Physical activity of moderate intensity and duration leads to healthy biological adaptationsin humans. However, very intense and prolonged exercise may induce disruption in redox balance, potentially increasing oxidative stress. In addition, exposure to environmental heat stress and associated hyperthermia further increases oxidative stress and mayinduce the expression of heat shock proteins. However, antioxidant supplementation isbelieved to minimise the effect of oxidative stress and may therefore help reduce or limitthe heat shock response to exercise heat stress.The first study (Chapter 4) examined whether exertional heat illness (EHI) casualtiesamong military recruits may exhibit greater disturbances in redox balance followingexercise compared to non-EHI controls. Nine (n=9) recruits were identified as havingsuspected EHI during the Loaded March (LM) on day 1, with a peak mean (SD) body coretemperature of 40.1 (0.5) °C. Fifteen (n=15) recruits were identified as having suspectedEHI during the Log Race (LR) on day 2, with a peak mean (SD) body core temperature of39.7 (0.5) °C. A further twenty-one (n=21) recruits, which successfully finished both LMand LR events, were treated as controls (CON). Interestingly, the plasma antioxidantconcentration was significantly elevated from pre to post-exercise (p<0.001) for EHI andCON groups, during both LM and LR events, with no changes on lipid peroxide proteincarbonyl concentrations. These data suggest there is no increase in lipid peroxide orprotein carbonyl level damage in response to intense hyperthermic military exercise,regardless of acute heat illness. It is possible that military training augments the body’sdefence capabilities, thus reducing oxidative stress and damage induced by free radicalproduction.To date there is a scarcity of data examining the effects of acute intake of antioxidantsupplements on oxidative stress and heat shock response during continuous exercise in ahot environment. Hence, the aims of the second study (Chapter 5) were to examine theeffects of acute ingestion of Quercetin (Q), Quercetin + vitamin C (QC) or placebo (P) 14hours before, 2 hours before and every 20 minutes during trials on oxidative stress andheat shock response. In this randomised, crossover study 10 recreationally active males(age 21±2 y, V̇ O2max 54.9±8.4 ml.kg.min-1) completed three running trials at 70% V̇ O2maxfor 60 minutes in the heat (33.0±0.3°C; 28.5±1.8% relative humidity). Exercise heat stresssignificantly elevated plasma quercetin (p=0.02), antioxidant power (FRAP) (p<0.001),plasma heat shock protein 70 (HSP70) (p=0.009) and plasma heat shock protein 90α(HSP90α) (p<0.001) over time, but no differences were detected between trials. Also, nochanges were observed in protein carbonyl concentration. Acute intake of quercetinsignificantly increased the level of plasma quercetin however, this did not affect the plasmaantioxidant capacity or heat shock response to exercise heat stress. The increases in plasma HSP70 and HSP90α concentrations might act as supplementary antioxidants,reducing the oxidative damage reflected in the absence of changes in protein carbonyl.Exercise heat stress is effective in inducing both intracellular HSP70 (muscle andperipheral blood mononuclear cell (PBMC)) and extracellular HSP70 (plasma)concentrations. Thus, the third study (Chapter 6) tested the hypothesis that this acutequercetin supplementation would induce similar trends in plasma HSP70 and intracellularHSP70 concentrations 2 days following exercise heat stress. In this randomised, crossoverstudy, 9 recreationally active males (age 22±2y, V̇ O2max 50.3±3.3ml.kg.min-1) completedthree running trials at 70% V̇ O2max for 60 minutes in the heat (32.9±0.3°C; 28.3±1.2%relative humidity). This study demonstrated that there is no positive relationship betweenboth intracellular of HSP70 (muscle and PBMC) and plasma HSP70 (eHSP70) 2 days following exercise heat stress. These data suggest that the release of eHSP70 couldoriginate from others tissue or cells. Additionally, the absence of differences between trialsin the expression of muscle HSP70, PBMC HSP70 and plasma HSP70 might indicate it is implausible that quercetin might inhibits the expression of HSP70 in plasma, muscle and PBMC 2 days following the exercise heat stress stimulus.Overall, the results from this thesis emphasise that the hyperthermia experienced in response to exercise and environmental heat stress could potentially influence the human redox response and heat shock response. Besides, there is reasonable evidence thatacute quercetin co-ingestion with vitamin C has the potential to improve the bioavailabilityand bioactive effects of quercetin, however, the effects of quercetin supplementation in reducing oxidative stress in response to exercise heat stress remains to be elucidated. In addition, the anti-oxidative ability of acute ingestion of quercetin to suppress the intracellular and extracellular heat shock response remains uncertain and worthy for further investigation.
|Date of Award||25 Jul 2018|
|Sponsors||Ministry of Higher Education|
|Supervisor||James Bilzon (Supervisor), James Turner (Supervisor) & James Betts (Supervisor)|
- antioxidant supplements, quercetin, oxidative stress, heat shock response, heat, hyperthermia, exercise.