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Lack of muscle fibre hypertrophy, myonuclear addition, and satellite cell pool expansion with resistance training in 83-94-year-old men and women.

If I recall correctly, I have heard some researchers suggest that sarcopenia can be completely avoided (or even successfully treated) with sufficient exercise and nutrition interventions. It's not clear whether this research group provided adequate nutritional intervention, but they reported that "12 weeks of heavy resistance training" was not sufficient to improve some muscle parameters in older men and women. To me, these results support the idea that age-related sarcopenia and frailty are caused by something other than inadequate exercise and nutrition.
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Decreased Sarcopenia in Aged Females with Young Ovary Transplants was Preserved in Mice that Received Germ Cell-Depleted Young Ovaries.

I recently reported on a study of ovary transplant in mice being associated with a significant lifespan extension (see PMID 30547325). The first and last author on that paper are the authors of this report, in which they state that ovarian transplantation in mice was also associated with "an improvement of body composition in both treatment groups" (those receiving ovaries with or without germ cells). I did not look into the full-text to determine exactly what they meant by this.
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Aging of the immune system causes reductions in muscle stem cell populations, promotes their shift to a fibrogenic phenotype, and modulates sarcopenia.

These results look remarkable; they suggest that old bone marrow cells have some sort of cell-intrinsic dysfunction (their transplantation into young mice reduced satellite cell number and promoted a fibrogenic phenotype). And some results suggested a cell-extrinsic dysfunction (conditioned media from young bone marrow cells promoted myoblast proliferation in vitro).
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Inhibition of the Activin Receptor Type-2B Pathway Restores Regenerative Capacity in Satellite Cell-Depleted Skeletal Muscle.

From scanning the introduction, this group appears to have explored the possibility of enhancing satellite cell regenerative ability for possible application in Duchenne muscular dystrophy. But assuming human aging is characterized by reduced satellite cell number, this technique might also be useful in human aging because that is partly what they tried to address here. One remarkable finding is that restoring the number of satellite cells appears to affect the tissue environment to enable better regeneration, suggesting a relation to parabiosis. In the introduction, they report: "We report here that treatment of satellite cell depleted muscle with an AcvR2B inhibitor prior to injury rescues regenerative potential concomitant with a near complete inhibition of ectopic fat formation and fibrosis. Using genetic lineage tracing, we found that the regenerated fibers originated from the residual pool of satellite cells in the satellite cell-depleted mice. These data reveal that a decline in satellite cells has a profound effect on the tissue environment compromising myogenic competence and that inhibition of the AcvR2B pathway restores the regenerative potential of a reduced satellite cell population."
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Is Iron Accumulation a Possible Risk Factor for Sarcopenia?

I don't recall seeing iron accumulation as a possible cause of sarcopenia. I retained this paper because the author asserts that iron accumulation has been found in skeletal muscle. Perhaps it is worth reading the study that reported this, which is probably mentioned in the full-text of this paper.
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Plasticity in central neural drive with short-term disuse and recovery – effects on muscle strength and influence of aging.

This group reports on some parameters of muscle function that deteriorate, and apparently do not easily recover, in older people, when they do recover in younger ones. They tested 4 days muscle disuse (immobilization) and subsequent active recovery, and observe that older people experience a greater decrease in voluntary muscle activation and muscle twitch force. These parameters are restored with active recovery in the young, but not in the older subjects.
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