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.

The inhibition of dipeptidyl peptidase-4 (DPP4) significantly enhances the wound closure rate in diabetic patients with chronic foot ulcers. DPP4 inhibitors are only prescribed for enteral, but topical administration, if feasible, to a wound would have more encouraging outcomes. Nanofibrous drug-eluting poly-D-L-lactide-glycolide (PLGA) membranes that sustainably release a high concentration of vildagliptin were prepared to accelerate wound healing in diabetes. Solutions of vildagliptin and PLGA in hexafluoroisopropanol were electrospun into nanofibrous biodegradable membranes. The concentration of the drug released in vitro from the vildagliptin-eluting PLGA membranes was evaluated, and it was found that effective bioactivity of vildagliptin can be discharged from the nanofibrous vildagliptin-eluting membranes for 30 days. Additionally, the electrospun nanofibrous PLGA membranes modified by blending with vildagliptin had smaller fiber diameters (336.0 ± 69.1 nm vs. 743.6 ± 334.3 nm, p < 0.001) and pore areas (3405 ± 1437 nm² vs. 8826 ± 4906 nm², p < 0.001), as well as a higher hydrophilicity value (95.2 ± 2.2° vs. 113.9 ± 4.9°, p = 0.004), and showed a better water-retention ability within 24 h compared with PLGA membranes. The vildagliptin-eluting PLGA membrane also enhanced the diabetic wound closure rate for two weeks (11.4 ± 3.0 vs. 18.7 ± 2.6 %, p < 0.001) and the level of the angiogenesis using CD31 expression (1.73 ± 0.39 vs. 0.45 ± 0.17 p = 0.006 for Western blot; 2.2 ± 0.5 vs. 0.7 ± 0.1, p < 0.001 for immunofluorescence). These results demonstrate that nanofibrous drug-eluting PLGA membranes loaded with vildagliptin are an effective agent for sustained drug release and, therefore, for accelerating cutaneous wound healing in the management of diabetic wounds.

It is important to use short breaks to accelerate post-exercise recovery in sports. Previous studies have revealed that vibration can reduce post-exercise muscle soreness. However, there is still high heterogeneity in the effects of vibration on cardiovascular autonomic activities, and most studies to date have focused on high-frequency vibration. This study aimed to investigate the effect of low-frequency lower-body vibration (LBV) on post-exercise changes in heart rate variability and peripheral arterial tone. Ten men and 9 women aged 20 to 25 were recruited for this study. Each subject visited the testing room three times with at least 2 days in between. Each time, the subject received one of the three different vibration frequencies (0, 5, and 15 Hz) in a random order in the sitting position for 10 minutes. LBV was performed immediately after a static standing (control) test and 3-min-step test. Heart rate variability and digital volume pulse wave were recorded during the vibration phase (V1: vibration 0-5 minutes; V2: 6-10 minutes) and the recovery phase (Rc1: recovery phase 11-15 minutes; Rc2: 16-20 minutes). The result of digital pulse wave analysis showed that the reflection index (RI) under 15 Hz decreased during V1. Heart rate of the 15-Hz group also decreased during Rc1 and Rc2. According to the analysis of heart rate variability, low-frequency power/high-frequency power (LF/HF) decreased and normalized high-frequency power (nHF) increased during V2, Rc1 and Rc2 under 15 Hz and, during Rc2 under 5 Hz vibration. This study confirmed that the application of low-frequency LBV after exercise can reduce peripheral vascular tone, accelerate heart rate recovery, decrease cardiac sympathetic nerve activity, and promote parasympathetic nerve activity. The effect was more pronounced at 15 Hz than at 5 Hz. The findings provide a method to accelerate cardiovascular autonomic recovery after exercise.

Cerebral tissue oxygen saturation (SctO₂) reflects cerebral perfusion and tissue oxygen consumption, which decline in some patients with heart failure with reduced ejection fraction (HFrEF) or stroke, especially during exercise. Its physiologic basis and clinical significance remain unclear. We aimed to investigate the association of SctO₂ with oxygen transport physiology and known prognostic factors during both rest and exercise in patients with HFrEF or stroke. Thirty-four HFrEF patients, 26 stroke patients, and 17 healthy controls performed an incremental cardiopulmonary exercise test using a bicycle ergometer. Integrated near-infrared spectroscopy and automatic gas analysis were used to measure cerebral tissue oxygenation and cardiac and ventilatory parameters. We found that SctO₂ (rest; peak) were significantly lower in the HFrEF (66.3±13.3%; 63.4±13.8%,) than in the stroke (72.1±4.2%; 72.7±4.5%) and control (73.1±2.8%; 72±3.2%) groups. In the HFrEF group, SctO₂ at rest (SctO_2rest) and peak SctO₂ (SctO_2peak) were linearly correlated with brain natriuretic peptide (BNP), peak oxygen consumption ( ), and oxygen uptake efficiency slope (r between -0.561 and 0.677, p < 0.001). Stepwise linear regression showed that SctO_2rest was determined by partial pressure of end-tidal carbon dioxide at rest (P_ETCO_2rest), hemoglobin, and mean arterial pressure at rest (MAP_rest) (adjusted R = 0.681, p < 0.05), while SctO_2peak was mainly affected by peak carbon dioxide production ( ) (adjusted R = 0.653, p < 0.05) in patients with HFrEF. In conclusion, the study delineates the relationship of cerebral saturation and parameters associated with oxygen delivery. Moreover, SctO_2peak and SctO_2rest are correlated with some well-recognized prognostic factors in HFrEF, suggesting its potential prognostic value.

This descriptive study aimed to explore the physiological factors that determine tolerance to exertion during high-intensity interval effort. Forty-seven young women (15–28 years old) were enrolled: 23 athletes from Taiwan national or national reserve teams and 24 moderately active females. Each participant underwent a maximal incremental INC (modified Bruce protocol) cardiopulmonary exercise test on the first day and high-intensity interval testing (HIIT) on the second day, both performed on a treadmill. The HIIT protocol involved alternation between 1-min effort at 120% of the maximal speed, at the same slope reached at the end of the INC, and 1-min rest until volitional exhaustion. Gas exchange, heart rate (HR), and muscle oxygenation at the right vastus lateralis, measured by near-infrared spectroscopy, were continuously recorded. The number of repetitions completed (R_lim) by each participant was considered the HIIT tolerance index. The results showed a large difference in the R_lim (range, 2.6–12.0 repetitions) among the participants. Stepwise linear regression revealed that the variance in the R_lim within the cohort was related to the recovery rates of oxygen consumption ( ), HR at the second minute after INC, and muscle tissue saturation index at exhaustion (R = 0.644). In addition, age was linearly correlated with R_lim (adjusted R = −0.518, p < 0.0001). In conclusion, the recovery rates for and HR after the incremental test, and muscle saturation index at exhaustion, were the major physiological factors related to HIIT performance. These findings provide insights into the role of the recovery phase after maximal INC exercise testing. Future research investigating a combination of INC and HIIT testing to determine training-induced performance improvement is warranted.