muscle loss (sarcopenia)
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Calorie restriction and periodic fasting has been shown to ameliorate the age-related loss of muscle mass (sarcopenia).


Long-Term Calorie Restriction Enhances Cellular Quality-Control Processes in Human Skeletal Muscle.

Cell Rep. 2016 Jan 26;14(3):422-8. doi: 10.1016/j.celrep.2015.12.042. Epub 2016 Jan 7.
Yang L1, Licastro D2, Cava E3, Veronese N4, Spelta F5, Rizza W6, Bertozzi B7,
Villareal DT8, Hotamisligil GS1, Holloszy JO7, Fontana L9.
 
Calorie restriction (CR) retards aging, acts as a hormetic intervention, and increases
serum corticosterone and HSP70 expression in rodents. 
However, less is known regarding
the effects of CR on these factors in humans. Serum cortisol and molecular
chaperones and autophagic proteins 
were measured in the skeletal muscle of subjects on CR diets for 3-15 years and in control volunteers. Serum cortisol was higher in the CR group than in age-matched sedentary and endurance athlete groups (15.6 ± 4.6 ng/dl versus 12.3 ± 3.9 ng/dl and 11.2 ± 2.7 ng/dl, respectively; p ≤ 0.001).  HSP70, Grp78,
beclin-1, and LC3 mRNA and/or protein levels were higher in the skeletal muscle of the CR group compared to controls.
 
Our data indicate that CR in humans is associated with sustained rises in serum cortisol, reduced inflammation, and increases in key molecular 
chaperones and autophagic mediators involved in cellular protein quality control and removal of dysfunctional proteins and organelles.


Caloric restriction delays aging-induced cellular phenotypes in rhesus monkey skeletal muscle.
Exp Gerontol. 2010 Sep 29.
McKiernan SH, Colman RJ, Lopez M, Beasley TM, Aiken JM, Anderson RM, Weindruch R.
Wisconsin National Primate Research Center, University of Wisconsin, Madison, WI 53715, United States; Department of Kineseology, University of Wisconsin, Madison, WI 53706, United States.
Sarcopenia is the age-related loss of skeletal muscle mass and function and is characterized by a reduction in muscle mass and fiber cross-sectional area, alterations in muscle fiber type and mitochondrial functional changes. In rhesus monkeys, calorie restriction (CR) without malnutrition improves survival and delays the onset of age-associated diseases and disorders including sarcopenia. We present a longitudinal study on the impact of CR on early stage sarcopenia in the upper leg of monkeys from ~16years to ~22years of age. Using dual-energy X-ray absorptiometry we show that CR delayed the development of maximum muscle mass and, unlike Control animals, muscle mass of the upper leg was preserved in CR animals during early phase sarcopenia. Histochemical analyses of vastus lateralis muscle biopsies revealed that CR opposed age-related changes in the proportion of Type II muscle fibers and fiber cross-sectional area. In contrast the number of muscle fibers with mitochondrial electron transport system enzyme abnormalities (ETS(ab)) was not significantly affected by CR. Laser capture microdissection of ETS(ab) fibers and subsequent PCR analysis of the mitochondrial DNA revealed large deletion mutations in fibers with abnormal mitochondrial enzyme activities. CR did not prevent stochastic mitochondrial deletion mutations in muscle fibers but CR may have contributed to the maintenance of affected fibers.

Sarcopenia of aging: underlying cellular mechanisms and protection by calorie restriction.
Biofactors. 2009 Jan-Feb;35(1):28-35.
Marzetti E, Anne Lees H, Eva Wohlgemuth S, Leeuwenburgh C.
Department of Aging and Geriatric Research, Institute on Aging, Division of Biology of Aging, University of Florida, Gainesville, FL 32610, USA.
Sarcopenia, the loss of muscle mass and function, is a common feature of aging and impacts on individual health and quality of life. Several cellular mechanisms have been involved in the pathogenesis of this syndrome, including mitochondrial dysfunction, altered apoptotic and autophagic signaling, and, more recently, trace metal dyshomeostasis. Calorie restriction (CR) without malnutrition has been shown to ameliorate the age-related loss of muscle mass in a variety a species. Mechanisms of protection span from preservation of mitochondrial functional and structural integrity to mitochondrial biogenesis, reduction of oxidative stress, and favorable modulation of apoptotic and autophagic signaling pathways. Importantly, preliminary evidence indicates that moderate CR may promote muscle mitochondrial biogenesis in middle-aged human subjects. Further research is warranted to investigate whether CR may represent a safe and efficient strategy to delay the onset and mitigate the progression of sarcopenia in older adults.











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