To further explore the limitations to maximal O2 consumption (V̇o2 max) in exercise-trained skeletal muscle, six cyclists performed graded knee-extensor exercise to maximum work rate (WRmax) in hypoxia (12% O2), hyperoxia (100% O2), and hyperoxia + femoral arterial infusion of adenosine (ADO) at 80% WRmax. Arterial and venous blood sampling and thermodilution blood flow measurements allowed the determination of muscle O2 delivery and O2 consumption. At WRmax, O2 delivery rose progressively from hypoxia (1.0 ± 0.04 l/min) to hyperoxia (1.20 ± 0.09 l/min) and hyperoxia + ADO (1.33 ± 0.05 l/min). Leg V̇o2 max varied with O2 availability (0.81 ± 0.05 and 0.97 ± 0.07 l/min in hypoxia and hyperoxia, respectively) but did not improve with ADO-mediated vasodilation (0.80 ± 0.09 l/min in hyperoxia + ADO). Although a vasodilatory reserve in the maximally working quadriceps muscle group may have been evidenced by increased leg vascular conductance after 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 nonexercising 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 V̇o2 max with significantly increased O2 delivery (hyperoxia + ADO), with a degree of uncertainty as to the site of this dilation, suggests an ADO-induced mismatch between O2 consumption and blood flow in the exercising limb.
The Determination of the Relationship Between Isokinetic Leg Strengths and Agility and Speed Performance of Elite Handball Players