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PP-PH02 Physiology 2<br />

Hot conditions increased significantly HR (+9 ±5 bpm) and Tskin (+5 ±1°C) independently <strong>of</strong> the simulated altitude (both P < 0.001),<br />

whereas altitude exposure reduced SpO2 independently <strong>of</strong> the environmental temperature (96 ±1 vs. 88 ±4% in sea level and hypoxic<br />

conditions, P < 0.001). [La] values failed to be significantly different within conditions (5.6 ±3.4, 8.7 ±2.6, 7.9 ±6.2 and 10.0 ±5.4 mmol.L-1<br />

in CON, HYP, HOT and H+H, respectively). There was no significant interaction effect between temperature and altitude on HR, Tskin,<br />

SpO2 and [La].<br />

However, our data displayed a significant (P = 0.011) interaction effect on time to exhaustion. This interaction was due to a slightly reduced<br />

effect <strong>of</strong> either a hot (-34.6 ±14.8% from CON to HOT vs. -25.6 ±19.9% from HYP to H+H) or an altitude (-35.7 ±14.5% from CON to<br />

HYP vs. -26.0 ±19.7% from HOT to H+H) exposure when the other stressor is already present. That suggests that some limiting factors for<br />

performance are common to both a hot and hypoxic environment. In line with this, subjects stopped exercising at equivalent Tcore (38.5<br />

±0.6, 38.2 ±0.6, 38.4 ±0.7 and 38.4 ±0.5°C) and RPE (18.7 ±1.7, 19.3 ±1.0, 19.2 ±1.3 and 19.3 ±0.9) in CON, HYP, HOT and H+H.<br />

Conclusion<br />

There is no cumulative effect <strong>of</strong> combining hot and hypoxic environment on cardiovascular, metabolic or perceived strains despite exercise<br />

performance being reduced.<br />

HYPERTHERMIA INDUCES OXIDATIVE STRESS IN RESTING BUT NOT IN EXERCISING HUMANS<br />

LAITANO, O., KALSI, K.K., POOK, M., TRANGMAR, S., OLIVEIRA, A.R., GONZÁLEZ-ALONSO, J.<br />

BRUNEL UNIVERSITY, UK. UNIVERSIDADE FEDERAL DO RIO GRANDE DO SUL, BRAZIL.<br />

Hyperthermia imposes a severe stress to multiple regulatory systems including the redox system which is important for maintaining<br />

cellular homeostasis in resting and exercising humans. Glutathione (GSH) protects cells against oxidation by providing a substrate for<br />

glutathione peroxidase. GSH removes hydrogen ions and organic peroxides resulting in the formation <strong>of</strong> oxidized glutathione (GSSG).<br />

Therefore, the GSH/GSSG ratio is a sensitive marker <strong>of</strong> oxidative stress. The aim <strong>of</strong> this study was to determine the effects <strong>of</strong> isolated<br />

hyperthermia on oxidative stress in resting and exercising humans. We hypothesized that isolated hyperthermia would increase oxidative<br />

stress as indicated by alterations in GSH metabolism reflecting a decrease in GSH/GSSG ratio ([GSH-GSSG]/[GSSG]). Eight healthy<br />

males took part in this study. Participants wore a water-perfused suit and performed a 6 min one-legged knee extensor exercise at 50%<br />

<strong>of</strong> their predetermined maximal peak power output both under control and hyperthermic conditions while maintaining euhydration by<br />

ingesting1.3 ± 0.3 L <strong>of</strong> water. Following the control trial and a 15 min resting period, hot water (~ 48°C) was perfused through the suit for<br />

~75 min in order to increase rectal temperature from 37.0 ± 0.3 to 38.3 ± 0.4 ºC and skin temperature from 33.1 ± 1.6 to 38.7 ± 0.9ºC.<br />

Blood samples were withdrawn before and at the fifth minute during both exercise bouts for determination <strong>of</strong> GSH and GSSG concentration<br />

by spectrophotometry assay. At rest, hyperthermia did not alter GSH (620 ± 289 vs 693 ± 379 µM, p= 0.093), but increased GSSG (6 ±<br />

4 vs 12 ± 8 µM, p = 0.012), thereby leading to a significant reduction in the GSH/GSSG ratio (127 ± 84 vs 64 ± 51 µM, p= 0.017). This indicates<br />

an independent hyperthermia-induced oxidative stress. Conversely, during exercise hyperthermia increased both GSH (569 ± 313<br />

vs 821 ± 440 µM, p = 0.036) and GSSG (6 ± 3 vs 16 ± 17 µM, p = 0.012). Consequently, GSH/GSSG ratio did not change (108 ± 71 vs 88 ±<br />

67, p = 0.208). In conclusion, these results in humans demonstrate that hyperthermia induces oxidative stress at rest but not during<br />

exercise because a parallel increase in antioxidant defense <strong>of</strong>fsets hyperthermia-induced oxidative stress.<br />

Supported by the Gatorade Sports Science Institute & Brazil’s Ministry <strong>of</strong> Education<br />

EFFECT OF WORKING IN HOT ENVIRONMENT ON HEALTH AND PHYSICAL ABILITIES: AN OIL AND GAS INDUSTRY<br />

STUDY<br />

RACINAIS, S., GIRARD, O., WALSH, A., KNEZ, W., GAOUA, N., GRANTHAM, J.<br />

ASPETAR<br />

Purpose: To investigate the alterations in physical work capacity occurring in the summer <strong>of</strong> a Middle Eastern country (Qatar – outside<br />

temperature between 40 and 50ºC).<br />

Methods: A group <strong>of</strong> 40 workers (oil and gas industry) with no previous experience <strong>of</strong> working in a Qatari summer volunteered to participate<br />

in a one-year follow-up project.<br />

- Blood pressure and arterial oxygen saturation were obtained during the pre-experimental screening (April, before their first summer) as<br />

well as before (6 a.m.) and after (4 p.m.) work in the summer (August) and the following winter (January). Handgrip force was measured<br />

at the same time.<br />

- Normalised physical activity (tri-axial accelerometer) and core temperature (ingestible pill) were recorded during the same working day.<br />

Results: Blood pressure recorded before work decreased (P < 0.001) from April to August (from 136 ±13 and 84 ±11 to 125 ±11 and 77 ±9<br />

mmHg for systolic and diastolic, respectively) but returned (P < 0.05) close to baseline values in January (130 ±16 and 80 ±11). Oxygen<br />

saturation decreased also (P < 0.01) from pre-screening (98.5 ±1%) to the summer (98.0 ±1%) and increased (P < 0.01) the following winter<br />

(98.5 ±1%). Both blood pressure and oxygen saturation were reduced (P &#8804; 0.05) following the day <strong>of</strong> work but without interaction<br />

with the period <strong>of</strong> the year. Maximal handgrip force was significantly lower (P < 0.005) in August (38 ±7 kg) than in January (40 ±8 kg)<br />

independently <strong>of</strong> time-<strong>of</strong>-day.<br />

Data at work. The normalised physical activity (acceleration) during the working hours was significantly (P < 0.02) lower in the summer<br />

(0.10 ±0.04 g) as compared to the winter (0.11 ±0.03 g). Average core temperature during work was significantly (P < 0.005) higher in<br />

August (37.4 ±0.2ºC) than in January (37.2 ±0.2ºC). However, no workers became hyperthermic as the highest observed value during the<br />

continuous recording was 38.3ºC.<br />

Discussion: The Company in which this survey was performed applies safety rules based on heat index (HI). The work/rest period (minutes)<br />

were reduced to 30/10 for a HI <strong>of</strong> 39-49, 20/10 for a HI <strong>of</strong> 50-53, and work stopped for a HI > 54. The summer data presented here<br />

were obtained on days with the highest HI (up to 53). Our data showed a reduced activity during the summer as a consequence <strong>of</strong> both<br />

these safety rules and the self-pacing <strong>of</strong> the worker. However, despite this reduced activity, central temperatures were higher in the<br />

summer month and workers presented with symptoms consistent with chronic fatigue (reduced blood pressure and saturation) associated<br />

with reduced maximal voluntary strength capacity.<br />

Conclusion: None <strong>of</strong> these alterations were dependent <strong>of</strong> being tested before or after work suggesting that there were not linked to acute<br />

fatigue due to the day <strong>of</strong> work but rather to the presence <strong>of</strong> chronic alterations persisting during the summer months.<br />

254 14 TH<br />

ANNUAL CONGRESS OF THE EUROPEAN COLLEGE OF SPORT SCIENCE

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