Author(s): DI DOMENICO, H.1,2, BOWEN, M.2, MOREL, B.2, Institution: FRENCH INSTITUTE OF SPORT (INSEP), Country: FRANCE, Abstract-ID: 1655

INTRODUCTION:
Critical Power (Pc) is a fundamental parameter for assessing endurance capabilities and optimizing race strategies and training plans [1]. While Pc is well established, its determination is often time-consuming and fatiguing due to existing protocols. The recently introduced Ramp Above Critical Level Endurance Test (RACLET) offers a novel, submaximal alternative for Pc assessment [2,3]. This study aims to i) validate the sensitivity of RACLET to variations in aerobic capacity by assessing its response to hypoxia, and ii) investigate hypoxia’s impact on force and velocity capacities under fatigue using the Force-Velocity-Endurance (FoVE) model [4].
METHODS:
12 participants (5 women, 7 men) completed two RACLET sessions under normoxia (FiO₂=20.9%) and severe hypoxia (FiO₂=13%) in a randomized crossover design. Participants cycled at 80 RPM on a modified Monark LC6 ergometer while following a progressively decreasing target power interspersed with six-pedal-stroke sprints every 30s. Power reached during sprints were modelled using derived equations based on: Pmax(t) =Pi–(1/Tau)*int(P(t)-Pc)dt, where P is the target power and Tau is a time constant [2,3]. Theoretical maximal force and velocity were extrapolated from the linear relationship during each sprint. Critical maximal force (F0c) and velocity (V0c) were calculated based on the FoVE model and the decay ratio derived from the decline in power throughout the RACLET [4]. Peripheral oxygen saturation (SpO₂) was monitored to confirm hypoxic exposure.
RESULTS:
The mean SpO₂ dropped from 96.0 ± 1.2 % (normoxia) to 72.6 ± 5.2 % (hypoxia), confirming the physiological impact of the intervention. Pc significantly decreased in hypoxia (194 ± 49 W) compared to normoxia (236 ± 61 W) (p<0.001, d=1.8), aligning with the literature. Decrease in Pc under hypoxia were mainly explained by decrease in V0c (-25.2 ± 3.4% in hypoxia compared to normoxia, p<0.01), while F0c were comparable between normoxia and hypoxia (p=0.71), aligning with previous studies suggesting that hypoxia predominantly affects velocity-related capacities rather than maximal force production during repeated sprint exercise [5].
CONCLUSION:
Beyond validating the RACLET’s sensitivity to hypoxic stress, this study demonstrates its utility in dynamically tracking the kinetics of mechanical impairment. By enabling the FoVE model to dissociate force and velocity alterations along time, the RACLET revealed that Pc alteration in hypoxia was driven by velocity loss rather than force capability. This protocol thus emerges as a versatile framework to investigate the mechanical etiology of fatigue under diverse environmental constraints (e.g., hypoxia, heat). Ultimately, it offers a time-efficient solution to monitor specific physiological adaptations and optimize training load prescription in challenging conditions.
[1] Vanhatalo et al., IJSPP, 2011
[2] Bowen et al., ECSS, 2024
[3] Bowen et al., EJAP, 2025
[4] Bowen et al., J Theo Biol, 2023
[5] Kasai et al., Sports Med Int Open, 2018