Non-technical summary The mechanisms determining exercise intolerance are poorly understood. A reduction in work efficiency in the form of an additional energy cost and oxygen requirement occurs during high-intensity exercise and contributes to exercise limitation. Muscle fatigue and subsequent recruitment of poorly efficient muscle fibres has been proposed to mediate this decline. These data demonstrate in humans, that muscle fatigue, generated in the initial minutes of exercise, is correlated with the increasing energy demands of high-intensity exercise. Surprisingly, however, while muscle fatigue reached a plateau, oxygen uptake continued to increase throughout 8 min of exercise. This suggests that additional recruitment of inefficient muscle fibres may not be the sole mechanism contributing to the decline in work efficiency during high-intensity exercise.Abstract During constant work rate (CWR) exercise above the lactate threshold (LT), the exponential kinetics of oxygen uptake (V O 2 ) are supplemented by aV O 2 slow component (V O 2 sc ) which reduces work efficiency. This has been hypothesised to result from 'fatigue and recruitment' , where muscle fatigue during supra-LT exercise elicits recruitment of additional, but poorly efficient, fibres to maintain power production. To test this hypothesis we characterised changes in the power-velocity relationship during sub-and supra-LT cycle ergometry in concert withV O 2 kinetics. Eight healthy participants completed a randomized series of 18 experiments consisting of: (1) a CWR phase of 3 or 8 min followed immediately by; (2) a 5 s maximal isokinetic effort to characterize peak power at 60, 90 and 120 rpm. CWR bouts were: 20 W (Con); 80% LT (Mod); 20% (H); 60% (VH); where is the difference between the work rate at LT andV O 2 max . TheV O 2 sc was 238 ± 128 and 686 ± 194 ml min −1 during H and VH, with no discernibleV O 2 sc during Mod. Peak power in Con was 1025 ± 400, 1219 ± 167 and 1298 ± 233 W, at 60, 90 and 120 rpm, respectively, and was not different after Mod (P > 0.05). Velocity-specific peak power was significantly reduced (P < 0.05) by 3 min of H (−103 ± 46 W) and VH (−216 ± 60 W), with no further change by 8 min. TheV O 2 sc was correlated with the reduction in peak power (R 2 = 0.49; P < 0.05). These results suggest that muscle fatigue is requisite for theV O 2 sc . However, the maintenance of velocity-specific peak power between 3 and 8 min suggests that progressive muscle recruitment is not obligatory. Rather, a reduction in mechanical efficiency in fatigued fibres is implicated.

To examine the effect (“cross-tolerance”) of heat acclimation (HA) on exercise performance upon exposure to acute hypobaric hypoxia (4350 m). Eight male cyclists residing at 1600 m performed tests of maximal aerobic capacity (VO2max) at 1600 m and 4350 m, a 16 km time-trial at 4350 m, and a heat tolerance test at 1600 m before and after 10 d HA at 40°C, 20% RH. Resting blood samples were obtained pre-and post- HA to estimate changes in plasma volume (ΔPV). Successful HA was indicated by significantly lower exercise heart rate and rectal temperature on day 10 vs. day 1 of HA and during the heat tolerance tests. Heat acclimation caused a 1.9% ΔPV, however VO2max was not significantly different at 1600 m or 4350 m. Time-trial cycling performance improved 28 sec after HA (p = 0.07), suggesting a possible benefit for exercise performance at acute altitude and that cross-tolerance between these variables may exist in humans. These findings do not clearly support the use of HA to improve exercise capacity and performance upon acute hypobaric hypoxia, however they do indicate that HA is not detrimental to either exercise capacity or performance.

Across various populations, verification testing is used to confirm VO(2)max attainment and has repeatedly shown similar VO(2)max values to those obtained from incremental exercise. Yet, many individuals show meaningful differences in VO(2)max between protocols, and an explanation for this is unknown. The aim of the study was to elucidate this phenomenon in 30 men and women of similar age, fitness, and physical activity using assessment of anaerobic power. On day 1, they completed the Wingate test, and returned at least 48 h later to complete incremental cycle ergometry followed by a verification protocol. During exercise, ventilation, pulmonary gas exchange data, and heart rate (HR) were continuously measured. Mean VO(2)max was similar (P > 0.05) between protocols (42.05 +/- 5.88 ml kg(-1) per min versus 42.03 +/- 5.75 ml kg(-1) per min, respectively), although seven subjects (23%) revealed a VO(2)max that was not 'verified' by the supramaximal protocol. Indices of power output and gas exchange data were similar (P > 0.05) between subjects who revealed a 'true' VO(2)max compared to those who did not, although peak and mean power was consistently higher in persons whose VO(2)max was not 'verified.' A previously established HRmax criterion for verification testing was not met in 17% of subjects. Additional study is merited to identify alternate determinants of VO(2)max, such as muscle activation via assessment of motor unit recruitment, and to investigate utility of verification testing to confirm VO(2)max attainment in elite athletes and the elderly.

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