To examine the effect of high-intensity interval training (HIIT) on metabolic syndrome (MetS) and body composition in cardiac rehabilitation (CR) patients with myocardial infarction (MI). We retrospectively screened 174 consecutive patients with MetS enrolled in CR following MI between 2015 and 2018. We included 56 patients who completed 36 CR sessions and pre-post dual-energy X-ray absorptiometry. Of these patients, 42 engaged in HIIT and 14 in moderate-intensity continuous training (MICT). HIIT included 4–8 intervals of high-intensity (30–60 s at RPE 15–17 [Borg 6–20]) and low-intensity (1–5 min at RPE < 14), and MICT included 20–45 min of exercise at RPE 12–14. MetS and body composition variables were compared between MICT and HIIT groups. Compared to MICT, HIIT demonstrated greater reductions in MetS (relative risk = 0.5, 95% CI 0.33–0.75, P < .001), MetS z-score (− 3.6 ± 2.9 vs. − 0.8 ± 3.8, P < .001) and improved MetS components: waist circumference (− 3 ± 5 vs. 1 ± 5 cm, P = .01), fasting blood glucose (− 25.8 ± 34.8 vs. − 3.9 ± 25.8 mg/dl, P < .001), triglycerides (− 67.8 ± 86.7 vs. − 10.4 ± 105.3 mg/dl, P < .001), and diastolic blood pressure (− 7 ± 11 vs. 0 ± 13 mmHg, P = .001). HIIT group demonstrated greater reductions in body fat mass (− 2.1 ± 2.1 vs. 0 ± 2.2 kg, P = .002), with increased body lean mass (0.9 ± 1.9 vs. − 0.9 ± 3.2 kg, P = .01) than the MICT. After matching for exercise energy expenditure, HIIT-induced improvements persisted for MetS z-score (P < .001), MetS components (P < .05), body fat mass (P = .002), body fat (P = .01), and lean mass (P = .03). Our data suggest that, compared to MICT, supervised HIIT results in greater improvements in MetS and body composition in MI patients with MetS undergoing CR.

Mounting evidence has firmly established that increased exercise capacity (EC) is associated with considerable improvements in the survival of patients with cardiovascular disease (CVD) and that antistress capacity is a prognostic predictor of adverse cardiovascular events in patients with CVD. Previous studies have indicated that aerobic exercise (AE) and supplementation with Rhodiola sacra (RS), a natural plant pharmaceutical, improve EC and enable resistance to stress; however, the underlying mechanism remains unclear. This study explored the ability of AE and RS, alone or combined, to improve EC and ameliorate exhaustive exercise‐ (EE‐) induced stress and elucidate the mechanism involved. We found that AE and RS significantly increased EC in mice and ameliorated EE‐induced stress damage in skeletal and cardiac muscles (SCM); furthermore, a synergistic effect was detected for the first time. To our knowledge, the present work is the first to report that AE and RS activate mitophagy, mitochondrial dynamics, and biogenesis in SCM, both in the resting state and after EE. These data indicate that AE and RS synergistically improve EC in mice and protect SCM from EE‐induced stress by enhancing mitochondrial quality control, including the activation of mitophagy, mitochondrial dynamics, and biogenesis, both at rest and after EE.

Exercise training has been demonstrated as an effective therapy for insulin resistance (IR) to relieve skeletal muscle metabolic disorders. Physiologic protective autophagy was found blocked by IR induced severe endoplasmic reticulum (ER) stress, which may lead to progression of IR. However, the mechanisms are not fully understood. Therefore, this study sought to investigate that how exercise training act on IR through an exploration into the mechanism of ER stress and high-fat diet (HFD)-blocked autophagy. A rodent model was adopted in mice via a HFD and an 8-week swim exercise training intervention. The mouse IR model was successfully established through HFD treatment: body mass, adipose weight, HOMA-IR index increased, as well as IRS1, inhibited in the muscle of HFD mice. Moreover, the AMPK/PGC1α pathway was depressed and IRE1, PERK, ATF6-related ER stress signaling was activated in the muscle of HFD mice. While autophagy factors, including BNIP3, LC3II/LC3I, and PINK1, decreased. However, additional 8-week exercise training during HFD was found to reverse all these changes and alleviate IR. Thus, exercise training could facilitate HFD-blocked protective autophagy via the activation of the AMPK/PGC1α pathway to relieve insulin resistance in mice. Our study provides experimental data for the prevention of T2DM and insulin resistance.