scholarly journals SR Ca2+ leak in skeletal muscle fibers acts as an intracellular signal to increase fatigue resistance

2019 ◽  
Vol 151 (4) ◽  
pp. 567-577 ◽  
Author(s):  
Niklas Ivarsson ◽  
C. Mikael Mattsson ◽  
Arthur J. Cheng ◽  
Joseph D. Bruton ◽  
Björn Ekblom ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fatigue ◽  
Signaling Pathway ◽  
Fatigue Resistance ◽  
Endurance Exercise ◽  
Mitochondrial Biogenesis ◽  
Muscle Fibers ◽  
Oxidative Capacity ◽  
Pharmacological Agents ◽  
Skeletal Muscle Fibers

Effective practices to improve skeletal muscle fatigue resistance are crucial for athletes as well as patients with dysfunctional muscles. To this end, it is important to identify the cellular signaling pathway that triggers mitochondrial biogenesis and thereby increases oxidative capacity and fatigue resistance in skeletal muscle fibers. Here, we test the hypothesis that the stress induced in skeletal muscle fibers by endurance exercise causes a reduction in the association of FK506-binding protein 12 (FKBP12) with ryanodine receptor 1 (RYR1). This will result in a mild Ca2+ leak from the sarcoplasmic reticulum (SR), which could trigger mitochondrial biogenesis and improved fatigue resistance. After giving mice access to an in-cage running wheel for three weeks, we observed decreased FKBP12 association to RYR1, increased baseline [Ca2+]i, and signaling associated with greater mitochondrial biogenesis in muscle, including PGC1α1. After six weeks of voluntary running, FKBP12 association is normalized, baseline [Ca2+]i returned to values below that of nonrunning controls, and signaling for increased mitochondrial biogenesis was no longer present. The adaptations toward improved endurance exercise performance that were observed with training could be mimicked by pharmacological agents that destabilize RYR1 and thereby induce a modest Ca2+ leak. We conclude that a mild RYR1 SR Ca2+ leak is a key trigger for the signaling pathway that increases muscle fatigue resistance.

scholarly journals Exercise: Teaching myocytes new tricks

2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
Cardiac Phenotype ◽  
Endurance Exercise Training ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

scholarly journals Hsp60 in Skeletal Muscle Fiber Biogenesis and Homeostasis: From Physical Exercise to Skeletal Muscle Pathology

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 224 ◽  
Author(s):  
Antonella Marino Gammazza ◽  
Filippo Macaluso ◽  
Valentina Di Felice ◽  
Francesco Cappello ◽  
Rosario Barone
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Pathological Condition ◽  
Treatment Options ◽  
Muscle Fibers ◽  
Mitochondrial Protein ◽  
Oxidative Capacity ◽  
Skeletal Muscle Fiber ◽  
Muscle Pathology ◽  
Skeletal Muscle Fibers

Hsp60 is a molecular chaperone classically described as a mitochondrial protein with multiple roles in health and disease, participating to the maintenance of protein homeostasis. It is well known that skeletal muscle is a complex tissue, rich in proteins, that is, subjected to continuous rearrangements, and this homeostasis is affected by many different types of stimuli and stresses. The regular exercise induces specific histological and biochemical adaptations in skeletal muscle fibers, such as hypertrophy and an increase of mitochondria activity and oxidative capacity. The current literature is lacking in information regarding Hsp60 involvement in skeletal muscle fiber biogenesis and regeneration during exercise, and in disease conditions. Here, we briefly discuss the functions of Hsp60 in skeletal muscle fibers during exercise, inflammation, and ageing. Moreover, the potential usage of Hsp60 as a marker for disease and the evaluation of novel treatment options is also discussed. However, some questions remain open, and further studies are needed to better understand Hsp60 involvement in skeletal muscle homeostasis during exercise and in pathological condition.

scholarly journals Perm1 enhances mitochondrial biogenesis, oxidative capacity, and fatigue resistance in adult skeletal muscle

2015 ◽  
Vol 30 (2) ◽  
pp. 674-687 ◽  
Author(s):  
Yoshitake Cho ◽  
Bethany C. Hazen ◽  
Paulo G. Gandra ◽  
Samuel R. Ward ◽  
Simon Schenk ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatigue Resistance ◽  
Mitochondrial Biogenesis ◽  
Oxidative Capacity ◽  
Adult Skeletal Muscle
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