Reductions in systemic and skeletal muscle blood flow and oxygen delivery limit maximal aerobic capacity in humans

Background-A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity ((V) over dot O(2)max) in humans. Severe heat stress drastically reduces (V) over dot O(2)max, but the mechanisms have never been studied. Methods and Results-To determine the main contributing factor that limits (V) over dot O(2)max with and without heat stress, we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures (+10degreesC and +1degreesC). Heat stress reduced (V) over dot O(2)max, 2-legged (V) over dot O-2, and time to fatigue by 0.4+/-0.1 L/min (8%), 0.5+/-0.2 L/min (11%), and 2.2+/-0.4 minutes (28%), respectively (all P<0.05), despite heart rate and core temperature reaching similar peak values. However, before exhaustion in both heat stress and normal conditions, cardiac output, leg blood flow, mean arterial pressure, and systemic and leg O-2 delivery declined significantly (all 5% to 11%, P<0.05), yet arterial O-2 content and leg vascular conductance remained unchanged. Despite increasing leg O-2 extraction, leg (V) over dot O-2 declined 5% to 6% before exhaustion in both heat stress and normal conditions, accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis. Conclusions-These results demonstrate that in trained humans, severe heat stress reduces (V) over dot O(2)max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O-2 delivery, and O-2 uptake. Furthermore, the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O-2 delivery to locomotive muscle.