The Acute Effects of Caffeine and Normobaric Hypoxia on Cardiorespiratory Exercise Responses in Healthy Adults: A Randomized Controlled Trial

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The ergogenic effects of caffeine for endurance performance at sea level are well established. However, whether caffeine enhances exercise capacity or modulates cardiorespiratory responses in hypoxia remains unclear. Twenty-nine healthy, active volunteers (14 women) completed four tests in a pseudorandomized order, comprising 10 min of steady-state cycling (40% normoxic maximal aerobic power) followed by incremental exercise tests to exhaustion. Participants consumed 6 mg/kg body mass anhydrous caffeine, or placebo, 45 min before exercise. Tests were performed while breathing room air or a hypoxic gas mixture (simulating ∼3,500 m). At peak exercise intensity, oxygen uptake was affected by condition (hypoxia vs. normoxia; 44.8 ± 7.3 vs. 51.4 ± 7.9 ml·kg-1·min-1; p < .001) but not supplement (caffeine vs. placebo; 48.2 ± 8.2 vs. 48.0 ± 8.4 ml·kg-1·min-1; p = .501). Maximal aerobic power and pulse oxygen saturation were lower in hypoxia (both p < .001), but unaffected by caffeine (p = .061 and .898, respectively). Pulmonary ventilation was unaffected by hypoxia (p = .154) or caffeine (p = .117). Heart rate was higher in normoxia and with caffeine (both p < .001). During steady-state cycling, hypoxia (p < .001) and caffeine (p = .026) increased pulmonary ventilation. However, the hypoxia-induced pulse oxygen saturation decrease (p < .001) was not attenuated with caffeine (interaction p = .283). Perceived exertion was higher in hypoxia (p < .001) and lower with caffeine (p = .026). Caffeine increased vastus lateralis oxygenation in hypoxia (caffeine vs. placebo; 52 ± 8 vs. 50 ± 10%; p = .020) but not in normoxia (caffeine vs. placebo; 59 ± 7 vs. 59 ± 8%; p > .999). Overall, caffeine did not enhance exercise capacity in either environmental condition. However, during steady-state cycling, caffeine enhanced pulmonary ventilation, reduced perceived exertion, and mitigated hypoxia-induced muscle oxygenation reductions.

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