Exogenous carbohydrate oxidation is reduced, and muscle glycogen oxidation is increased, when carbohydrate is ingested during prolonged exercise in hot conditions. Heat acclimation (HA) has been shown to reduce reliance on endogenous carbohydrates at least in the absence of exogenous carbohydrate provision during exercise. However, the effects of HA on exogenous carbohydrate oxidation remains unclear. This study aimed to determine whether 9-days of HA can reverse the decline in exogenous carbohydrate oxidation rates observed during endurance exercise performed in a hot environment.
Seventeen participants (10 males, 7 females; age: 24±7 years; V̇O2peak: 52.2±7.1 mL/kg/min) completed three experimental trials, cool (COOL), hot (HOT), and post-HA (POST). HA was isothermic (body core temperature maintained at ≥38.5ºC) and involved nine consecutive days (one rest day permitted) of 95-minutes cycling in 40ºC and 20% relative humidity (RH). Each experimental trial was preceded by 48-h of standardised diet and exercise and consisted of 90-minutes of stationary cycle ergometer exercise (45% Wmax) after an overnight fast in either cool (COOL: 20ºC, 20%; RH) or hot (HOT/POST: 40ºC, 20% RH) ambient conditions. On experimental trial days, skeletal muscle biopsies were obtained from the vastus lateralis before and after exercise for subsequent muscle glycogen analysis. During exercise, participants ingested beverages containing glucose at a rate of 90 g/h, enriched with U13C6-glucose to determine exogenous carbohydrate oxidation rates. Every 15-minutes, substrate oxidation rates were assessed via indirect calorimetry. Before HA, COOL and HOT were completed in a randomised order. Effects of condition on outcomes were estimated from linear mixed models with data reported as least squares means (95% confidence limits; P values).
Mean rectal temperature during exercise was higher in HOT (38.2ºC [38.0-38.3] ºC) than COOL (38.0 [37.8-38.1] ºC, p<0.0001), and lower in POST (37.9 [37.8-38.1] ºC) than HOT (p<0.0001). Mean heart rate was higher in HOT (155 [150-161] beats/min) than COOL (130 [124-135] beats/min, p<0.0001). Heart rate decreased in POST (146 [141-152] beats/min) compared to HOT (p<0.0001) and remained elevated relative to COOL (p<0.0001). Total carbohydrate oxidation rates did not differ across trials (1.85 [1.70-2.00], 1.80 [1.65-1.94], and 1.82 [1.66-1.99] g/min for COOL, HOT, and POST, respectively; p>0.05). Exogenous carbohydrate oxidation rates (Figure 1) were lower in HOT (0.37 [0.31-0.43] g/min) than COOL (0.51 [0.45-0.57] g/min; p<0.0001) and remained lower at POST (0.38 [0.31-0.44] g/min) than COOL (p<0.0001). POST and HOT exogenous carbohydrate oxidation rates were the same (p=0.805). Net muscle glycogen utilisation was lower in POST than HOT (p=0.027) and not different between (p>0.05) COOL (163 [117-209] mmol/kg DM), HOT (200 [155-245] mmol/kg DM) and POST (112 [56-168] mmol/kg DM).
HA caused phenotypic thermoregulatory and cardiovascular adaptions. However, despite improving thermoregulatory responses to exercise, HA did not reverse the reduction in exogenous carbohydrate oxidation rates observed during exercise in a hot environment.
