Exercise Intensity but Not Cadence Affects the Dynamics of Muscle Oxygenation and Pulmonary Oxygen Uptake at the Onset of Exercise in Trained Cyclists

Purpose: This study examined how exercise intensity and pedaling cadence influence the on-transient kinetics of pulmonary oxygen uptake (˙VO2) and muscle oxygenation in trained cyclists. Specifically, we evaluated responses during transitions to moderate-, heavy-, and severe-intensity cycling at 2 cadences (60 and 90 rev·min-1), focusing on ˙VO2, deoxygenated hemoglobin/myoglobin (Δ deoxy[heme]), and tissue oxygen saturation (StO2). Methods: Sixteen well-trained male cyclists completed 6 laboratory sessions, including a graded ramp test and step transitions to 3 intensity domains at both cadences. ˙VO2 was measured breath-by-breath, while muscle oxygenation of the right vastus lateralis was continuously recorded using near-infrared spectroscopy. ˙VO2 and Δ deoxy[heme] kinetics were modeled with monoexponential functions, and StO2 desaturation rate (StO2-slope) was assessed using linear regression over the first 25 seconds following the transition. Two-way analyses of variance were used to analyze the effects of intensity and cadence. Results: Exercise intensity significantly influenced the amplitude and temporal characteristics of ˙VO2 and Δ deoxy[heme] responses (P < .001). ˙VO2 showed shorter time delays but longer time constants at higher intensities, while Δ deoxy[heme] amplitude and StO2-slope increased significantly from moderate- to severe-intensity (P < .001). Cadence affected ˙VO2 only in the moderate domain, with higher values at 90 rev·min-1. Δ deoxy[heme] and StO2 kinetics were unaffected by cadence at all intensities (P > .05). Conclusion: Exercise intensity, not cadence, is the primary driver of systemic and muscle oxygen kinetics in trained cyclists. Peripheral oxygen extraction appears robust across cadences, supporting the use of intensity-based training to target muscular adaptations.