Voluntary hyperventilation-induced hypocapnia enhances wingate test performance without altering energy system contributions.

High-intensity exercise challenges acid-base homeostasis, often limiting performance due to hydrogen ion (H⁺) accumulation. This study investigated the effects of voluntary hyperventilation-induced hypocapnia (a state of reduced carbon dioxide levels in the blood) on Wingate test performance and energy system contributions in team sport athletes. Seventeen male athletes performed 30-second Wingate tests under control and hyperventilation conditions, separated by 2-3 days. Hyperventilation involved 5 min of controlled breathing with a tidal volume of 1000 mL and a respiratory frequency of 30 breaths·min⁻¹ to induce hypocapnia before the test. Performance metrics (peak and mean power), energy system contributions (oxidative, glycolytic, ATP-PCr), and blood lactate accumulation (Δ[BLa⁻]) were assessed using breath-by-breath gas analysis and capillary blood samples. Paired t-tests revealed that hyperventilation significantly increased relative peak power (12.7 ± 1.55 vs. 11.9 ± 1.05 W·kg⁻¹, p = 0.007) and mean power (9.0 ± 0.65 vs. 8.6 ± 0.67 W·kg⁻¹, p = 0.005) compared to control. However, no differences were observed in energy system contributions (oxidative: 20.1 ± 3.9% vs. 20.4 ± 2.3%; glycolytic: 41.1 ± 4.7% vs. 41.4 ± 3.7%; ATP-PCr: 38.9 ± 5.5% vs. 38.4 ± 4.2%), total energy expenditure, or Δ[BLa⁻] (12.6 ± 1.9 vs. 12.8 ± 1.2 mmol·L⁻¹). These findings suggest that hyperventilation enhances anaerobic performance without altering energy metabolism, potentially through improved buffering capacity, neuromuscular activation, or oxygen redistribution. All values are reported as mean ± standard deviation (SD). This endogenous strategy offers a practical approach to optimize short-duration, high-intensity efforts, though further research is needed to refine its application across varied protocols and populations.