Wu 2017 Sci Rep

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Wu LH, Chang SC, Fu TC, Huang CH, Wang JS (2017) High-intensity interval training improves mitochondrial function and suppresses thrombin generation in platelets undergoing hypoxic stress. Sci Rep 7:4191.

» PMID: 28646182 Open Access

Wu LH, Chang SC, Fu TC, Huang CH, Wang JS (2017) Sci Rep

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.


Bioblast editor: Kandolf G O2k-Network Lab: TW Taoyuan Wang JS


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Hypoxia  Organism: Human  Tissue;cell: Blood cells, Platelet  Preparation: Intact cells, Permeabilized cells 


Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, CIV, NS, ROX  HRR: Oxygraph-2k 

BMI, VO2max