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Limitations to vasodilatory capacity and O_{2 max} in trained human skeletal muscle

¹Department of Medicine, University of California San Diego, La Jolla, California; and ²School of Applied Science, University of Glamorgan, Glamorgan, South Wales, United Kingdom

Submitted 20 December 2006 ; accepted in final form 24 January 2007

To further explore the limitations to maximal O₂ consumption (O_{2 max}) in exercise-trained skeletal muscle, six cyclists performed graded knee-extensor exercise to maximum work rate (WR_max) in hypoxia (12% O₂), hyperoxia (100% O₂), and hyperoxia + femoral arterial infusion of adenosine (ADO) at 80% WR_max. Arterial and venous blood sampling and thermodilution blood flow measurements allowed the determination of muscle O₂ delivery and O₂ consumption. At WR_max, 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 O_{2 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 O_{2 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.

exercise; blood flow; vasodilatory reserve

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