Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging

2019 ◽  
Vol 81 (1) ◽  
pp. 19-41 ◽  
Author(s):  
David A. Hood ◽  
Jonathan M. Memme ◽  
Ashley N. Oliveira ◽  
Matthew Triolo
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Mitochondrial Function ◽  
High Functioning ◽  
Muscle Disuse ◽  
Skeletal Muscle Mitochondria ◽  
Single Bout ◽  
Atp Supply ◽  
And Function ◽  
Exercise And Aging

Mitochondria are critical organelles responsible for regulating the metabolic status of skeletal muscle. These organelles exhibit remarkable plasticity by adapting their volume, structure, and function in response to chronic exercise, disuse, aging, and disease. A single bout of exercise initiates signaling to provoke increases in mitochondrial biogenesis, balanced by the onset of organelle turnover carried out by the mitophagy pathway. This accelerated turnover ensures the presence of a high functioning network of mitochondria designed for optimal ATP supply, with the consequence of favoring lipid metabolism, maintaining muscle mass, and reducing apoptotic susceptibility over the longer term. Conversely, aging and disuse are associated with reductions in muscle mass that are in part attributable to dysregulation of the mitochondrial network and impaired mitochondrial function. Therefore, exercise represents a viable, nonpharmaceutical therapy with the potential to reverse and enhance the impaired mitochondrial function observed with aging and chronic muscle disuse.

Testosterone suppression does not exacerbate disuse atrophy and impairs muscle recovery that is not rescued by high protein

2020 ◽  
Vol 129 (1) ◽  
pp. 5-16 ◽  
Author(s):  
Erik D. Hanson ◽  
Andrew C. Betik ◽  
Cara A. Timpani ◽  
John Tarle ◽  
Xinmei Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adverse Effects ◽  
Muscle Mass ◽  
Caloric Intake ◽  
Disuse Atrophy ◽  
Muscle Recovery ◽  
Testosterone Levels ◽  
Muscle Disuse ◽  
Low Testosterone ◽  
And Function

Low testosterone levels during skeletal muscle disuse did not worsen declines in muscle mass and function, although hypogonadism may attenuate recovery during subsequent reloading. Diets high in casein did not improve outcomes during immobilization or reloading. Practical strategies are needed that do not compromise caloric intake yet provide effective protein doses to augment these adverse effects.

Denervation-induced mitochondrial dysfunction and autophagy in skeletal muscle of apoptosis-deficient animals

2012 ◽  
Vol 303 (4) ◽  
pp. C447-C454 ◽  
Author(s):  
Michael F. N. O′Leary ◽  
Anna Vainshtein ◽  
Heather N. Carter ◽  
Yuan Zhang ◽  
David A. Hood
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Mass ◽  
Contractile Activity ◽  
Double Knockout ◽  
Muscle Disuse ◽  
Subsarcolemmal Mitochondria ◽  
And Function ◽  
Species Production ◽  
Potential Signal

Skeletal muscle undergoes remarkable adaptations in response to chronic decreases in contractile activity, such as a loss of muscle mass, decreases in both mitochondrial content and function, as well as the activation of apoptosis. Although these adaptations are well known, questions remain regarding the signaling pathways that mediated these changes. Autophagy is an organelle turnover pathway that could contribute to these adaptations. The purpose of this study was to determine whether denervation-induced muscle disuse would result in the activation of autophagy gene expression in both wild-type (WT) and Bax/Bak double knockout (DKO) animals, which display an attenuated apoptotic response. Denervation caused a reduction in muscle mass for WT and DKO animals; however, there was a 40% attenuation in muscle atrophy in DKO animals. Mitochondrial state 3 respiration was significantly reduced, and reactive oxygen species production was increased by two- to threefold in both WT and DKO animals. Apoptotic markers, including cytosolic AIF and DNA fragmentation, were elevated in WT, but not in DKO animals following denervation. Autophagy proteins including LC3II, ULK1, ATG7, p62, and Beclin1 were increased similarly following denervation for both WT and DKO. Interestingly, denervation markedly increased the localization of LC3II to subsarcolemmal mitochondria, and this was more pronounced in the DKO animals. Thus denervation-induced muscle disuse activates both apoptotic and autophagic signaling pathways in muscle, and autophagic protein expression does not exhibit a compensatory increase in the presence of attenuated apoptosis. However, the absence of Bax and Bak may represent a potential signal to trigger mitophagy in muscle.

scholarly journals Subpopulation-specific differences in skeletal muscle mitochondria in humans with obesity: insights from studies employing acute nutritional and exercise stimuli

2020 ◽  
Vol 318 (4) ◽  
pp. E538-E553
Author(s):  
Nisreen Wahwah ◽  
Katon A. Kras ◽  
Lori R. Roust ◽  
Christos S. Katsanos
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Subcellular Location ◽  
Metabolic Dysfunction ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Experimental Approaches ◽  
And Function

Mitochondria from skeletal muscle of humans with obesity often display alterations with respect to their morphology, proteome, biogenesis, and function. These changes in muscle mitochondria are considered to contribute to metabolic abnormalities observed in humans with obesity. Most of the evidence describing alterations in muscle mitochondria in humans with obesity, however, lacks reference to a specific subcellular location. This is despite data over the years showing differences in the morphology and function of subsarcolemmal (found near the plasma membrane) and intermyofibrillar (nested between the myofibrils) mitochondria in skeletal muscle. Recent studies reveal that impairments in mitochondrial function in obesity with respect to the subcellular location of the mitochondria in muscle are more readily evident following exposure of the skeletal muscle to physiological stimuli. In this review, we highlight the need to understand skeletal muscle mitochondria metabolism in obesity in a subpopulation-specific manner and in the presence of physiological stimuli that modify mitochondrial function in vivo. Experimental approaches employed under these conditions will allow for more precise characterization of impairments in skeletal muscle mitochondria and their implications in inducing metabolic dysfunction in human obesity.

scholarly journals Skeletal muscle mitochondrial respiration in a model of age-related osteoarthritis is impaired after dietary rapamycin

2021 ◽  
Author(s):  
Christian J Elliehausen ◽  
Dennis M Minton ◽  
Alexander D Nichol ◽  
Adam R Konopka
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Guinea Pigs ◽  
Muscle Size ◽  
Skeletal Muscle Mitochondria ◽  
Age Related ◽  
End Stage ◽  
And Function ◽  
Permeabilized Muscle

A decline in skeletal muscle mitochondrial function is associated with the loss of skeletal muscle size and function during knee osteoarthritis (OA). We have recently reported that the 12-weeks of dietary rapamycin (Rap, 14ppm), with or without metformin (Met, 1000ppm), increased plasma glucose and OA severity in male Dunkin Hartley (DH) guinea pigs, a model of naturally occurring, age-related OA. The purpose of the current study was to determine if increased OA severity after dietary Rap and Rap+Met was accompanied by impaired skeletal muscle mitochondrial function. Mitochondrial respiration and hydrogen peroxide (H2O2) emissions were evaluated in permeabilized muscle fibers via high-resolution respirometry and fluorometry using either a saturating bolus or titration of ADP. Rap and Rap+Met decreased complex I (CI)-linked respiration and increased ADP sensitivity, consistent with previous findings in patients with end-stage OA. Rap also tended to decrease mitochondrial H2O2 emissions, however, this was no longer apparent after normalizing to respiration. The decrease in CI-linked respiration was accompanied with lower CI protein abundance. This is the first inquiry into how lifespan extending treatments Rap and Rap+Met can influence skeletal muscle mitochondria in a model of age-related OA. Collectively, our data suggest that Rap with or without Met inhibits CI-linked capacity and increases ADP sensitivity in DH guinea pigs that have greater OA severity.

scholarly journals NEUROMUSCULAR CHANGES WITH AGING AND SARCOPENIA

2018 ◽  
pp. 1-3
Author(s):  
B.C. Clark
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Function ◽  
Skeletal Muscle Mass ◽  
The Past ◽  
Conceptual Definition ◽  
Age Related ◽  
Per Se ◽  
Definition Of ◽  
And Function

Sarcopenia was originally conceptualized as the age-related loss of skeletal muscle mass. Over the ensuing decades, the conceptual definition of sarcopenia has changed to represent a condition in older adults that is characterized by declining muscle mass and function, with “function” most commonly conceived as muscle weakness and/or impaired physical performance (e.g., slow gait speed). Findings over the past 15-years, however, have demonstrated that changes in grip and leg extensor strength are not primarily due to muscle atrophy per se, and that to a large extent, are reflective of declines in the integrity of the nervous system. This article briefly summarizes findings relating to the complex neuromuscular mechanisms that contribute to reductions in muscle function associated with advancing age, and the implications of these findings on the development of effective therapies.

scholarly journals Sarcopenia in women with hip fracture: A comparison of hormonal biomarkers and their relationship to skeletal muscle mass and function

2020 ◽  
Vol 6 (3) ◽  
pp. 139-145
Author(s):  
Ming Li Yee ◽  
Raphael Hau ◽  
Alison Taylor ◽  
Mark Guerra ◽  
Peter Guerra ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Hip Fracture ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
And Function

scholarly journals Absence of insulin signalling in skeletal muscle is associated with reduced muscle mass and function: evidence for decreased protein synthesis and not increased degradation

AGE ◽  
2010 ◽  
Vol 32 (2) ◽  
pp. 209-222 ◽  
Author(s):  
Elaine D. O’Neill ◽  
John P. H. Wilding ◽  
C. Ronald Kahn ◽  
Holly Van Remmen ◽  
Anne McArdle ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Insulin Signalling ◽  
And Function
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