Purpose: Acute high-intensity unaccustomed eccentric exercise performed by naive subjects is accompanied by disturbances in muscle damage biomarkers. The aim of the study was to investigate whether a causal relationship indeed exists between eccentric exercise and muscle damage.
Methods: Twenty-four men randomly assigned into a concentric only or an eccentric-only training group and performed 10 weeks of isokinetic resistance exercise (one session/week of 75 maximal knee extensors actions). Physiological markers of muscle function and damage (i.e., range of motion, delayed onset muscle soreness, isometric, concentric and eccentric peak torque) were assessed prior to and 1-3 and 5 days post each session. Biochemical markers of muscle damage (creatine kinase) and inflammation (C-reactive protein) were measured prior and 2 days post each session.
Results: After the first bout, eccentric exercise induced greater muscle damage compared to concentric exercise; however, during the nine following sessions, this effect progressively diminished, while after the 10th week of training, no alterations in muscle damage biomarkers were observed after either exercise protocol. Additionally, strength gains at the end of the training period were comparable between the two groups and were mode-specific.
Conclusion: (1) eccentric exercise per se does not affect muscle damage biomarkers; (2) muscle damage occurs as a result of muscle unaccustomedness to this action type; (3) exercise-induced muscle damage is not a prerequisite for increased muscle strength. Collectively, we believe that muscle unaccustomedness to high-intensity eccentric exercise, and not eccentric exercise per se, is the trigger for muscle damage as indicated by muscle damage biomarkers.
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Sci Rep
January 2025
Clinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, 213 Borowska St, Wroclaw, 50-556, Poland.
Oxidative stress is proven to increase cardiovascular risk and to diminish healthy life expectancy. Sleep bruxism (SB) is a prevalent masticatory muscle activity during sleep characterized by heterogeneous etiology and inadequately recognized pathophysiology. Recent theories have proposed a potential association between SB and oxidative stress.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, Republic of Korea.
Background: The cellular prion protein (PrP), a glycoprotein encoded by the PRNP gene, is known to modulate muscle mass and exercise capacity. However, the role of PrP in the maintenance and regeneration of skeletal muscle during ageing remains unclear.
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Biomater Transl
November 2024
Organoid Research Center, Institute of Translational Medicine, Shanghai University, Shanghai, China.
The skeletal system, composed of bones, muscles, joints, ligaments, and tendons, serves as the foundation for maintaining human posture, mobility, and overall biomechanical functionality. However, with ageing, chronic overuse, and acute injuries, conditions such as osteoarthritis, intervertebral disc degeneration, muscle atrophy, and ligament or tendon tears have become increasingly prevalent and pose serious clinical challenges. These disorders not only result in pain, functional loss, and a marked reduction in patients' quality of life but also impose substantial social and economic burdens.
View Article and Find Full Text PDFCase Rep Crit Care
January 2025
Department of Anesthesiology and Intensive Care Medicine, Kreiskliniken Günzburg-Krumbach, Krumbach, Germany.
Drug-induced rhabdomyolysis has become increasingly prevalent due to the rising use of medications such as statins, antidepressants, and antipsychotics. These can lead to muscle cell destruction and the release of myoglobin, potentially causing kidney damage. Recent advancements include the use of CytoSorb hemoadsorption as a promising therapy to remove myoglobin and other potentially toxic substances from the bloodstream.
View Article and Find Full Text PDFJ Ginseng Res
January 2025
College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
DNA damage is a driver of cancer formation, leading to the impairment of repair mechanisms in cancer cells and rendering them susceptible to DNA-damaging therapeutic approaches. The concept of "synthetic lethality" in cancer clinics has emerged, particularly with the use of PARP inhibitors and the identification of DNA damage response (DDR) mutation biomarkers, emphasizing the significance of targeting DDR in cancer therapy. Novel approaches aimed at genome maintenance machinery are under development to further enhance the efficacy of cancer treatments.
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