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1 Medicine, University of California San Diego, La Jolla, California, United States
2 School of Applied Sciences, Hypoxia Research Unit, Mid-Glamorgan, United Kingdom
* To whom correspondence should be addressed. E-mail: rrichardson{at}ucsd.edu.
To further explore the limitations to maximal oxygen consumption (VO2max) in exercise-trained skeletal muscle, six cyclists performed graded knee-extensor exercise (KE) to maximum work rate (WRmax) in hypoxia (12 % O2), hyperoxia (100% O2), and hyperoxia with a femoral arterial infusion of adenosine at 80% WRmax (Hyper + ADO). Arterial and venous blood sampling and thermodilution blood flow measurements allowed the determination of muscle O2 delivery and VO2. At WRmax, O2 delivery rose progressively from hypoxia (1.0 ± 0.04 l/min) to hyperoxia (1.20 ± 0.09 l/min) and hyper + ADO (1.33 ± 0.05 l/min). Leg VO2max) varied with O2 availability (hypoxia = 0.81 ± 0.05 l/min; hyperoxia = 0.97 ± 0.07 l/min), but did not improve with adenosine-mediated vasodilation (hyper + ADO = 0.80 ± 0.09 l/min). Although a vasodilatory reserve in the maximally working quadriceps muscle group may have been evidenced by increased leg vascular conductance following ADO infusion beyond that observed in hyperoxia (increased blood flow, but no change in blood pressure), we recognize the possibility that the ADO infusion may have provoked vasodilation in non-exercising tissue of this limb. Together, these findings imply that maximally exercising skeletal muscle may maintain some vasodilatory capacity, but the lack of improvement in leg VO2max with significantly increased O2delivery (hyper + ADO), with a degree of uncertainty as to the site of this dilation suggests an adenosine-induced mismatch between VO2max and blood flow in the exercising limb.
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