Document Detail

Heat and exercise acclimation increases intracellular levels of Hsp72 and inhibits exercise-induced increase in intracellular and plasma Hsp72 in humans.
MedLine Citation:
PMID:  20414820     Owner:  NLM     Status:  MEDLINE    
In order to verify the effects of heat and exercise acclimation (HA) on resting and exercise-induced expression of plasma and leukocyte heat shock protein 72 (Hsp72) in humans, nine healthy young male volunteers (25.0 ± 0.7 years; 80.5 ± 2.0 kg; 180 ± 2 cm, mean ± SE) exercised for 60 min in a hot, dry environment (40 ± 0°C and 45 ± 0% relative humidity) for 11 days. The protocol consisted of running on a treadmill using a controlled hyperthermia technique in which the work rate was adjusted to elevate the rectal temperature by 1°C in 30 min and maintain it elevated for another 30 min. Before and after the HA, the volunteers performed a heat stress test (HST) at 50% of their individual maximal power output for 90 min in the same environment. Blood was drawn before (REST), immediately after (POST) and 1 h after (1 h POST) HST, and plasma and leukocytes were separated and stored. Subjects showed expected adaptations to HA: reduced exercise rectal and mean skin temperatures and heart rate, and augmented sweat rate and exercise tolerance. In HST1, plasma Hsp72 increased from REST to POST and then returned to resting values 1 h POST (REST: 1.11 ± 0.07, POST: 1.48 ± 0.10, 1 h POST: 1.22 ± 0.11 ng mL(-1); p < 0.05). In HST2, there was no change in plasma Hsp72 (REST: 0.94 ± 0.08, POST: 1.20 ± 0.15, 1 h POST: 1.17 ± 0.16 ng mL(-1); p > 0.05). HA increased resting levels of intracellular Hsp72 (HST1: 1 ± 0.02 and HST2: 4.2 ± 1.2 density units, p < 0.05). Exercise-induced increased intracellular Hsp72 expression was observed on HST1 (HST1: REST, 1 ± 0.02 vs. POST, 2.9 ± 0.9 density units, mean ± SE, p < 0.05) but was inhibited on HST2 (HST2: REST, 4.2 ± 1.2 vs. POST, 4.4 ± 1.1 density units, p > 0.05). Regression analysis showed that the lower the pre-exercise expression of intracellular Hsp72, the higher the exercise-induced increase (R = -0.85, p < 0.05). In conclusion, HA increased resting leukocyte Hsp72 levels and inhibited exercise-induced expression. This intracellular adaptation probably induces thermotolerance. In addition, the non-increase in plasma Hsp72 after HA may be related to lower stress at the cellular level in the acclimated individuals.
Flávio de Castro Magalhães; Fabiano Trigueiro Amorim; Renata L Freitas Passos; Michele Atalla Fonseca; Kenya Paula Moreira Oliveira; Milene Rodrigues Malheiros Lima; Juliana Bohen Guimarães; João Batista Ferreira-Júnior; Angelo R P Martini; Nilo R V Lima; Danusa Dias Soares; Edilamar Menezes Oliveira; Luiz Oswaldo Carneiro Rodrigues
Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-23
Journal Detail:
Title:  Cell stress & chaperones     Volume:  15     ISSN:  1466-1268     ISO Abbreviation:  Cell Stress Chaperones     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-14     Completed Date:  2011-02-04     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  9610925     Medline TA:  Cell Stress Chaperones     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  885-95     Citation Subset:  IM    
Laboratory of Biochemistry of Physical Activity, University of São Paulo, São Paulo, Brazil.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Body Temperature
HSP72 Heat-Shock Proteins / blood*,  metabolism
Heart Rate
Hot Temperature*
Leukocytes / immunology,  metabolism
Regression Analysis
Sweating / physiology
Reg. No./Substance:
0/HSP72 Heat-Shock Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Natural products and their role in cancer therapy.
Next Document:  The Canadian STOP-PAIN project - Part 2: What is the cost of pain for patients on waitlists of multi...