Pflugers Arch - Eur J Physiol (2004) 448: 422–430
EXERCI SE, TEMPERATURE REG U LAT I ON
Ross Tucker . Laurie Rauch . Yolande X.R. Harley . Timothy D. Noakes
Impaired exercise performance in the heat is associated with an anticipatory reduction in skeletal muscle recruitment
Received: 6 August 2003 / Accepted: 20 November 2003 / Published online: 8 May2004
# Springer-Verlag 2004
Abstract Exercise in the heat causes “central fatigue”, associated with reduced skeletal muscle recruitment during sustained isometric contractions. A similar mech- anism may cause fatigue during prolonged dynamic
Keywords Exercise . Heat . Fatigue . Brain . Electromyography . Cycling time-trial . Thermoregulation . Teleoanticipation
exercise inthe heat. The aim of this study was to
determine whether centrally regulated skeletal muscle recruitment was altered during dynamic exercise in hot (35°C) compared with cool (15°C) environments. Ten male subjects performed two self-paced, 20-km cycling time-trials, one at 35°C (HOT condition) and one at 15°C (COOL condition). Rectal temperature rose significantly in bothconditions, reaching maximum values at 20 km of
39.2±0.2°C in HOT and 38.8±0.1°C in COOL (P<0.005
HOT vs. COOL). Core temperatures at all other distances were not different between conditions. Power output and integrated electromyographic activity (iEMG) of the quadriceps muscle began to decrease early in the HOT trial, when core temperatures, heart rates and ratings of perceived exertion (RPE)were similar in both conditions. iEMG was significantly lower in HOT than in COOL at 10 and 20 km, while power output was significantly reduced in the period from 80% to 100% of the trial duration in the HOT compared with COOL condition. Thus, reduced power output and iEMG activity during self-paced exer- cise in the heat occurs before there is any abnormal increase in rectal temperature, heartrate or perception of effort. This adaptation appears to form part of an anticipatory response which adjusts muscle recruitment and power output to reduce heat production, thereby ensuring that thermal homeostasis is maintained during exercise in the heat.
R. Tucker (*) . L. Rauch . Y. X. Harley . T. D. Noakes MRC/UCT Bioenergetics of Exercise Research Unit, University of Cape Town, SportsScience Institute of South Africa,
PO Box 115, 7725 Newlands , South Africa e-mail: firstname.lastname@example.org
Exercise performance is impaired during both self-paced [16, 35] and externally regulated [5, 7, 25, 26] exercise in the heat. The biological mechanisms explaining this impairment are, however, poorly understood. Originally it wasbelieved that an increase in the oxygen-independent contribution to energy production , resulting from a reduction in skeletal muscle blood flow [6, 30] secondary to reduced stroke volume and cardiac output , explained this phenomenon.
It is now known, however, that fatigue during exercise in the heat is not caused by reductions in cardiac output or exercising muscle blood flow, or byimpaired substrate availability or utilization, or by the accumulation of lactate or K+ [8, 19, 20, 32]. Such fatigue has been observed to occur at a core temperature of approximately 40°C [7, 24], irrespective of the rate of heat storage, the pre-exercise core temperature  or the extent of prior heat acclima- tization [20, 21]. It has thus been proposed that fatigue during exercise in the heat isassociated with a “critical core temperature limiting exercise performance” , in which a high body temperature directly affects central nervous functions [19, 24].
Recently, Nybo and Nielsen  showed that force production and voluntary activation percentage in the exercised muscle groups (knee extensors) were lower during a sustained isometric maximal voluntary contrac- tion (MVC)...
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