Background: Chronic low back pain (CLBP) is a common health problem. Pilates is a unique exercise therapy. This meta-analysis aims to evaluate the efficacy of Pilates on pain, functional disorders, and quality of life in patients with chronic low back pain (CLBP). Methods: PubMed, Web of Science, CNKI, VIP, Wanfang Data, CBM, EBSCO, and Embase were searched. Randomized controlled trials of Pilates in the treatment of CLBP were collected based on the inclusion and exclusion criteria. The meta-analysis was performed using RevMan 5.4 and Stata 12.2. Results: 19 randomized controlled trials with a total of 1108 patients were included. Compared with the controls, the results showed the following values: Pain Scale [standard mean difference; SMD = −1.31, 95%CI (−1.80, −0.83), p < 0.00001], Oswestry Disability Index (ODI) [mean difference; MD = −4.35, 95%CI (−5.77, −2.94), p < 0.00001], Roland–Morris Disability Questionnaire (RMDQ) [MD = −2.26, 95%CI (-4.45, −0.08), p = 0.04], 36-item Short-Form (SF-36) (Physical Function (PF) [MD = 5.09, 95%CI (0.20, 9.99), p = 0.04], Role Physical (RP) [MD = 5.02, 95%CI (−1.03, 11.06), p = 0.10], Bodily Pain (BP) [MD = 8.79, 95%CI (−1.57, 19.16), p = 0.10], General Health (GH) [MD = 8.45, 95%CI (−5.61, 22.51), p = 0.24], Vitality (VT) [MD = 8.20, 95%CI(−2.30, 18.71), p = 0.13], Social Functioning (SF) [MD = −1.11, 95%CI (−7.70, 5.48), p = 0.74], Role Emotional (RE) [MD = 0.86, 95%CI (−5.53, 7.25), p = 0.79], Mental Health (MH) [MD = 11.04, 95%CI (−12.51, 34.59), p = 0.36]), Quebec Back in Disability Scale (QBPDS) [MD = −5.51, 95%CI (−23.84, 12.81), p = 0.56], and the sit-and-reach test [MD = 1.81, 95%CI (−0.25, 3.88), p = 0.09]. Conclusions: This meta-analysis reveals that Pilates may have positive efficacy for pain relief and the improvement of functional disorders in CLBP patients, but the improvement in quality of life seems to be less obvious. Registration: PROSPERO CRD42022348173.

Mitochondria-associated endoplasmic reticulum membranes (MAMs) are important components of intracellular signaling and contribute to the regulation of intracellular Ca²⁺/lipid homeostasis, mitochondrial dynamics, autophagy/mitophagy, apoptosis, and inflammation. Multiple studies have shown that proteins located on MAMs mediate cardioprotection. Exercise preconditioning (EP) has been shown to protect the myocardium from adverse stimuli, but these mechanisms are still being explored. Recently, a growing body of evidence points to MAMs, suggesting that exercise or EP may be involved in cardioprotection by modulating proteins on MAMs and subsequently affecting MAMs. In this review, we summarize the latest findings on MAMs, analyzing the structure and function of MAMs and the role of MAM-related proteins in cardioprotection. We focused on the possible mechanisms by which exercise or EP can modulate the involvement of MAMs in cardioprotection. We found that EP may affect MAMs by regulating changes in MFN2, MFN1, AMPK, FUNDC1, BECN1, VDAC1, GRP75, IP3R, CYPD, GSK3β, AKT, NLRP3, GRP78, and LC3, thus playing a cardioprotective role. We also provided direction for future studies that may be of interest so that more in-depth studies can be conducted to elucidate the relationship between EP and cardioprotection.

Background: Sarcopenia is prevalent in older adults and affects their quality of life and overall health, low handgrip strength is one of the main manifestations of sarcopenia. Resistance training is an effective intervention for improving muscle strength in older adults, but the optimal dose of resistance training remains unclear. Therefore, the aim of this meta-analysis was to investigate the dose-response relationship between different doses of resistance training and grip strength in older adults.Methods: This systematic review and network meta-analysis included a search in PubMed, Embase, and the Cochrane Library for randomized controlled trials from inception to 19 October 2024 of resistance training for patients with senile sarcopenia. Comprehensive data extraction covered dose, resistance training protocol, demographics, and study duration. Systematic review with Bayesian network meta-analysis (NMA) methodology was employed and results were presented as 95% credible intervals (Crl).Results: A total of 13 studies involving 711 participants (mean age: 68.29 ± 5.30 years; mean BMI: 24.03 ± 3.43; female: 79.5%) were included in this study. The results of our network meta-analysis showed that resistance training variables (e.g., frequency, intensity, period, and training volume) were effective in improving handgrip strength in older patients with sarcopenia. Among them, the effective dose range for frequency of resistance training was 2–5 times/week, resistance training intensity was 30%–75%, resistance training period was 4–24 weeks, resistance training exercise was 3–17 exercises per set, resistance training repetitions was 10–24 reps, resistance training sets was 2–8 sets, resistance training volume was 528–2,200 reps per week. The optimal dose of resistance training to improve handgrip strength in older adults with sarcopenia is 3 times per week (MD = 7.02, 95% CrI [4.62, 9.42]), 49% 1RM (MD = 7.11, 95% CrI [2.69, 11.52]), 19 weeks (MD = 7.87, 95% CrI [3.89, 11.85]), 15 exercises (MD = 8.16, 95% CrI [3.65, 12.66]), 16 reps (MD = 7.62; 95% CrI [4.77, 10.46]), 6 sets (MD = 8.63; 95% CrI [5.06, 12.21]), 1,400 reps/week (MD = 8.45; 95% CrI [5.50, 11.40]).Conclusion: Resistance training effectively improves handgrip strength in older adults with sarcopenia. A recommended 19-week program includes 3 sessions per week at 49% 1RM, featuring 15 exercises per set, 6 sets, and 16 repetitions per exercise, totaling up to 1,400 reps weekly.Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/recorddashboard.

Background: The proportion of women is higher than men in depression. This is mainly due to women's physiological regulation is different from men, especially in puberty, menstruation, pregnancy, menopause, among others. Therefore, treating depressive women is still a health challenge. Besides, recent studies of exercise therapy have a more outstanding performance in treating depression, especially in contrast to drug therapy and psychotherapy. Its main advantages are convenience, quickness, no side effects, real-time, and long-term effectiveness. Objective: The aim of this study was to systematically review the clinical efficacy of exercise on women with depressive symptoms. Methods: Searching PubMed, The Cochrane Library, and Embase databases to collect randomized controlled trials about exercise in the treatment of depressive women. After literature screening, data extraction, and literature quality evaluation, the meta-analysis of acquirement data was performed with RevMan5.3 software. Results: A total of 2294 patients were included in 25 different articles totally. Meta-analysis shows that compared with the control group, exercise could relieve female depression (standard mean difference [95% confidence interval, CI] = −0.64 [−0.89 to −0.39], Z = 4.99, P < .001). Subgroup analysis shows that different types of exercise have significant effects in improving depression symptoms. Exercise therapy has better effect on depressive patients induced by physiology or disease than ordinary depressive patients. Conclusion: Exercise can significantly improve depressive symptoms in women.

Cardiovascular disease (CVD) remains a leading cause of death globally, posing a major public health challenge. Due to the complexity of CVD's etiology, understanding its pathogenesis has been a significant challenge and research focus. In recent years, the communication between organelles has gained increasing attention, with mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) emerging as a key structural component that facilitates dialogue between the mitochondria and the ER. Numerous studies have highlighted that proteins located in MAMs may play a role in the development of CVD. Among these, mitofusin 2 (MFN2), a protein found on the outer mitochondrial and ER membranes, has garnered particular interest due to its widespread presence in MAMs. This review aims to sort out current research on MFN2, focusing on its potential involvement in myocardial protection through its mediation of MAMs. We discuss how MFN2-mediated MAMs may contribute to the protection against various CVDs, including myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, dilated cardiomyopathy, pathological myocardial hypertrophy, cardiotoxicity, and heart failure. However, given the functional diversity of MFN2, the current body of research remains controversial, and further studies are urgently needed to clarify its precise mechanisms of action.

Cardiovascular disease (CVD) is a serious public health risk, and prevention and treatment efforts are urgently needed. Effective preventive and therapeutic programs for cardiovascular disease are still lacking, as the causes of CVD are varied and may be the result of a multifactorial combination. Mitophagy is a form of cell-selective autophagy, and there is increasing evidence that mitophagy is involved in cardioprotective processes. Recently, many studies have shown that FUN14 domain-containing protein 1 (FUNDC1) levels and phosphorylation status are highly associated with many diseases, including heart disease. Here, we review the structure and functions of FUNDC1 and the path-ways of its mediated mitophagy, and show that mitophagy can be effectively activated by dephosphorylation of Ser13 and Tyr18 sites, phosphorylation of Ser17 site and ubiquitination of Lys119 site in FUNDC1. By effectively activating or inhibiting excessive mitophagy, the quality of mitochondria can be effectively controlled. The main reason is that, on the one hand, improper clearance of mitochondria and accumulation of damaged mitochondria are avoided, and on the other hand, excessive mitophagy causing apoptosis is avoided, both serving to protect the heart. In addition, we explore the possible mechanisms by which FUNDC1-mediated mitophagy is involved in exercise preconditioning (EP) for cardioprotection. Finally, we also point out unresolved issues in FUNDC1 and its mediated mitophagy and give directions where further research may be needed.