Physiological adaptations of stroke patients after high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) remain unclear. This study determined the HIIT and MICT effects on aerobic capacity, cerebral oxygenation, peak cardiac output (CO), and serum brain-derived neurotrophic factor (BDNF) in stroke patients. We included 23 stroke patients with age about 55 years and stroke duration>24 months; participants completed 36 sessions of exercise training for 30min; 13 were randomly assigned to perform MICT at 60% of peak oxygen consumption (VO2peak) and 10 to perform HIIT at alternating 80% (3min) and 40% (3min) VO2peak. Before and after interventions, we evaluated VO2peak, peak CO, arteriovenous oxygen difference (AV O2diff), bilateral frontal cortex oxygenation (relative changes of oxyhemoglobin Δ[O2Hb], deoxyhemoglobin Δ[HHb], and total hemoglobin Δ[THb] levels), serum brain-derived neurotrophic factor (BDNF) level, and fluorescent cell staining for neuron morphology and percentage of cell-bearing neurites (% neurites). HIIT induced significant increases in VO2peak (P=0.008), CO (P=0.038), Δ[HHb] (P=0.046), Δ[THb] (P=0.046), and serum BDNF level (P=0.012). The improvement in VO2peak was significantly greater with HIIT than MICT (20.7% vs. 9.8%, P=0.031), as was AV O2diff (P=0.041), Δ[HHb] (P=0.027), and serum BDNF level (P<0.001). HIIT facilitated neuron dendritic protrusions (greater % neurites, P=0.012) with prominent redistribution of mitochondria. As compared with MICT, HIIT-improved aerobic capacity by increasing systemic tissue O2 extraction in stroke patients. Increased cerebral O2 utilization in the involved hemisphere was also identified after HIIT. These physiological adaptations may be associated with increased serum BDNF level. In vitro dendritic growth in neurons treated with serum from HIIT participants may imply significant effects on neuron activities as compared with MICT. CLINICALTRIALS. NCT04135391.

Objective— Alternating shear stress, which resembles the flow condition in stenotic arteries, induces platelet aggregation. This study investigated how exercise training and deconditioning influence alternating shear-induced platelet aggregation (ASIPA) and clarify the mechanisms underlying ASIPA. Methods and Results— Thirty healthy male sedentary subjects were randomly divided into control and trained groups. The trained men were trained on a bicycle ergometer at ≈60% of maximal oxygen consumption for 30 minutes per day, 5 days per week for 8 weeks, and then were deconditioned for 8 weeks. The experimental results indicate the following: (1) short-term strenuous exercise increases the extent of ASIPA and is accompanied by increased the von Willebrand factor (vWF) binding and P-selectin expression on platelets in both the control and trained groups, whereas the enhancement of platelet function decreases after exercise training in trained subjects; (2) at rest and immediately after exercise, ASIPA and the vWF binding and P-selectin expression on platelets are reduced by training, but remain unchanged in the control group; and (3) deconditioning reverses the effects of training on resting and postexercise state. Conclusions— Exercise training suppresses the extent of ASIPA, probably by reducing vWF binding to platelets and P-selectin expression on platelets. However, deconditioning reverses the training effects.

Background: Age-related sarcopenia meaningfully increases the risks of functional limitations and mortality in the older adults. Although circulating microRNAs (c-miRNAs) are associated with aging-related cellular senescence and inflammation, the relationships between c-miRNAs and sarcopenia in the older adults remain unclear. This study investigates whether circulating myo-miRNAs and inflammation-related miRNAs are associated with sarcopenia in the older adults. Methods: This investigation recruited 77 eligible subjects (41 males and 36 females) from 597 community-dwelling older adults, and then divided them into normal (n = 24), dynapenic (loss of muscular function without mass, n = 35), and sarcopenic groups (loss of muscular function with mass, n = 18). Moreover, myo- (c-miRNA-133a and c-miRNA-486) and inflammation- (c-miRNA-21 and c-miRNA-146a) related miRNAs, as well as, inflammatory-related cytokine and peroxide levels in plasma were determined using quantitative polymerase chain reaction and ELISA, respectively. Results: Sarcopenic group exhibited lesser skeletal muscle mass index (SMI), handgrip strength, and gait speed, as well as, lower c-miR-486 and c-miR-146a levels, compared to those of normal and dynapenic groups. Moreover, c-miR-486 level was positively related to SMI (r = 0.334, P = 0.003), whereas c-miR-146a level was positively associated with SMI (r = 0.240, P = 0.035) and handgrip strength (r = 0.253, P = 0.027). In the receiver operating characteristic analysis for predicting sarcopenia, the area under the curve in c-miR-486 was 0.708 (95% confidence interval: 0.561–0.855, P = 0.008) and c-miR-146a was 0.676 (95% CI: 0.551–0.801, P = 0.024). However, no significant relationships were observed between SMI/handgrip strength/gait speed and plasma myeloperoxidase/interleukin-1훽/interleukin-6 levels. Conclusions: Myo-miRNA (c-miR-486) and inflammation-related miRNA (c-miR-146a) are superior to inflammatory peroxide/cytokines in plasma for serving as critical biomarkers of age-related sarcopenia.

Hypoxic preconditioning prevents cerebrovascular/cardiovascular disorders by increasing resistance to acute ischemic stress, but severe hypoxic exposure disturbs vascular hemodynamics. This study compared how various exercise regimens with/without hypoxia affect hemodynamics and oxygenation in cardiac, muscle, and cerebral tissues during severe hypoxic exposure. Sixty sedentary males were randomly divided into five groups. Each group ( n = 12) received one of five interventions: 1) normoxic (21% O₂) resting control, 2) hypoxic (15% O₂) resting control, 3) normoxic exercise (50% maximum work rate under 21% O₂; N-E group), 4) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O₂; H-RE group), or 5) hypoxic-absolute exercise (50% maximum work rate under 15% O₂; H-AE group) for 30 min/day, 5 days/wk, for 4 wk. A recently developed noninvasive bioreactance device was used to measure cardiac hemodynamics, and near-infrared spectroscopy was used to assess perfusion and oxygenation in the vastus lateralis (VL)/gastrocnemius (GN) muscles and frontal cerebral lobe (FC). Our results demonstrated that the H-AE group had a larger improvement in aerobic capacity compared with the N-E group. Both H-RE and H-AE ameliorated the suppression of cardiac stroke volume and the GN hyperemic response (Δtotal Hb/min) and reoxygenation rate by acute 12% O₂exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (Δtotal Hb) and O₂extraction [ΔdeoxyHb] of the VL muscle during the 12% O₂exercise. Although acute 12% O₂exercise decreased oxygenation (ΔO₂Hb) of the FC, none of the 4-wk interventions influenced the cerebral perfusion and oxygenation during normoxic/hypoxic exercise tests. Therefore, we conclude that moderate hypoxic exercise training improves cardiopulmonary fitness and increases resistance to disturbance of cardiac hemodynamics by severe hypoxia, concurrence with enhancing O₂delivery/utilization in skeletal muscles but not cerebral tissues.