Intracellular signaling specificity in skeletal muscle in response to different modes of exercise

Nader, Gustavo A.; Esser, Karyn A.

doi:10.1152/jappl.2001.90.5.1936

Cited by 300 publications

(307 citation statements)

References 48 publications

(57 reference statements)

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“…Akt activity is increased in response to numerous stimuli, including a wide variety of growth factors and hormones activating phosphatidylinositol 3-kinase (PI3-kinase) (18)(19)(20). Akt can also be activated by mechanisms independent of PI3-kinasefor example, in response to increases in intracellular Ca 2+ or cAMP, as occurs with increased muscle contractile activity (21)(22)(23)(24)(25).…”

Section: Resultsmentioning

confidence: 99%

Musclin is an activity-stimulated myokine that enhances physical endurance

Subbotina

Sierra

Zhu

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

136

154

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Exercise remains the most effective way to promote physical and metabolic wellbeing, but molecular mechanisms underlying exercise tolerance and its plasticity are only partially understood. In this study we identify musclin-a peptide with high homology to natriuretic peptides (NP)-as an exercise-responsive myokine that acts to enhance exercise capacity in mice. We use human primary myoblast culture and in vivo murine models to establish that the activity-related production of musclin is driven by Ca 2+ -dependent activation of Akt1 and the release of musclin-encoding gene (Ostn) transcription from forkhead box O1 transcription factor inhibition. Disruption of Ostn and elimination of musclin secretion in mice results in reduced exercise tolerance that can be rescued by treatment with recombinant musclin. Reduced exercise capacity in mice with disrupted musclin signaling is associated with a trend toward lower levels of plasma atrial NP (ANP) and significantly smaller levels of cyclic guanosine monophosphate (cGMP) and peroxisome proliferator-activated receptor gamma coactivator 1-α in skeletal muscles after exposure to exercise. Furthermore, in agreement with the established musclin ability to interact with NP clearance receptors, but not with NP guanyl cyclase-coupled signaling receptors, we demonstrate that musclin enhances cGMP production in cultured myoblasts only when applied together with ANP. Elimination of the activity-related musclin-dependent boost of ANP/ cGMP signaling results in significantly lower maximum aerobic capacity, mitochondrial protein content, respiratory complex protein expression, and succinate dehydrogenase activity in skeletal muscles. Together, these data indicate that musclin enhances physical endurance by promoting mitochondrial biogenesis.osteocrin | mitochondria | skeletal muscle | exercise | natriuretic peptide

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Section: Resultsmentioning

confidence: 99%

Musclin is an activity-stimulated myokine that enhances physical endurance

Subbotina

Sierra

Zhu

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

136

154

View full text Add to dashboard Cite

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“…Therefore, we may have missed the peak activation of some or all proteins. However, endurance-type muscle contraction, which does not result in muscle hypertrophy, is also known to increase phosphorylation of p70S6K during the early phase of the recovery period but returns to basal level by 6 h after contraction (30). Similarly, the rat squat training model has also been used as an animal resistance exercise model, which results in increased anabolic signaling activity (4,11,25).…”

Section: Discussionmentioning

confidence: 99%

mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle

Ogasawara

Kobayashi

Tsutaki

et al. 2013

Journal of Applied Physiology

117

107

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“…Consistent with its role in regulation of protein synthesis, signaling through mTOR occurs in muscle after high force contractions/ mechanical loading and is maintained for many hours (18 -36 h) after a single bout of loading (10). In contrast, mTOR signaling is only transiently (Ͻ6 h) upregulated after low force contractions that do not elicit growth of skeletal muscle (10,73). Also considered in this review is that mTOR receives and integrates many different upstream signals that can function as either activators or inhibitors of activity and many of these upstream regulators are known to be active in muscle following mechanical loading.…”

Section: Mtor Signaling and Protein Synthesismentioning

confidence: 93%

Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals

Miyazaki

Esser²

2009

Journal of Applied Physiology

Self Cite

163

142

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Miyazaki M, Esser KA. Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals. J Appl Physiol 106: 1367-1373, 2009; doi:10.1152/japplphysiol.91355.2008.-Growth and maintenance of skeletal muscle mass is critical for long-term health and quality of life. Skeletal muscle is a highly adaptable tissue with well-known sensitivities to environmental cues such as growth factors, cytokines, nutrients, and mechanical loading. All of these factors act at the level of the cell and signal through pathways that lead to changes in phenotype through multiple mechanisms. In this review, we discuss the animal and cell culture models used and the signaling mechanisms identified in understanding regulation of protein synthesis in response to mechanical loading/resistance exercise. Particular emphasis has been placed on 1) alterations in mechanical loading and regulation of protein synthesis in both in vivo animal studies and in vitro cell culture studies and 2) upstream mediators regulating mammalian target of rapamycin signaling and protein synthesis during skeletal muscle hypertrophy. mechanical stretch; REDD2; overload; IGF-1; amino acids IT IS WIDELY ACCEPTED that repeated bouts of resistance exercise/ high-force contractions produce compensatory growth of skeletal muscle (35,42,47,95). The increase in skeletal muscle mass results from rates of protein synthesis increased more than changes in protein degradation with the net result being an accumulation of protein and increased fiber area (66,96). While the effect of resistance exercise/contraction on muscle mass has long been recognized, the mechanisms underlying the link between high resistance contractions and muscle growth are, to date, not fully understood.One of the important variables contributing to the growth response in skeletal muscle is the application of mechanical loading. For this review we use mechanical loading very generally as the application of force on the muscle or muscle cell. This force on the muscle can occur via active cross-bridge interactions (such as during concentric, isometric, or eccentric contractions) in a gravity-based environment or via external application of force such as passive stretching. The most established animal model for studying skeletal muscle hypertrophy in response to mechanical loading was described by Dr. A. L. Goldberg (38) and was referred to as work-induced muscle growth. This model is now commonly known as the synergist ablation/mechanical overload model and is a surgical model that involves cutting of the tendon and removal of the gastrocnemius muscle, resulting in loading and compensatory growth of the remaining plantar flexors, the plantaris, and soleus muscles. These muscles are involved in maintenance of posture and walking so are loaded by the body weight of the animal. Muscle mass changes are fairly rapid and the growth is robust, ranging from 40 to 200% depending on the muscle and species studied (7,37,38,53,56). Many labs use this model in their research programs to study mole...

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Intracellular signaling specificity in skeletal muscle in response to different modes of exercise

Cited by 300 publications

References 48 publications

Musclin is an activity-stimulated myokine that enhances physical endurance

Musclin is an activity-stimulated myokine that enhances physical endurance

mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle

Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals

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