A map of the phosphoproteomic alterations that occur after a bout of maximal-intensity contractions. This was one of the first studies to quantify the extensive phosphorylation events that occur in human skeletal muscle in response to exercise. Global phosphoproteomic analysis of human skeletal muscle reveals a network of exercise-regulated kinases and AMPK substrates. Compensatory regulation of HDAC5 in muscle maintains metabolic adaptive responses and metabolism in response to energetic stress. Genetic impairment of AMPKα2 signaling does not reduce muscle glucose uptake during treadmill exercise in mice. Effects of α-AMPK knockout on exercise-induced gene activation in mouse skeletal muscle. Role of AMPKα2 in basal, training-, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle. Muscle hypertrophy in prediabetic men after 16 wk of resistance training. Divergent response of metabolite transport proteins in human skeletal muscle after sprint interval training and detraining. Effect of short-term training on GLUT-4 mRNA and protein expression in human skeletal muscle. Maintenance of skeletal muscle mitochondria in health, exercise, and aging. Fatal congenital heart glycogenosis caused by a recurrent activating R531Q mutation in the gamma 2-subunit of AMP-activated protein kinase (PRKAG2), not by phosphorylase kinase deficiency. Mutations in the gamma(2) subunit of AMP-activated protein kinase cause familial hypertrophic cardiomyopathy: evidence for the central role of energy compromise in disease pathogenesis. Isoform-specific and exercise intensity-dependent activation of 5’-AMP-activated protein kinase in human skeletal muscle. Plasma catecholamines and essential hypertension. Adrenaline increases skeletal muscle glycogenolysis, pyruvate dehydrogenase activation and carbohydrate oxidation during moderate exercise in humans. Exercise, GLUT4, and skeletal muscle glucose uptake. The role of CaMKII in regulating GLUT4 expression in skeletal muscle. This was the first study to quantify CaMKII activation in human skeletal muscle in response to exercise. Exercise increases Ca 2+-calmodulin-dependent protein kinase II activity in human skeletal muscle. Dual role of calmodulin in autophosphorylation of multifunctional CaM kinase may underlie decoding of calcium signals. AMPK: an energy-sensing pathway with multiple inputs and outputs. This study uncovered the exercise intensity-dependent activation of AMPK in human skeletal muscle. Effect of exercise intensity on skeletal muscle AMPK signaling in humans. Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle. Skeletal muscle hypertrophy after aerobic exercise training. Physiological basis of brief vigorous exercise to improve health. Concurrent exercise training: do opposites distract? J. Molecular mechanisms of muscle plasticity with exercise. Training for endurance and strength: lessons from cell signaling. T.) (American Physiological Society, 1996). Exercise: Regulation and Integration of Multiple Systems (eds Rowell, L. Exercise metabolism in 2016: health benefits of exercise - more than meets the eye! Nat. Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Lack of exercise is a major cause of chronic diseases. The possibility of designing therapeutic interventions based on these molecular mechanisms is addressed, using relevant examples that have exploited this approach.īooth, F. This Review provides an overview of the beneficial adaptive responses to exercise and details the molecular mechanisms involved. With this knowledge also comes the opportunity to design new therapeutic strategies based on the biology of exercise for a variety of chronic conditions where regular exercise might be a challenge. Our understanding of the epigenetic and transcriptional mechanisms that mediate the skeletal muscle gene expression response to exercise as well as of their upstream signalling pathways has advanced substantially in the past 10 years. This adaptive response increases oxidative capacity and influences the function of myokines and extracellular vesicles that signal to other tissues. The phenotypic alterations observed in skeletal muscle are partly mediated by transcriptional responses that occur following each individual bout of exercise. It is well appreciated that regular exercise improves metabolism and the metabolic phenotype in a number of tissues. Exercise is fundamental for good health, whereas physical inactivity underpins many chronic diseases of modern society.
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