Aging begins long before evident loss of function arises. As researchers point out here, efforts to better map and intervene in the progression of these pre-symptomatic changes are not the primary focus of medical research and development. But attaining any degree of control over aging also implies the same degree of prevention of aging, meaning the ability to intervene early with therapies that repair the damage that would otherwise lead to greater dysfunction. Any rejuvenation therapy that shows efficacy in late stage disease should be even better as a way to prevent emergency of disease. Nonetheless, the historical focus on late stage disease in aging has already successful misdirected medical research and clinical practice into less beneficial approaches, and may continue to do so absent a cultural shift to focus more on prevention.
Aging is a multifactorial process that progressively disrupts cellular and tissue homeostasis, affecting all organ systems at distinct rates and predisposing individuals to chronic diseases such as cancer, type II diabetes, and sarcopenia. Among these systems, skeletal muscle plays a central role in healthspan decline, yet the precise onset of its deterioration remains unclear. Most studies emphasize late-life models, overlooking the transitional phase of middle age, when initial alterations emerge. Evidence indicates that middle-aged muscle exhibits aberrant metabolism, impaired insulin sensitivity, and an early, gradual reduction in mass, suggesting that decline begins long before overt sarcopenia, a pathologic loss of muscle mass and functionality after middle age.
Indeed, most of the in vivo research about skeletal muscle aging focuses on comparisons between old and young organisms, creating a gap in the field regarding mid-age alterations. This creates two problems: (i) it overlooks non-linear biomarkers that return to basal values in old age after an organism initiates compensatory response mechanisms, and (ii) it presents treatment mainly as a damage-control strategy after molecular and morphological alterations are already established. These "palliative" treatments may partially promote lifespan but have a limited impact on healthspan.
Therefore, we seek to summarize and identify biomarkers indicative of the onset of skeletal muscle aging from in vivo studies on young adults and middle-aged humans and rodents in an attempt to identify some of the chronological alterations. This review aims to contribute insights for future research seeking to prevent or delay the onset of sarcopenia.
Link: https://doi.org/10.3390/ijms262010145
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