Effects of active and passive hyperthermia on heat shock protein 70 (HSP70).
The purpose of this study was to delineate the effects of hyperthermia and physical exercise on the heat shock protein 70 (HSP70) response in circulating peripheral blood mononuclear cells (PBMCs). Six healthy, young (age: 24 +/- 3 yrs), moderately trained males (VO(2max): 48.9 +/- 2.7 ml x kg x min(-1)) undertook two experimental trials in a randomised fashion in which the core temperature (T (c)) was increased and then maintained at 39 degrees C during a 90 min bout by either active (AH) or passive (PH) means. AH involved subjects cycling at 90% of their lactate threshold in attire designed to impede heat loss mechanisms. In the PH trial, subjects were immersed up to the neck in a hot bath (40.2 +/- 0.4 degrees C), once the critical T (c) was achieved, intermittent cycling and water immersions were prescribed for the AH and PH conditions, respectively, to maintain the T (c) at 39 degrees C. HSP70 was measured intracellularly pre, post and 4 h after trials, from circulating PBMCs using an ELISA technique. T (c) reached 39 degrees C quicker in PH than during AH trials (PH: 21 +/- 4 min vs. AH: 39 +/- 6 min; P < 0.01), thereafter T (c) was maintained around 39 degrees C (PH: 39.1 +/- 0.2 degrees C; AH: 38.8 +/- 0.3 degrees C; P > 0.05). AH induced a marked leukocytosis in all sub-sets (P < 0.05). PH generated significant monocytosis and granulocytosis (P < 0.05), without changes in lymphocyte counts (P > 0.05). There were no significant increases in intracellular HSP70 at 0 h (AH: Delta - 21.1 +/- 44.8; PH: Delta + 12.5 +/- 32.4 ng/mg TP/10(3)/microl PBMCs; P > 0.05) and 4 h (AH: Delta - 30.0 +/- 40.1; PH: Delta + 36.3 +/- 70.4 ng/mg TP/10(3)/microl PBMCs; P > 0.05) post active and passive heating. Peak HSP70 expressed as a fold-change from rest was also not increased by AH (1.1 +/- 0.9; P > 0.05) or PH (3.2 +/- 4.8; P > 0.05). There were no significant differences between the AH and PH trials at any time-point, and the HSP70 response appeared to be individual specific. These results did not allow us to delineate the effects of hyperthermia and other exercise associated stressors on the heat shock response and therefore further work is warranted.
Lovell
R
R
Applied Physiology Laboratory, University of Hull, Hull, UK. r.j.lovell@hull.ac.uk
Madden
L
L
McNaughton
L R
LR
Carroll
S
S
D000328:Adult; D001642:Bicycling / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D001833:Body Temperature Regulation; D002118:Calcium / Q000097:blood; D015444:Exercise / Q000502:physiology*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D006358:Hot Temperature; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006979:Hyperthermia, Induced; D019344:Lactic Acid / Q000097:blood; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male
D001786:Blood Glucose; D018840:HSP70 Heat-Shock Proteins; D019344:Lactic Acid; D002118:Calcium