Abstract
This study elucidates how high-intensity interval training (HIT) and moderate-intensity continuous training (MCT) affect mitochondrial functionality and thrombin generation (TG) in platelets following hypoxic exercise (HE, 100 W under 12% O2 for 30 min). Forty-five healthy sedentary males were randomized to engage either HIT (3-minute intervals at 40% and 80%VO2max, n = 15) or MCT (sustained 60%VO2max, n = 15) for 30 minutes/day, 5 days/week for 6 weeks, or to a control group (CTL, n = 15) that did not received exercise intervention. Before the intervention, HE (i) reduced the ATP-linked O2 consumption rate (OCR), the reserve capacity of OCR, and the activities of citrate synthase (CS) and succinate dehydrogenase (SDH), (ii) lowered mitochondrial membrane potential (MP) and elevated matrix oxidant burden (MOB) in platelets, and (iii) enhanced dynamic TG in platelet-rich plasma (PRP), which responses were attenuated by pretreating PRP with oligomycin or rotenone/antimycin A. However, 6-week HIT (i) increased mitochondrial OCR capacity with enhancing the CS and SDH activities and (ii) heightened mitochondrial MP with depressing MOB in platelets following HE, compared to those of MCT and CTL. Moreover, the HIT suppressed the HE-promoted dynamic TG in PRP. Hence, we conclude that the HIT simultaneously improves mitochondrial bioenergetics and suppresses dynamic TG in platelets undergoing hypoxia.
Highlights
Increased thrombin activity is an essential pathogenic process of cardiovascular diseases[8]
We further hypothesize that high-intensity interval exercise training (HIT) effectively reduces platelet-induced thrombin generation (TG) undergoing hypoxic stress, which is associated with alleviating platelet mitochondrial dysfunction cause by hypoxia
To answer the abovementioned questions, this study evaluated how two isovolumic exercise regimens [i.e., HIT (3-minute intervals at 40% and 80%VO2max) and moderate-intensity continuous exercise training (MCT, sustained 60%VO2max)] for 6 weeks affected (i) mitochondrial oxidative phosphorylation (OXPHOS) and oxidative stress, (ii) mitochondrial biogenesis, and (iii) dynamic TG in platelets following hypoxic exercise (HE, 100 W under 12% O2 for 30 min)
Summary
Increased thrombin activity is an essential pathogenic process of cardiovascular diseases[8]. A previous study has indicated that exercise training decreased the coagulant factor expression and PS exposure of platelets and the shedding of procoagulant microparticles from platelets, thereby depressing dynamic TG in platelets[11]. Our investigation revealed that high-intensity interval exercise training (HIT) that consists of alternating mild-(40%VO2max) and high-(80%VO2max) intensity exercise significantly suppressed neutrophil-promoted blood coagulation by down-regulating expression of procoagulant factors under hypoxic condition[13]. We further hypothesize that HIT effectively reduces platelet-induced TG undergoing hypoxic stress, which is associated with alleviating platelet mitochondrial dysfunction cause by hypoxia. The aim of the present study is to establish an effective exercise strategy for improving individual aerobic capacity and simultaneously ameliorating the risk of platelet mitochondrial dysfunction and subsequent TG evoked by hypoxic stress
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