Downhill running and exercise in hot environments increase leukocyte Hsp72 (HSPA1A) and Hsp90α (HSPC1) gene transcripts.
Stressors within humans and other species activate Hsp72 and Hsp90α mRNA transcription, although it is unclear which environmental temperature or treadmill gradient induces the largest increase. To determine the optimal stressor for priming the Hsp system, physically active but not heat-acclimated participants (19.8 ± 1.9 and 20.9 ± 3.6 yr) exercised at lactate threshold in either temperate (20°C, 50% relative humidity; RH) or hot (30°C, 50% RH) environmental conditions. Within each condition, participants completed a flat running (temperate flat or hot flat) and a downhill running (temperate downhill or hot downhill) experimental trial in a randomized counterbalanced order separated by at least 7 days. Venous blood samples were taken immediately before (basal), immediately after exercise, and 3 and 24 h postexercise. RNA was extracted from leukocytes and RT-quantitative PCR conducted to determine Hsp72 and Hsp90α mRNA relative expression. Leukocyte Hsp72 mRNA was increased immediately after exercise following downhill running (1.9 ± 0.9-fold) compared with flat running (1.3 ± 0.4-fold; P = 0.001) and in hot (1.9 ± 0.6-fold) compared with temperate conditions (1.1 ± 0.5-fold; P = 0.003). Leukocyte Hsp90α mRNA increased immediately after exercise following downhill running (1.4 ± 0.8-fold) compared with flat running (0.9 ± 0.6-fold; P = 0.002) and in hot (1.6 ± 1.0-fold) compared with temperate conditions (0.9 ± 0.6-fold; P = 0.003). Downhill running and exercise in hot conditions induced the largest stimuli for leukocyte Hsp72 and Hsp90α mRNA increases.
Muscle Cellular and Molecular Physiology Research Group, Institute of Sport and Physical Activity Research, Department of Sport Science and Physical Activity, University of Bedfordshire, Bedford, United Kingdom; james.tuttle1987@gmail.com.
James A
JA
Tuttle
Muscle Cellular and Molecular Physiology Research Group, Institute of Sport and Physical Activity Research, Department of Sport Science and Physical Activity, University of Bedfordshire, Bedford, United Kingdom;
Paul C
PC
Castle
Muscle Cellular and Molecular Physiology Research Group, Institute of Sport and Physical Activity Research, Department of Sport Science and Physical Activity, University of Bedfordshire, Bedford, United Kingdom; School of Exercise and Health Sciences, Edith Cowan University, Perth, Australia.
Alan J
AJ
Metcalfe
Department of Sport and Physical Activity, Edgehill University, Ormskirk, United Kingdom; and.
Adrian W
AW
Midgley
Muscle Cellular and Molecular Physiology Research Group, Institute of Sport and Physical Activity Research, Department of Sport Science and Physical Activity, University of Bedfordshire, Bedford, United Kingdom;
Lee
L
Taylor
National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, United Kingdom;
Mark P
MP
Lewis
D000222:Adaptation, Physiological; D000293:Adolescent; D000328:Adult; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D018841:HSP90 Heat-Shock Proteins / Q000378:metabolism*; D064368:Healthy Volunteers; D006358:Hot Temperature; D006801:Humans; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D063806:Myalgia; D011897:Random Allocation; D012420:Running / Q000502:physiology*; D055815:Young Adult
D018840:HSP70 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; C533585:HSP90AA2P protein, human; C490786:HSPA1A protein, human
exercise heat stress; heat shock response; thermotolerance