0000000000661222
AUTHOR
Esther Garcia-dominguez
Physical exercise in the prevention and treatment of Alzheimer's disease
Highlights • Low levels of physical activity are a risk factor associated with Alzheimer's disease. • Older adults who exercise are more likely to maintain cognition. • Exercise modulates amyloid β turnover, inflammation, synthesis, and release of neurotrophins, and cerebral blood flow.
Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction
Muscle repair without stem cells Skeletal muscle is a mechanical organ that endures cellular damage after contraction. Lesions caused by external injury can be repaired by muscle stem cells, which fuse with injured cells or create entirely new myofibers. Roman et al . describe a cell-autonomous repair process that is independent of muscle stem cells (see the Perspective by McNally and Demonbreun). After localized damage, myonuclei migrate to injury sites and locally deliver messenger RNA for cellular reconstruction. This myofiber self-repair represents a model for understanding the restoration of muscle architecture in health and disease. —BAP
Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.
Background: Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. Methods: Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigate…
Glucosamine Supplementation Improves Physical Performance in Trained Mice
Introduction D-Glucosamine (GlcN) is one of the most widely consumed dietary supplements and complementary medicines in the world and has been traditionally used to attenuate osteoarthritis in humans. GlcN extends lifespan in different animal models. In humans, its supplementation has been strongly associated with decreased total mortality and improved vascular endothelial function. GlcN acts as a suppressor of inflammation and by inhibiting glycolysis, it can activate the metabolism of stored fat and mitochondrial respiration. Methods The conventional human GlcN dose is 1,500 mg x day-1 but extensive evidence indicates that much higher doses are well tolerated. GlcN is one of the supplemen…
Redox-related biomarkers in physical exercise
Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake's group calculating the content of free radicals in skeletal muscle in resting conditions in 1954, many discoveries have been made in the field. The first section of this review is devoted to highlight the main research findings and fundamental changes in the exercise redox biology discipline. It includes: i) the first steps in free radical research, ii) the relation between exercise and oxidative damage, iii) the redox regulation of muscle fatigue, iv) the sources of free radicals during muscle contractions, and v) the role of reactive oxygen species as regulato…