The effect of blood-flow restricted strength and sprint training on skeletal muscle mitochondrial function in persons with COPD: a randomised controlled study

<bold>Introduction:</bold> Blood-flow restricted training (BFRT) was recently introduced to pulmonary rehabilitation. It remains unknown whether it has the potential to ameliorate the skeletal muscle mitochondrial dysfunction associated with COPD. <bold>Aim:</bold> We aimed to investigate the effects of BFRT (as low-load strength and sprint training) vs high-load strength training and sprint training (HL) on mitochondrial function in persons with stable COPD. <bold>Methods:</bold> We randomly assigned participants to 6 weeks lower limb BFRT (strength: 70% occlusion pressure, 30% 1-repetition maximum; sprint: 30s all-out sprints, 70% occlusion pressure during breaks) or HL (strength: 70% 1-repetition maximum; sprint: 30s all-out sprints). Primary outcome was mitochondrial respiratory capacity and H₂O₂ emission (Oroboros O2k) in permeabilised muscle fibres sampled from vastus lateralis biopsies before and after the intervention. We secondarily investigated maximal voluntary strength. <bold>Results:</bold> The study is ongoing. To date, 11 participants (69 [67, 72] years, FEV₁ 61 [49, 70] % pred.) completed the study, 3 dropped out. Mitochondrial complex I + II state 3 respiration changed by -0.20 (−1.08, 1.40) pmol O₂/s/mg ww in the BFRT group and by 2.72 (2.27, 3.78) in the HL group. Maximal mitochondrial H₂O₂ emission changed by -0.08 (−1.62, 0.40) pmol H₂O₂/s/mg ww in the BFRT group and by 0.25 (−1.43, 0.61) in the HL group. Both groups increased maximal voluntary strength without clinically relevant between-group differences. <bold>Conclusions:</bold> Six weeks of BFRT may reduce overactivity of mitochondrial complex I + II-linked respiration and maximal H₂O₂ emission in comparison to HL.