Published Online
on January 27, 2003

A more recent version of this article appeared on February 18, 2003

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Submitted on July 18, 2002
Revised on October 24, 2002
Accepted on October 24, 2002

Reductions in Systemic and Skeletal Muscle Blood Flow and Oxygen Delivery Limit Maximal Aerobic Capacity in Humans

José González-Alonso PhD^* and José A.L. Calbet MD, PhD

From The Copenhagen Muscle Research Centre (J.G.-A.), Rigshospitalet, University of Copenhagen, Denmark, and the Department of Physical Education (J.A.L.C.), University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain.

^* To whom correspondence should be addressed. E-mail: jga{at}cmrc.dk.

Background--A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity (VO₂max) in humans. Severe heat stress drastically reduces VO₂max, but the mechanisms have never been studied.

Methods and Results--To determine the main contributing factor that limits VO₂max 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 (+10°C and +1°C). Heat stress reduced VO₂max, 2-legged VO₂, 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 O₂ delivery declined significantly (all 5% to 11%, P<0.05), yet arterial O₂ content and leg vascular conductance remained unchanged. Despite increasing leg O₂ extraction, leg VO₂ 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 VO₂max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O₂ delivery, and O₂ 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 O₂ delivery to locomotive muscle.

Key words: hemodynamics • blood flow, regional • cardiac output • hemodynamics • heat stress

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