Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Purpose: We aimed to compare individual hypertrophic responses to resistance training in which overload progressed either by adjusting the load (LOADProg) or by increasing the number of repetitions (REPSProg). Furthermore, we investigated whether greater responsiveness to one protocol was associated with chronic changes in myonuclei and satellite cells, proteolysis and extracellular matrix (ECM) remodeling biomarkers.
Methods: Thirty-seven untrained participants had their legs randomized into LOADProg and REPSProg and underwent 10 weeks of training. Muscle cross-sectional area (mCSA) ultrasound and muscle biopsies were performed pre- and post-training. Based on mCSA changes between protocols, we applied a criterion of 2 typical errors (5.7%) to create 4 clusters.
Results: Twelve participants (~ 34%) showed greater mCSA increases after REPSProg (14.2 ± 7.6%) than LOADProg (3.4 ± 8.7%, p = 0.004). Seven participants (~ 19%) responded better to LOADProg (21.5 ± 7.5% vs. 12 ± 7.5%, p = 0.041). Thirteen participants (~ 35%) showed no differences between protocols (p = 0.852). Five participants were nonresponders (mCSA changes smaller than the 5.7% threshold) for both protocols. There were no significant differences (p > 0.05) in myonuclear content, proteolysis, or ECM remodeling markers within any of the clusters. However, for those who responded better to REPSProg, this protocol promoted greater satellite cell changes (108.6 ± 77.0%) than LOADProg (48.9 ± 63.1%, p = 0.015).
Conclusion: Our findings suggest that overload progression models may influence individual responsiveness to RT-induced muscle hypertrophy. Additionally, progression through increased repetitions was associated with a chronic addition of satellite cells. However, responsiveness was not explained by chronic changes in myonuclei, proteolysis or ECM remodeling biomarkers.
Trial Registration: This study is registered in the Brazilian Registry of Clinical Trials (RBR-57v9mrb).
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s00421-025-05817-y | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
DNA methylation subtypes dictate metastatic heterogeneity of osteosarcoma via distinct tumor-stromal interactions: Multi-omics profiling and decitabine validation.
Int J Biol Macromol
September 2025
Faculty of Applied Sciences, Macao Polytechnic University, Macao. Electronic address:
Osteosarcoma (OS), the most prevalent primary bone malignancy in adolescents, is characterized by aggressive progression and early metastasis. However, the epigenetic drivers of its metastatic heterogeneity remain poorly understood. Herein, we integrated bulk DNA methylation profiling and single-cell RNA sequencing (scRNA-seq) to elucidate the epigenetic mechanisms driving OS metastatic heterogeneity.
View Article and Find Full Text PDFPrim-O-glucosylcimifugin attenuates intestinal fibrosis by modulating TGF-β/MAPK signaling and ECM remodeling.
Life Sci
September 2025
KM Convergence Research Division, Korea Institute of Oriental Medicine, Republic of Korea; Korean Convergence Medical Science Major, KIOM School, University of Science & Technology (UST), Daejeon, 34054, Republic of Korea. Electronic address:
Background: Intestinal fibrosis is a severe and progressive complication of inflammatory bowel disease (IBD), particularly Crohn's disease (CD), for which no effective anti-fibrotic therapies currently exist.
Purpose: This study aimed to investigate the anti-fibrotic efficacy and underlying mechanisms of Prim-O-glucosylcimifugin (POG), a natural chromone derivative, in TGF-β1-stimulated human intestinal fibroblasts.
Methods: Fibrosis was modeled in human intestinal fibroblast cell lines (CCD-18Co) and human primary intestinal myofibroblasts (HIMF) using TGF-β1.
Chemoselective Characterization of New Extracellular Matrix Deposition in Bioengineered Tumor Tissues.
Adv Mater
September 2025
Department of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA, 15213, USA.
In both native and engineered tissues, the extracellular matrix (ECM) supports and regulates nearly all aspects of cellular pathophysiology, and in response, cells extensively remodel their surrounding extracellular environments through new ECM protein deposition. Understanding this intricate bi-directional cell-ECM interaction is key to tissue engineering, but it remains challenging to investigate. This is partly due to the limited sensitivity of conventional proteomics to capture low-abundance newly synthesized ECM (newsECM).
View Article and Find Full Text PDFMechanosensitive biochemical imprinting of the talin interaction with DLC1 regulates RhoA activity and cardiomyocyte remodeling.
Sci Adv
September 2025
School of Engineering and Materials Science, Queen Mary University of London, UK.
During heart disease, the cardiac extracellular matrix (ECM) undergoes a structural and mechanical transformation. Cardiomyocytes sense the mechanical properties of their environment, leading to phenotypic remodeling. A critical component of the ECM mechanosensing machinery, including the protein talin, is organized at the cardiomyocyte costamere.
View Article and Find Full Text PDFIschemic stroke of undetermined source as a priming event for brain metastasis: a case report and systematic literature review.
Front Oncol
August 2025
Stroke Unit, Emergency Department, Umberto I Hospital, Sapienza University of Rome, Rome, Italy.
The association between ischemic stroke (IS) and malignancy is well established. Cancer-related strokes are predominantly embolic and classified as embolic strokes of undetermined source (ESUS). While malignancy-associated coagulopathy represents the primary pathogenic mechanism, neoplastic embolization of circulating tumor cells is another potential etiology, particularly in cases of cardiac and pulmonary malignancies.
View Article and Find Full Text PDF