Muscle mass and strength are very important for exercise performance. Training-induced musculoskeletal injuries usually require periods of complete immobilization to prevent any muscle contraction of the affected muscle groups. Disuse muscle wasting will likely affect every sport practitioner in his or her lifetime. Even short periods of disuse results in significant declines in muscle size, fiber cross sectional area, and strength. To understand the molecular signaling pathways involved in disuse muscle atrophy is of the utmost importance to develop more effective countermeasures in sport science research. We have divided our review in four different sections. In the first one we discuss the molecular mechanisms involved in muscle atrophy including the main protein synthesis and protein breakdown signaling pathways. In the second section of the review we deal with the main cellular, animal, and human atrophy models. The sources of reactive oxygen species in disuse muscle atrophy and the mechanism through which they regulate protein synthesis and proteolysis are reviewed in the third section of this review. The last section is devoted to the potential interventions to prevent muscle disuse atrophy with especial consideration to studies on which the levels of endogenous antioxidants enzymes or dietary antioxidants have been tested.
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http://dx.doi.org/10.1016/j.redox.2020.101531 | DOI Listing |
Cureus
December 2024
Department of Rehabilitation Medicine, School of Medicine, Showa University, Tokyo, JPN.
Tetanus is a rare but life-threatening neurological disorder caused by neurotoxins produced by . Although mortality rates have significantly decreased with modern intensive care, severe cases remain challenging due to prolonged Intensive Care Unit (ICU) stays, complications, and rehabilitation barriers. We report the case of an 81-year-old male with a history of hypertension and femoral neck fracture who developed severe tetanus following a contaminated forehead laceration.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Aerospace Medical Training, School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Skeletal muscle atrophy, which is induced by factors such as disuse, spaceflight, certain medications, neurological disorders, and malnutrition, is a global health issue that lacks effective treatment. Hindlimb unloading is a commonly used model of muscle atrophy. However, the underlying mechanism of muscle atrophy induced by hindlimb unloading remains unclear, particularly from the perspective of the myocyte proteome and metabolism.
View Article and Find Full Text PDFHead Neck
January 2025
Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
Background: Radiotherapy (RT) in head and neck cancer (HNC) can cause multiple side effects such as nausea, pain, taste loss, fatigue, oral mucositis, xerostomia, and acute radiation-associated dysphagia (RAD). These factors threaten patients' oral intake (OI) during this RT. Reduced OI can cause weight loss, dehydration, malnutrition, and various comorbidities.
View Article and Find Full Text PDFSports Med
January 2025
School of Behavioural and Health Sciences, Australian Catholic University, Melbourne, VIC, Australia.
Following anterior cruciate ligament (ACL) injury, quadriceps muscle atrophy persists despite rehabilitation, leading to loss of lower limb strength, osteoarthritis, poor knee joint health and reduced quality of life. However, the molecular mechanisms responsible for these deficits in hypertrophic adaptations within the quadriceps muscle following ACL injury and reconstruction are poorly understood. While resistance exercise training stimulates skeletal muscle hypertrophy, attenuation of these hypertrophic pathways can hinder rehabilitation following ACL injury and reconstruction, and ultimately lead to skeletal muscle atrophy that persists beyond ACL reconstruction, similar to disuse atrophy.
View Article and Find Full Text PDFFront Sports Act Living
January 2025
Department of Physical Therapy, University of Nevada, Las Vegas, Las Vegas, NV, United States.
Introduction: In individuals with chronic post-stroke hemiparesis, slow walking speed is a significant concern related to inadequate propulsion of the paretic limb. However, an overlooked factor is this population's altered morphology of the Achilles tendon, which may compromise the propulsive forces by the paretic limb. This study aimed to explore changes in Achilles tendon morphology, including gross thickness and intra-tendinous collagen fiber bundle organization, following stroke-induced brain lesions.
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