Effects of acute or chronic heat exposure, exercise and dehydration on plasma cortisol, IL-6 and CRP levels in trained males

Authors: Costello, J.T., Rendell, R., Furber, M., Massey, H.C., Tipton, M.J., Young, J.S. and Corbett, J.

http://eprints.bournemouth.ac.uk/30230/

Journal: Cytokine

Publisher: Academic Press

ISSN: 1043-4666

This data was imported from PubMed:

Authors: Costello, J.T., Rendell, R.A., Furber, M., Massey, H.C., Tipton, M.J., Young, J.S. and Corbett, J.

http://eprints.bournemouth.ac.uk/30230/

Journal: Cytokine

Volume: 110

Pages: 277-283

eISSN: 1096-0023

DOI: 10.1016/j.cyto.2018.01.018

This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males [mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg-1 min-1] undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2-5 and 7-10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL-1 [0.9], post-exercise: 1.8 pg mL-1 [1.0], P = .032) and when euhydrated (pre-exercise: 1.0 pg mL-1 [1.4], post-exercise: 1.6 pg mL-1 [2.1], P = .048). Plasma cortisol levels were also elevated but only during permissive dehydration (P = .032). Body mass loss was strongly correlated with Δcortisol (r = -0.688, P = .003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.

This data was imported from Scopus:

Authors: Costello, J.T., Rendell, R.A., Furber, M., Massey, H.C., Tipton, M.J., Young, J.S. and Corbett, J.

http://eprints.bournemouth.ac.uk/30230/

Journal: Cytokine

Volume: 110

Pages: 277-283

eISSN: 1096-0023

ISSN: 1043-4666

DOI: 10.1016/j.cyto.2018.01.018

© 2018 Elsevier Ltd This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males [mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg−1 min−1] undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2–5 and 7–10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL−1 [0.9], post-exercise: 1.8 pg mL−1 [1.0], P =.032) and when euhydrated (pre-exercise: 1.0 pg mL−1 [1.4], post-exercise: 1.6 pg mL−1 [2.1], P =.048). Plasma cortisol levels were also elevated but only during permissive dehydration (P =.032). Body mass loss was strongly correlated with Δcortisol (r = −0.688, P =.003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.

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