Purpose Low-intensity resistance training combined with blood flow restriction (LIBFR) has been proposed as an alternative to conventional resistance training, but its effects on bone metabolism remain unclear. This review compared LIBFR with high-intensity resistance training (HIRT), low-intensity resistance training (LIRT) and non-exercise on bone formation and resorption markers and bone mineral density (BMD). Methods MEDLINE (PubMed), Cochrane Library (CENTRAL), EMBASE, APA and Global Health (EBSCO) were searched up to 20th May 2026 for clinical trials in adults assessing bone-specific alkaline phosphatase (BSAP), cross-linked C-telopeptides of type I collagen (CTX-I) or BMD. Risk of bias was assessed with RoB 2 and certainty of evidence with GRADE. Meta-analyses were performed where applicable. Results Eight studies (nine reports; n = 211 participants) were included. Compared with HIRT, LIBFR resulted in significantly lower BSAP (MD = −2.72 [95% CI −5.17 to −0.28]) and CTX-I (MD = −0.08 [95% CI −0.13 to −0.03]), with no difference in BMD. Compared with LIRT, BSAP and CTX-I did not differ, but BMD was significantly higher in a single study (MD = 0.04 [95% CI 0.03 to 0.05]). Compared with non-exercise, LIBFR significantly reduced CTX-I and BMD, with no difference in BSAP. The certainty of evidence was very low for all comparisons. Conclusion LIBFR reduced BSAP and CTX-I compared with HIRT, and CTX-I compared with non-exercise. BMD findings were mixed: higher versus LIRT, similar versus HIRT and lower versus non-exercise. Given the very low certainty of evidence, these findings should be interpreted with caution.
Purpose Atrial fibrosis is a key structural substrate of atrial fibrillation and atrial cardiomyopathy. Thrombospondin-1 (TSP-1) and thrombospondin-2 (TSP-2) regulate TGF-β signaling and matrix organization, but their roles in human atrial remodeling remain incompletely understood. Therefore, this study aimed to compare atrial TSP-1 and TSP-2 expression in mitral and aortic valve disease and examine their associations with fibrosis, inflammation, and adhesion-related remodeling. Methods This observational cross-sectional study included 67 cardiac surgery patients: 30 with mitral valve disease, 23 with aortic valve disease, and 14 undergoing coronary artery bypass grafting without significant valvular disease. Left and right atrial tissues were examined using RT-qPCR, ELISA, histology, and immunofluorescence. Molecular assays used pooled tissue preparations. Systemic inflammation was evaluated using the neutrophil-to-lymphocyte ratio. Results TSP-1 and TSP-2 transcript levels were increased in both valve disease groups, alongside greater collagen deposition and increased inflammatory gene expression. Transcript changes were particularly marked in left atrial tissue from patients with mitral valve disease. TSP-1 protein was significantly increased in right atrial tissue from the mitral valve group, whereas TSP-2 protein did not differ significantly between groups. Cadherin transcript levels were also altered. The neutrophil-to-lymphocyte ratio was higher in both valve disease groups than in the surgical comparator group. Conclusions Atrial TSPs expression was associated with fibrotic and inflammatory remodeling in valvular heart disease. Differences between transcript and protein findings and the use of pooled preparations warrant cautious interpretation. These observational findings require validation in independent cohorts and do not establish causality.
