Blood flow restricted resistance exercise and reductions in oxygen tension attenuate mitochondrial H2O2 emission rates in human skeletal muscle

Low‐load blood flow restricted resistance exercise (BFR‐RE) training has been proposed to induce comparable adaptations to traditional resistance exercise (RE) training, however, the acute signalling events remain unknown. Although a suggested mechanism of BFR‐RE is an increase in reactive oxygen species (ROS) production, oxygen partial pressure (urn:x-wiley:00223751:media:tjp13683:tjp13683-math-0006) is reduced during BFR‐RE, and the influence of O2 tension on mitochondrial redox balance remains ambiguous. We therefore aimed to determine whether skeletal muscle mitochondrial bioenergetics were altered following an acute bout of BFR‐RE or RE, and to further examine the role of urn:x-wiley:00223751:media:tjp13683:tjp13683-math-0007 in this response. Accordingly, muscle biopsies were obtained from 10 males at rest and 2 h after performing three sets of single‐leg squats (RE or BFR‐RE) to failure at 30% one‐repetition maximum. We determined that mitochondrial respiratory capacity and ADP sensitivity were not altered in response to RE or BFR‐RE. Although maximal (succinate) and submaximal (non‐saturating ADP) mitochondrial ROS emission rates were unchanged following RE, BFR‐RE attenuated these responses by ∼30% compared to pre‐exercise, occurring along with a reduction in skeletal muscle tissue oxygenation during BFR‐RE (P < 0.01 vs. RE). In a separate cohort of participants, evaluation of mitochondrial bioenergetics in vitro revealed that mild O2 restriction (50 µm) dramatically attenuated maximal (∼4‐fold) and submaximal (∼50‐fold) mitochondrial ROS emission rates and the fraction of electron leak to ROS compared to room air (200 µm). Combined, these data demonstrate that mitochondrial ROS emissions are attenuated following BFR‐RE, a response which may be mediated by a reduction in skeletal muscle urn:x-wiley:00223751:media:tjp13683:tjp13683-math-0008.

This is the peer reviewed version of the following article: Petrick, H.L., Pignanelli, C., Barbeau, P.‐A., Churchward‐Venne, T.A., Dennis, K.M.J.H., van Loon, L.J.C., Burr, J.F., Goossens, G.H. and Holloway, G.P. (2019), Blood flow restricted resistance exercise and reductions in oxygen tension attenuate mitochondrial H2O2 emission rates in human skeletal muscle. J Physiol, 597: 3985-3997. https://doi.org/10.1113/JP277765, which has been published in final form at https://doi.org/10.1113/JP277765 . This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.