Key result
Adding CO2 during heat stress fails to improve VO2max despite restoring middle cerebral artery velocity.
Why the study?
Heat-induced hyperventilation may reduce PaCO2 and cerebral perfusion, potentially impairing exercise performance, but this mechanism's impact on fatigue in heat was unclear.
Does restoring heat stress-associated reduction in middle cerebral artery velocity by adding CO2 to inspiration improve exercise performance in volunteers?
Does restoring heat stress-associated reduction in middle cerebral artery velocity by adding CO2 to inspiration improve exercise performance in volunteers?
Absolute Event Rate: 4.1% vs 4.6%
p-value: p=<0.05
Restoring cerebral perfusion and oxygenation during heat stress does not prevent the reduction in exercise performance, suggesting other mechanisms limit performance in the heat.
Adding CO2 fails to restore exercise capacity in heat; leaves open non-cerebral mechanisms of performance limitation for targeted trials.
Heat-induced hyperventilation may reduce PaCO2 and thereby cerebral perfusion and oxygenation and in turn exercise performance. To test this hypothesis, eight volunteers completed three incremental exercise tests to exhaustion: (a) 18 °C ambient temperature (CON); (b) 38 °C (HEAT); and (c) 38 °C with addition of CO2 to inspiration to prevent the hyperventilation-induced reduction in PaCO2 (HEAT + CO2 ). In HEAT and HEAT + CO2 , rectal temperature was elevated prior to the exercise tests by means of hot water submersion and was higher (P < 0.05) than in CON. Compared with CON, ventilation was elevated (P < 0.01), and hence, PaCO2 reduced in HEAT. This caused a reduction (P < 0.05) in mean cerebral artery velocity (MCAvmean ) from 68.6 ± 15.5 to 53.9 ± 10.0 cm/s, which was completely restored in HEAT + CO2 (68.8 ± 5.8 cm/s). Cerebral oxygenation followed a similar pattern. V ˙ O 2 m a x was 4.6 ± 0.1 L/min in CON and decreased (P < 0.05) to 4.1 ± 0.2 L/min in HEAT and remained reduced in HEAT + CO2 (4.1 ± 0.2 L/min). Despite normalization of MCAvmean and cerebral oxygenation in HEAT + CO2 , this did not improve exercise performance, and thus, the reduced MCAvmean in HEAT does not seem to limit exercise performance.
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Keiser et al. (2015) studied Healthy volunteers (n=8). Heat stress (38 °C) with or without inspired CO2 vs. 18 °C ambient temperature (CON) was evaluated on VO2max (p=<0.05). Restoring middle cerebral artery velocity by adding CO2 during heat stress did not improve exercise performance, with VO2max remaining reduced at 4.1 L/min compared to 4.6 L/min in control (P<0.05).
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