Breathing 40% O(2) can attenuate postcontraction hyperaemia or muscle fatigue caused by static forearm contraction, depending on timing.

Little is known of the role of O(2)-dependent mechanisms in the hyperaemia associated with static muscle contraction or recovery from fatigue. Thus, in recreationally active, young, male subjects, forearm contraction was performed twice at 100% maximal voluntary effort until exhaustion, with a 7 min recovery period, whilst 40% O(2) (hyperoxia) was breathed during the contractions only, or during recovery only, or room air (normoxia) was breathed throughout. When hyperoxia was limited to the contractions, postcontraction increases in forearm blood flow, measured by venous occlusion plethysmography, were ∼25% lower (P < 0.05, n = 10) than during normoxia throughout. Furthermore, the postcontraction increase in venous lactate and fall in pH were attenuated (P < 0.05, n = 8). However, there was no effect on fatigue; time to voluntary exhaustion of contraction 2 was ∼25% less than for contraction 1 in both conditions. By contrast, when hyperoxia was limited to recovery (n = 10), there was no effect on postcontraction increases in forearm blood flow, but fatigue was ameliorated; time to voluntary exhaustion of contraction 2 was comparable to that of contraction 1. These results allow the novel conclusions that, even during static forearm contraction at 100% maximal voluntary effort, additional O(2) dissolved in plasma can attenuate the contribution made by O(2)-dependent dilator substances to postcontraction hyperaemia and that these substances may be released from the muscle fibres or blood vessel wall. Furthermore, they indicate that even in recreationally active individuals, recovery from fatigue can be improved by additional O(2) made available during recovery, and the O(2)-dependent mechanisms that contribute to fatigue are different from those that induce postcontraction hyperaemia.