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(Circulation. 2003;107:824.)
© 2003 American Heart Association, Inc.

Clinical Investigation and Reports

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

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.

Correspondence to José González-Alonso, PhD, The Copenhagen Muscle Research Centre, Rigshospitalet, Section 7652, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark. 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 (O₂max) in humans. Severe heat stress drastically reduces O₂max, but the mechanisms have never been studied.

Methods and Results— To determine the main contributing factor that limits O₂max 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 O₂max, 2-legged O₂, 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 O₂ 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 O₂max 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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