Heat shock does not attenuate low-frequency fatigue.
Whole-body hyperthermia or heat shock confers protection to myocardial contractility against reperfusion-induced injury. The purpose of this study was to determine whether heat shock could provide similar protection to skeletal muscle contractility against low-frequency fatigue. Male Sprague-Dawley rats (6 rats/group) were heat shocked at 41.5 degrees C for 15 min either 24 h or 4 days prior to fatiguing stimulation to compare the contractile responses of the plantaris muscle with those of a nonheated group. Both 24 h and 4 days after heat shock, the 72-kDa heat shock protein (HSP72) was elevated above control levels. There were no differences between the heat-shocked and non-heat-shocked animals in measures of contractility prior to fatiguing contractions or in resistance to fatigue. Heat-shock preconditioning did not lead to improved postfatigue force recovery above control responses and, in fact, delayed the recovery of force. This study does not support the use of heat-shock therapy to improve skeletal muscle contractile performance under fatiguing conditions.
Thomas
J A
JA
School of Kinesiology, The University of Western Ontario, London, Canada.
Noble
E G
EG
D000818:Animals; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000032:analysis / Q000502:physiology; D006358:Hot Temperature; D008297:Male; D009119:Muscle Contraction; D018763:Muscle Fatigue; D051381:Rats; D017207:Rats, Sprague-Dawley
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins