Premium
Serum EMAP‐II in Young and Older Men During Prolonged Exercise in Temperate and Hot Conditions
Author(s) -
Cote Melissa,
Journeay W.,
McCormick James,
Notley Sean,
Kenny Glen
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.00291
Subject(s) - medicine , cytokine , inflammation , proinflammatory cytokine , immune system , immunology , physiology
Recent evidence has revealed a complex interplay between circulating inflammatory cytokines (e.g. TNF‐α, IL‐6) and susceptibility to heat illness, particularly in older adults who demonstrate dysregulation in the inflammatory response. Endothelial monocyte‐activating polypeptide II (EMAP‐II) is a pro‐inflammatory cytokine involved in a number of inflammatory and immune responses. However, the EMAP‐II response, as it relates to exercise‐heat stress is not known. This may be a particularly important cytokine mediating the inflammatory response in older adults, who are known to be at a higher risk for developing heat injury following the strain imposed by prolonged exercise heat stress. Therefore, the purpose of this study was to characterize the EMAP‐II response in young and older men during prolonged exercise in temperate and hot conditions. We evaluated the hypothesis that as observed with other key inflammatory cytokines, end‐exercise serum EMAP‐II concentrations would increase in hot compared to temperate conditions, albeit to a greater extent in young relative to older adults. To achieve this, serum EMAP‐II was measured in 12 young (21 years [SD 3]) and 12 older (59 years [SD 4]) men prior to and following prolonged exercise (180‐min or until volitional fatigue) performed at a metabolic rate of ~200 W/m2 (~3.5 METs) in temperate (21.9°C, 35% relative humidity (RH)) and hot environments (41.4°C, 35% RH) as part of a broader study. Exercise time (min) was compared between groups using a Mann‐Whitney U test. Rectal temperature, averaged over the final 5 min of exercise, and EMAP‐II (quantified via ELISA) at baseline and end‐exercise were analysed using a linear mixed model, with each participant's exercise time considered as a covariate for end‐exercise data. All participants completed 180 min in temperate conditions, although exercise time was reduced to a similar extent in hot conditions in young (median [IQR]; 175 min [108, 180]) vs. older men (180 min [139, 180]; p=0.551). End‐exercise rectal temperature did not differ significantly between groups (p=0.755) but it was higher in hot vs. temperate conditions across groups (mean [SD]; 38.9°C [0.3] vs. 37.5°C [0.3]; p<0.001). Across conditions, EMAP‐II was higher in young vs. older men at baseline (2.18 [0.49] vs. 1.57 [0.48] ng/mL; p=0.003) and end‐exercise (2.32 [0.64] vs. 1.75 [0.48] ng/mL; p=0.009). End‐exercise EMAP‐II was also higher in hot compared to temperate conditions across groups (2.19 [0.53] vs.1.89 [0.70] ng/mL; p=0.003), albeit that increase did not differ significantly between groups (p=0.096). Our findings demonstrate that prolonged exercise in hot, but not temperate conditions, increased EMAP‐II in both young and older men, albeit aging did not significantly influence the magnitude of that increase. However, given aging was associated with an overall reduction in circulating EMAP‐II concentrations, further studies are warranted to assess this response.