4.3 Article

Effects of ATP-induced leg vasodilation on Vo2 peak and leg O2 extraction during maximal exercise in humans

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00746.2005

Keywords

muscle sympathetic nerve activity; fatigue; performance

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During maximal whole body exercise Vo(2) peak is limited by O-2 delivery. In turn, it is though that blood flow at near-maximal exercise must be restrained by the sympathetic nervous system to maintain mean arterial pressure. To determine whether enhancing vasodilation across the leg results in higher O-2 delivery and leg Vo(2) during near-maximal and maximal exercise in humans, seven men performed two maximal incremental exercise tests on the cycle ergometer. In random order, one test was performed with and one without (control exercise) infusion of ATP (8 mg in 1 ml of isotonic saline solution) into the right femoral artery at a rate of 80 mu g center dot kg body mass(-1) center dot min(-1). During near-maximal exercise (92% of Vo(2) peak), the infusion of ATP increased leg vascular conductance (+ 43%, P < 0.05), leg blood flow (+ 20%, 1.7 l/min, P < 0.05), and leg O-2 delivery (+ 20%, 0.3 l/min, P < 0.05). No effects were observed on leg or systemic Vo(2). Leg O-2 fractional extraction was decreased from 85 +/- 3 (control) to 78 +/- 4% (ATP) in the infused leg (P < 0.05), while it remained unchanged in the left leg (84 +/- 2 and 83 +/- 2%; control and ATP; n = 3). ATP infusion at maximal exercise increased leg vascular conductance by 17% (P < 0.05), while leg blood flow tended to be elevated by 0.8 l/min (P < 0.08). However, neither systemic nor leg peak Vo(2) values where enhanced due to a reduction of O-2 extraction from 84 +/- 4 to 76 +/- 4%, in the control and ATP conditions, respectively (P < 0.05). In summary, the Vo(2) of the skeletal muscles of the lower extremities is not enhanced by limb vasodilation at near-maximal or maximal exercise in humans. The fact that ATP infusion resulted in a reduction of O-2 extraction across the exercising leg suggests a vasodilating effect of ATP on less-active muscle fibers and other noncontracting tissues and that under normal conditions these regions are under high vasoconstrictor influence to ensure the most efficient flow distribution of the available cardiac output to the most active muscle fibers of the exercising limb.

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