This study elucidates how interval and continuous exercise regimens affect the mitochondrial functionality of lymphocytes under hypoxic stress. Sixty healthy sedentary males were randomly assigned to engage in either high-intensity interval training (HIIT, 3 min intervals at 80% and 40% VO_2max, n = 20) or moderate-intensity continuous training (MICT, sustained 60% VO_2max, n = 20) for 30 min/day, 5 days/week for 6 weeks or were assigned to a control group that did not receive exercise intervention (n = 20). Lymphocyte phenotypes/mitochondrial functionality under hypoxic exercise (HE, 100 W under 12% O₂) were determined before and after the various interventions. Before the intervention, HE (i) increased the mobilization of senescent (CD57⁺/CD28⁻) lymphocytes into the blood, (ii) decreased the ATP-linked O₂ consumption rate (OCR), the reserve capacity of OCR, and the citrate synthase activity in the mitochondria, and (iii) lowered the mitochondrial membrane potential (MP) and elevated the matrix oxidant burden (MOB) of lymphocytes. However, both HIIT and MICT significantly (i) decreased blood senescent lymphocyte counts, (ii) enhanced the mitochondrial OCR with increased citrate synthase and succinate dehydrogenase activities, (iii) increased mitochondrial MP and decreased MOB and (iv) increased the ratio of mitofusin to DRP-1 in lymphocytes after HE. Thus, we concluded that either HIIT or MICT effectively improves lymphocyte mitochondrial functionality by enhancing oxidative phosphorylation and suppressing oxidative damage under hypoxic conditions.

Introduction: Improved myocardial contractility is a critical circulatory adaptation to exercise training. However, the types of exercise that enhance left ventricular (LV) contractile and diastolic functions have not yet been established. This study investigated how high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) influence LV mechanics during exercise. Methods: Fifty-four healthy sedentary men were randomized to engage in either HIIT (3-min intervals at 40% and 80% of V˙O_2max, n = 18) or MICT (sustained 60% of V˙O_2max, n = 18) for 30 min·d⁻¹, 5 d·wk⁻¹ for 6 wk or to a control group (n = 18) that did not engage in exercise intervention. LV mechanics during semiupright bicycle exercise tests were measured by two-dimensional speckle-tracking echocardiography. Results: Before the interventions, acute bicycle exercise increased (i) peak basal/apical radial and circumferential and peak longitudinal strains and strain rates, (ii) peak basal/apical rotations and torsion, and (iii) peak systolic twisting and early diastolic untwisting velocities in the LV. After the interventions, the HIIT group exhibited greater LV mass and diastolic internal diameter as well as higher ratio of E wave to A wave and early diastolic propagation velocity than did the MICT group. Despite decreased peak apical rotation and torsion, HIIT enhanced peak apical radial strain and strain rate as well as shortened the time to reach peak untwisting velocity in the LV during exercise. However, the LV mechanics during exercise were unchanged in the control group. Conclusion: HIIT but not MICT induces eccentric myocardial hypertrophy. Moreover, HIIT effectively improves the LV mechanics during exercise by increasing contractile and diastolic functions.

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% VO_2peak for 30 min/day, 5 days/week for 4 weeks), and those remaining received only the TRP (control group). The peak exercise capacity (VO_2peak) 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 VO_2peak (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 VO_2peak 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.

Acute hypoxic exposure increases vascular thrombotic risk. The release of procoagulant-rich microparticles from neutrophils accelerates the pathogenesis of inflammatory thrombosis. The present study explicates the manner in which interval and continuous exercise regimens affect neutrophil-derived microparticle (NDMP) formation and neutrophil/NDMP-mediated thrombin generation (TG) under hypoxic condition. A total of 60 sedentary males were randomized to perform either aerobic interval training [AIT; 3-min intervals at 40% and 80% V̇O2max (maximal O2 consumption)] or moderate continuous training (MCT; sustained 60% V̇O2max) for 30 min/day, 5 days/week for 5 weeks, or to a control (CTL) group who did not receive any form of training. At rest and immediately after hypoxic exercise test (HE, 100 W under 12% O2 for 30 min), the NDMP characteristics and dynamic TG were measured by flow cytometry and thrombinography respectively. Before the intervention, HE (i) elevated coagulant factor VIII/fibrinogen concentrations and shortened activated partial thromboplastin time (aPTT), (ii) increased total and tissue factor (TF)-rich/phosphatidylserine (PS)-exposed NDMP counts and (iii) enhanced the peak height and rate of TG promoted by neutrophils/NDMPs. Following the 5-week intervention, AIT exhibited higher enhancement of V̇O2max than did MCT. Notably, both MCT and AIT attenuated the extents of HE-induced coagulant factor VIII/fibrinogen elevations and aPTT shortening. Furthermore, the two exercise regimens significantly decreased TF-rich/PS-exposed NDMP formation and depressed neutrophil/NDMP-mediated dynamic TG at rest and following HE. Hence, we conclude that AIT is superior to MCT for enhancing aerobic capacity. Moreover, either AIT or MCT effectively ameliorates neutrophil/NDMP-promoted TG by down-regulating expression of procoagulant factors during HE, which may reduce thrombotic risk evoked by hypoxia. Moreover, either AIT or MCT effectively ameliorates neutrophil/NDMP-promoted TG by down-regulating expression of procoagulant factors during HE, which may reduce thrombotic risk evoked by hypoxia.