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"Although exercise is helpful in treating sarcopenia, it is not always a viable option clinically, and there are no pharmaceutical interventions for sarcopenia. " Here, we show that chronic treatment with pan-adiponectin receptor agonist AdipoRon enhanced muscle function in male mice by a mechanism related to muscle metabolism and tissue remodeling. In aged mice, AdipoRon therapy improved skeletal muscle function in vivo and ex vivo. In addition, the ability of AdipoRon to induce AMPK and PGC1a was preserved in nonhuman primate cultured cells. These results show that AdipoRon is an effective agent for sarcopenia in mice and show that its effects extend to primates, suggesting that it may also be a good drug for sarcopenia in clinical use. ".
Source link: https://doi.org/10.7554/eLife.71282
"Skeletal muscle is the primary tissue for maintaining glucose homeostasis through glucose uptake by insulin-dependent and -independent mechanisms. " Skeletal muscle is also sensitive to exercise-meditated glucose transport, and as a result, exercise is a foundation for glucose control in people with type 2 diabetes. A series of activities is required to achieve a slew of events. This report will investigate the physiology of each of these steps in healthy people, determine the causes of glucose elevations, and identify the causes by which exercise can raise glucose levels.
Source link: https://doi.org/10.3390/nu14030647
"Cardiovasomobility is a novel term that covers the integration of cardiovascular and skeletal muscle function in health and disease with a crucial change caused by physical activity or a lack thereof. " Physical fitness improves health, according to compliant results, but a sedentary, inactive, or inactive lifestyle contributes to cardiovascular and skeletal muscle dysfunction, which contributes to disease progression. Due to the inability of cross-sectional studies, finding causative factors for vascular and skeletal muscle abnormalities, particularly in humans, has been difficult. This review provides an overview of the experimental studies of disuse and inactivity, as well as the integrated responses of the vainculature and skeletal muscle in reaction to disuse/inactivity. Within the context of cardiovasomobility, experimental manipulation of physical activity provides valuable insight into the causes of vascular and skeletal muscle dysregulation that limit mobility, degrade quality of life, and hastented the onset of disease. ".
Source link: https://doi.org/10.1152/japplphysiol.00607.2021
"Skeletal muscle from the late gestation sheep fetus with intrauterine growth restriction has been shown to have reduced oxidative metabolism. " We tested the hypothesis that IUGR fetal skeletal muscle has reduced capacity for oxidative phosphorylation during late gestation using a sheep model of placental insufficiency and IUGR. We analyzed mitochondrial respiration in permeabilized muscle fibers from biceps femoris and soleus from control and IUGR fetal sheep.
Source link: https://doi.org/10.1152/ajpregu.00222.2021
"Skeletal muscle atrophy is a hallmark of significant spinal cord injury caused by neurological insult and paralysis. " Among many forms of disuse atrophy, including ubiquitin-proteasome signaling and others, signaling cascades that lead to SCI-induced muscle loss is common. The most effective muscle repair after severe SCI is combined with physical rehabilitation regimens and drugs targeting the underlying molecular pathways.
Source link: https://doi.org/10.1016/j.coph.2021.07.023
"We hypothesized that mice overexpressing calpastatin, an endogenous calpain reducer, solely in skeletal muscle," the aging muscle phenotype. Aging also reduced the diaphragm and EDL peak force in old WT mice by 48 percent and 23%, respectively, and decreased the force-time integral during a fatiguing protocol by 48 percent and 29 percent. In contrast, we found that CalpOX mice had a significant increase in diaphragm and EDL peak force in old mice, similar to that found in young mice. P = 0. 0006. NEW & NOTEWORTHY This is the first study to investigate the role of calpastatin overexpression in aging rodents. We found CalpOX mice from 20. 55 mo in WT mice to 24 mo in CalpOX mice.
Source link: https://doi.org/10.1152/japplphysiol.00883.2020
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