Caffeine improves supramaximal cycling but not the rate of anaerobic energy release

Abstract

The purpose of this study was to determine if improved supramaximal exercise performance in trained cyclists following caffeine ingestion was associated with enhanced O₂ uptake ($\dot{V}{\text{O}}_{2}$ kinetics), increased anaerobic energy provision (accumulated O₂—AO₂—deficit), or a reduction in the accumulation of metabolites (for example, K⁺) associated with muscular fatigue. Six highly trained male cyclists ($\dot{V}{\text{O}}_{2}$peak 68 ± 8 mL kg⁻¹ min⁻¹) performed supramaximal (120% $\dot{V}{\text{O}}_{2}$peak) exercise bouts to exhaustion on an electronically braked cycle ergometer, following double-blind and randomized ingestion of caffeine/placebo (5 mg kg⁻¹). Time to exhaustion (TE), $\dot{V}{\text{O}}_{2}$ kinetics, AO₂ deficit, blood lactate (La⁻), plasma potassium (K⁺), caffeine and paraxanthine concentrations were measured. Caffeine ingestion elicited significant increases in TE (14.8%, p < 0.01) and AO₂ deficit (6.5%, p < 0.05). In contrast, no changes were observed in AO₂ deficit at isotime, $\dot{V}{\text{O}}_{2}$ kinetics, blood [La⁻] at exhaustion or peak [K⁺] following caffeine ingestion. However, [K⁺] was significantly reduced (13.4%, p < 0.01) during warm-up cycling immediately prior to the onset of the supramaximal bout for the caffeine trials, compared with placebo. It appears that caffeine ingestion is beneficial to supramaximal cycling performance in highly trained men. The reduced plasma [K⁺] during submaximal warm-up cycling may prolong the time taken to reach critical [K⁺] at exhaustion, thus delaying fatigue. Considering caffeine ingestion did not change $\dot{V}{\text{O}}_{2}$ kinetics or isotime AO₂ deficit, increases in absolute AO₂ deficit may be a consequence of prolonged TE, rather than causal.