, thigh peak O2 consumption, blood flow, vascular conductance, and O2 delivery were greater in the T vs. the UT thigh (1.4 +/- 0.2 vs. 1.1 +/- 0.1 l/min, 8.4 +/- 0.8 vs. 7.2 +/- 0.8 l/min, 42 +/- 6 vs. 35 +/- 4 ml x min(-1) x mmHg(-1), 1.71 +/- 0.18 vs. 1.51 +/- 0.15 l/min, respectively) but were not enhanced with hyperoxia. Oxygen extraction was elevated in the T vs. the UT thigh, whereas arteriovenous O2 difference tended to be higher (78 +/- 2 vs. 72 +/- 4%, P < 0.05; 160 +/- 8 vs. 154 +/- 11 ml/l, respectively; P = 0.098) but again were unaltered with hyperoxia. In conclusion, the present results demonstrate that the increase in quadriceps muscle O2 uptake with training is largely associated with increases in blood flow and O2 delivery, with smaller contribution from increases in O2 extraction. Furthermore, the elevation in peak muscle blood flow and vascular conductance with endurance training seems to be related to an enhanced vasodilatory capacity of the vasculature perfusing the quadriceps muscle that is unaltered by moderate hyperoxia.
authors.affiliation: Human Biology and Nutritional Sciences, University of Guelph, Ontario, Canada N1G 2W1. marinamo@cancerboard.ab.ca.
authors.forename: M
authors.initials: M
authors.lastname: Mourtzakis
authors.forename: J
authors.initials: J
authors.lastname: González-Alonso
authors.forename: T E
authors.initials: TE
authors.lastname: Graham
authors.forename: B
authors.initials: B
authors.lastname: Saltin
mesh_terms: D000328:Adult; D002196:Capillaries / Q000473:pathology; D002319:Cardiovascular System / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood; D015444:Exercise; D006439:Hemodynamics; D006801:Humans; D018496:Hyperoxia / Q000503:physiopathology*; D007717:Knee; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010101:Oxygen Consumption; D010806:Physical Education and Training; D010807:Physical Endurance; D013848:Thigh
chemical_list: D002395:Catecholamines; D019344:Lactic Acid