scholarly journals Effects of Exercise and Aging on Skeletal Muscle

2017 ◽  
Vol 8 (3) ◽  
pp. a029785 ◽  
Author(s):  
Giovanna Distefano ◽  
Bret H. Goodpaster
2005 ◽  
Vol 35 (5) ◽  
pp. 413-427 ◽  
Author(s):  
Graeme L Close ◽  
Anna Kayani ◽  
Aphrodite Vasilaki ◽  
Anne McArdle

2010 ◽  
Vol 1800 (3) ◽  
pp. 223-234 ◽  
Author(s):  
Vladimir Ljubicic ◽  
Anna-Maria Joseph ◽  
Ayesha Saleem ◽  
Giulia Uguccioni ◽  
Melania Collu-Marchese ◽  
...  

2019 ◽  
Vol 81 (1) ◽  
pp. 19-41 ◽  
Author(s):  
David A. Hood ◽  
Jonathan M. Memme ◽  
Ashley N. Oliveira ◽  
Matthew Triolo

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.


2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Heather N Carter ◽  
Ayesha Saleem ◽  
Michael F.N. O'Leary ◽  
Olga Ostojic ◽  
David A. Hood

2016 ◽  
Vol 121 (5) ◽  
pp. 1053-1058 ◽  
Author(s):  
Koyal Garg ◽  
Marni D. Boppart

Skeletal muscle is endowed with a remarkable capacity for regeneration, primarily due to the reserve pool of muscle resident satellite cells. The satellite cell is the physiologically quiescent muscle stem cell that resides beneath the basal lamina and adjacent to the sarcolemma. The anatomic location of satellite cells is in close proximity to vasculature where they interact with other muscle resident stem/stromal cells (e.g., mesenchymal stem cells and pericytes) through paracrine mechanisms. This mini-review describes the components of the muscle stem cell niche, as well as the influence of exercise and aging on the muscle stem cell niche. Although exercise promotes ECM reorganization and stem cell accumulation, aging is associated with dense ECM deposition and loss of stem cell function resulting in reduced regenerative capacity and strength. An improved understanding of the niche elements will be valuable to inform the development of therapeutic interventions aimed at improving skeletal muscle regeneration and adaptation over the life span.


2014 ◽  
Vol 42 (4) ◽  
pp. 965-970 ◽  
Author(s):  
Brian McDonagh ◽  
Giorgos K. Sakellariou ◽  
Malcolm J. Jackson

Skeletal muscle represents a physiologically relevant model for the application of redox proteomic techniques to dissect its response to exercise and aging. Contracting skeletal muscles generate ROS (reactive oxygen species) and RNS (reactive nitrogen species) necessary for the regulation of many proteins involved in excitation–contraction coupling. The magnitude and species of ROS/RNS generated by contracting muscles will have downstream effects on specific protein targets and cellular redox signalling. Redox modifications on specific proteins are essential for the adaptive response to exercise and skeletal muscle can develop a dysregulated redox response during aging. In the present article, we discuss how redox proteomics can be applied to identify and quantify the reversible modifications on susceptible cysteine residues within those redox-sensitive proteins, and the integration of oxidative and non-oxidative protein modifications in relation to the functional proteome.


Author(s):  
D. E. Philpott ◽  
A. Takahashi

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.


Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.


Sign in / Sign up

Export Citation Format

Share Document