Back to results

University of Hull

The effects of hydration status on markers of oxidative and cellular stress during prolonged exercise in hyperthermic environments

Abstract

dc:description.abstract

The relationships between hyperthermia, dehydration and oxidative stress have been thoroughly studied  separately within the literature both in vitro and in vivo. However, no in vivo attempts have been made to  manipulate the hydration status of individuals to investigate the resulting changes in oxidative and cellular stress during and after exercise in hyperthermic conditions and what effect these changes may have on  exercise performance.The purpose of the first experiment was to investigate the effects of exercise-induced dehydration with and without hyperthermia on oxidative stress. Seven healthy male trained cyclists (mean ± SD) age: 36 ± 6 yrs, height: 177.4 ± 6.5 cm, weight: 72.8 ± 7.0 kg, and power output (PO) at lactate threshold (LT): 199.3 ± 19.0 Watts (W) completed 90 min cycling exercise at 95% LT followed by a 5 km time trial (TT) in four conditions: 1) euhydration in a warm environment (EU-W, control), 2) dehydration in a warm environment (DE-W), 3) euhydration in a thermoneutral environment (EU-T), and 4) dehydration in a thermoneutral environment (DE-T) (W: 33.9 ± 0.9°C; T: 23.0 ± 1.0°C). Whole blood oxidised glutathione (GSSG) increased significantly post exercise in dehydration trials only (DE-W: p < 0.01, DE-T: p = 0.03), and while not significant, whole blood total glutathione (TGSH) and plasma thiobarbituric acid reactive substances (TBARS) tended to increase post exercise in dehydration trials (p = 0.08 for both). Intracellular monocyte heat shock protein 72 (HSP72) concentration was increased (p = 0.01) while intracellular lymphocyte HSP32 concentration was decreased for all trials (p = 0.02). Exercise-induced dehydration led to an increase in GSSG concentration while maintenance of euhydration attenuated these increases regardless of environmental condition. Additionally, evidence of increased cellular stress (measured via HSP) was found during all trials independent of body mass loss and environment. Finally, total distance covered during 90 min and PO during both 90 min and 5 km TT performance were reduced during only the DE-W trial, likely a result of combined cellular stress, hyperthermia and dehydration. These findings highlight the importance of fluid consumption during exercise to attenuate thermal and oxidative stress during prolonged exercise in the heat.The purpose of the second experiment was to investigate the effect of prolonged exercise-induced dehydration with and without hyperthermia on cellular and oxidative stress markers in untrained individuals, to serve as a comparison to the results of the first experimental chapter. Seven untrained male university students (mean ± SD) age: 21 ± 3 yrs, height: 181.1 ± 9.2 cm, weight: 76.8 ± 8.8 kg, and PO at LT 100.0 ± 13.0 W, who were unacclimatised to heat, participated in this study. Subjects completed the same experimental protocol as outlined in experimental chapter one, in warm (33.9 ± 1.0°C) and thermoneutral (22.9 ± 1.0°C) environments. Whole blood GSSG increased an average of 32% (p < 0.01) as a result of prolonged exercise, however unlike the trained subjects of experiment one, there was no effect of body mass loss on GSSG (p = 0.63). Similarly, intracellular monocyte HSP72 concentration increased 14% (p < 0.01) as a result of prolonged cycling regardless of body mass loss and environmental heat stress, analogous to subjects in experiment one. While there were no significant changes as a result of hydration or environment, a relationship was found between GSSG concentration and body mass loss (r2 = 0.5, p = 0.05), while HSP72 was correlated with body temperature and levels of heat storage (r2 = 0.5, p = 0.01). Similar to the trained individuals in experiment one, PO during the 90 min (7%, p < 0.01) and TT (14%, p < 0.01) were decreased while thermoregulation was impaired during DE-W only. These results demonstrate the increased level of stress in untrained subjects as a result of exercise and highlight the importance of participation in recommended physical activity to aid in positive cellular adaptations leading to superior antioxidant defences to aid in disease prevention.In light of the findings from the first experimental chapter that dehydration can significantly influence oxidative stress in trained subjects, the purpose of the third experimental chapter was to compare pre-exercise hyperhydration with plain water (W) or water with glycerol (G) to no hyperhydration (C) on markers of oxidative stress prior to and after a 90 min TT. Seven trained male cyclists and triathletes (age: 28 ± 8 yrs, height: 178.4 ± 7.8 cm, and mass: 73.2 ± 9.6 kg) covered as much distance as possible during a 90 min cycle after G, W or C. Blood was collected pre ingestion (PRE), post ingestion/pre exercise (PI), immediately post exercise (PE) and 1 hour post exercise (1HR) and analysed for whole blood TGSH, GSSG, and plasma levels of lipid hydroperoxides (LOOH) and protein carbonyls (PC). TGSH concentration increased post exercise in W and C (p < 0.01) while PC concentration increased post exercise during C only (p = 0.03). Additionally, GSSG concentration was greater PI and PE in C compared to G (p = 0.05, and p < 0.01, respectively), likely due to the inferior amount of fluid retained during C compared to the G and W trials. Therefore, it appears that both pre exercise hyperhydration with ad libitum fluid ingestion during exercise is sufficient to attenuate rises in exercise-induced oxidative stress.The novel findings presented in this thesis indicate fluid ingestion plays a vital role in providing cellular protection from oxidative stress. These results suggest that individuals participating in prolonged exercise should consume adequate fluid during exercise to avoid dehydration, matching fluid intake with body mass loss. Additionally, individuals who wish to hyperhydrate prior to exercise may enhance their ability to delay dehydration and thus enhance their cellular protection from oxidative stress.

Degree

thesis:*
Name dc:type.qualificationname
PhD
Level dc:type.qualificationlevel
Doctoral
Grantor dc:publisher.institution
University of Hull
Year dc:date.issued
2011

Author and committee

dc:creator, dc:contributor.*
Author dc:creator
  • Hillman, Angela R.
Advisor dc:contributor.advisor
  • Siegler, Jason

Subjects

dc:subject × 1

Rights

Language dc:language
en

Identifiers

dc:identifier.*
Identifier
oai:hull-repository.worktribe.com:4211865
OAI identifier oai:identifier
oai:hull-repository.worktribe.com:4211865

Chain of custody

source
Harvested from
University of Hull
Base URL
hull-repository.worktribe.com/oaiprovider
Last updated
2026-07-24
Source record
OAI-PMH GetRecord
citation

Hillman, Angela R.. The effects of hydration status on markers of oxidative and cellular stress during prolonged exercise in hyperthermic environments. Doctoral thesis, University of Hull, 2011. https://hull-repository.worktribe.com/4211865/1/Thesis