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.

Highlights

  • Stroke, caused by cerebral vascular atherosclerosis/thrombosis or intracranial hemorrhage, is the leading cause of long-term disability, which produces enormous global health and economic burdens [1,2]

  • A randomized clinical study for 61 chronic stroke patients showed exercise training (ET) improved cardiovascular fitness [3] and a scientific overview encouraged post-stroke survivors to consider the importance of ET in regaining activities of daily living [4], controversy persists regarding how ET influences the hemostasis in stroke patients or stroke prevention [1,5]

  • Recent investigations further demonstrated that high-intensity interval training improved the platelet mitochondrial bioenergetics, which might reduce the risk of thrombosis in healthy sedentary individuals [14] and heart failure (HF) patients [15]

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Summary

Introduction

Stroke, caused by cerebral vascular atherosclerosis/thrombosis or intracranial hemorrhage, is the leading cause of long-term disability, which produces enormous global health and economic burdens [1,2]. Stroke-induced functional impairment reduces exercise capacity, which negatively affects the ability of patients to perform their daily activities. This limitation further decreases their independence and quality of life [1,2]. Regular exercise improves physical performance and aerobic capacity, which is concurrent with reducing the risk of major vascular thrombotic events [11]. Recent investigations further demonstrated that high-intensity interval training improved the platelet mitochondrial bioenergetics, which might reduce the risk of thrombosis in healthy sedentary individuals [14] and heart failure (HF) patients [15]. The effects of ET on platelet mitochondrial bioenergetics in stroke patients have not been extensively reviewed

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