Exercise Training Enhances Platelet Mitochondrial Bioenergetics in Stroke Patients: A Randomized Controlled Trial

Abstract

Exercise training (ET) may impact physical fitness by affecting mitochondrial functions. This study aimed to elucidate the effect of ET on aerobic capacity and platelet mitochondrial bioenergetics (MTB) in stroke patients. Among the 30 stroke patients who underwent the traditional rehabilitation program (TRP), 15 were randomly assigned to have ET (50–60% VO2peak for 30 min/day, 5 days/week for 4 weeks), and those remaining received only the TRP (control group). The peak exercise capacity (VO2peak) and platelet MTB, including oxidative phosphorylation (OXPHOS) and the electron transport chain (ETC), were measured through automatic gas analysis and high-resolution respirometry, respectively. The results demonstrated that ET significantly increased the VO2peak (17.7%) and O2 uptake efficiency slope (31.9%) but decreased the ventilation versus CO2 production slope (−7.65%). Patients who underwent ET also had significantly enhanced platelet mitochondrial OXPHOS and ETC by activating the FADH2 (Complex II)-dependent pathway, but depressed plasma myeloperoxidase (−28.4%) and interleukin-6 levels (−29.9%). Moreover, changes in VO2peak levels were positively correlated with changes in platelet OXPHOS and ETC capacities. In conclusion, ET increases the platelet MTB by enhancing Complex II activity in stroke patients. The exercise regimen also enhances aerobic fitness and depresses oxidative stress/pro-inflammatory status in stroke patients.