Arterial Oxygen Content and Fatigue

Functional consequences of arterial O 2 content on exercise performance and locomotor muscle fatigue (LMF). 8 male cyclists completed 3 constant workload trials on a bicycle ergometer to exhaustion (314 W). The rides were randomized and performed at the identical workload in NORM (F I O 2 [%] / C a O 2 [ml/dl]: 0.21 / 21), HYPER (1.0 / 24), or HYPO (0.15 / 18). To quantify LMF induced by the 3 trials, 2 different assessment methods were applied. Quadriceps twitch force, in response to supramaximal magnetic stimuli of the femoral nerve (1–100 Hz) was assessed pre and post exercise. Changes in myoelectrical activity [integrated EMG (iEMG) and mean power frequency (MPF)] of the vastus lateralis were measured throughout the trials. Exercise times were significantly different between HYPO vs NORM vs HYPER (4.5 ± 0.4, 8.1 ± 0.6, 19.4 ± 4.0 min, respectively). A decrease in contractile function from baseline occurred after NORM / HYPO / HYPER (mean of all stimulation frequencies: −26.3 ± 3.4%, −24.7 ± 2.3%, −23.7 ± 3.5%, respectively), these changes were not significantly different from each other. iEMG progressively increased throughout exercise in NORM and HYPO, however, after an initial increase, iEMG began to fall after the 3 rd minute in HYPER. MPF changed reciprocally with iEMG. We previously showed that C a O 2 during strenuous exercise at equal workloads and durations markedly affects LMF. However, for the performance test to exhaustion, despite up to 4‐fold differences in exercise duration, LMF at end‐exercise was not influenced by Δ C a O 2 . Together these data suggest the existence of a certain limit or threshold for “peripheral fatigue” and that feedback (from the muscle itself) prevents further increases in motor output, i.e. “central fatigue”. C a O 2 determines the rate of fatigue accumulation.