While a number of studies have investigated whether heat stress elevates muscle glycogen utilization, the results have been equivocal (Nielsen et al. 1990; Febbraio et al. 1994). No study has investigated muscle metabolism during running under heat stress. Therefore, with University Ethical Committee approval and informed written consent, nine sportsmen performed a prolonged, intermittent, high-intensity shuttle running test in hot (HT) and moderate (MT) environmental conditions (dry bulb temperature: HT 32·9 ± 0·4°C, MT 16·5 ± 0·1°C, P < 0·01; relative humidity: HT 28·4 ± 1·1 %, MT 62·6 ± 0·6 %, P < 0·01). The test was based on repeated 20 m shuttle runs. Subjects performed 60 m of walking, a 15 m sprint, 60 m of 'cruising' (85 % O2,max) and 60 m of 'jogging' (45 % O2,max) for 15 min followed by a 3 min rest. This exercise-rest pattern was continued until volitional exhaustion. All subjects performed the HT first followed, 14 days later, by the moderate trial. Subjects performed their two trials at the same time of day and food intake and physical activity were replicated in the 2 days prior to each trial. Subjects drank water ad libitum during exercise. Heart rate, blood lactate and glucose, plasma adrenaline and noradrenaline and serum cortisol were measured and then analysed using a two-way ANOVA (repeated measures on two factors: trial × time). Distance run, decline in sprint performance, muscle temperature and mixed muscle glycogen utilization (in the vastus lateralis) were analysed using a t test for correlated samples. All data are presented as means ± S.E.M. Distance run was reduced by 49 % (HT 11216 ± 1411 m, MT 21644 ± 1629 m, P < 0·01), and the decline in average 15 m sprint performance was greater (HT 0·17 ± 0·05 s, MT 0·09 ± 0·03 s, P < 0·05) in HT. Average heart rates, blood lactate and glucose were higher throughout exercise in the heat (main effect trial, P < 0·01; interaction trial-time, P < 0·01). Plasma adrenaline (HT 1·27 ± 0·28 nmol l-1, MT 0·77 ± 0·12 nmol l-1, main effect trial, P < 0·01) and noradrenaline (HT 17·5 ± 2·1 nmol l-1, MT 10·0 ± 1·6 nmol l-1, main effect trial, P < 0·01), and serum cortisol (HT 649 ± 28 nmol l-1, MT 472 ± 38 nmol l-1, main effect trial, P < 0·05, n = 5) mean exercise concentrations were greater in the HT. Muscle temperature was higher in the HT (HT end-point vs. same time point in MT, 40·2 ± 0·3 vs. 39·3 ± 0·2°C, P < 0·01). Muscle glycogen utilization appeared to be greater in the heat (HT 193·2 ± 19·5 mmol (kg dry wt)-1, MT 143·8 ± 23·9 mmol (kg dry wt)-1, P = 0·055, n = 8), and for seven out of the eight subjects the heat-induced increase in utilization ranged from 19 to just over 200 %. However, at the end of exercise in the HT the glycogen remaining in the muscle was much higher than that seen at the actual end of exercise in the MT (HT 207·4 ± 34·3 mmol (kg dry wt)-1, MT 126·5 ± 46·8 mmol (kg dry wt)-1, P < 0·01, n = 8). Rectal temperature (Trec) was higher in the HT (HT end-point vs. same time point in MT, 39·60 ± 0·15 vs. 38·75 ± 0·10°C, interaction trial-time, P < 0·01), and there was a very strong relationship between distance completed and rate of rise in Trec in the HT (HT, r = -0·90, P < 0·01; MT, r = -0·76, P < 0·05). These results support the idea that fatigue in the heat was associated with hyperthermia, and that elevated muscle glycogen utilization does not explain the earlier onset of fatigue seen in the HT.
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