Abstract
The decline in the mass and function of bone and muscle is an inevitable consequence of healthy aging with early onset and accelerated decline in those with chronic disease. Termed osteo-sarcopenia, this condition predisposes the decreased activity, falls, low-energy fractures, and increased risk of co-morbid disease that leads to musculoskeletal frailty. The biology of osteo-sarcopenia is most understood in the context of systemic neuro-endocrine and immune/inflammatory alterations that drive inflammation, oxidative stress, reduced autophagy, and cellular senescence in the bone and muscle. Here we integrate these concepts to our growing understanding of how bone and muscle senses, responds and adapts to mechanical load. We propose that age-related alterations in cytoskeletal mechanics alter load-sensing and mechano-transduction in bone osteocytes and muscle fibers which underscores osteo-sarcopenia. Lastly, we examine the evidence for exercise as an effective countermeasure to osteo-sarcopenia.
Highlights
With advancing age, a threshold of decline in the mass and function of bone and muscle marks the onset of musculoskeletal frailty
Given the imperative to address osteo-sarcopenia together, rather than individually, in order to recover from the cycle of frailty, we focus the remainder of this review on the action of microtubules in aging as a potential target for a collective solution
We present the concept that among the deficits contributing to musculoskeletal frailty is a defect in mechano-transduction
Summary
A threshold of decline in the mass and function of bone and muscle marks the onset of musculoskeletal frailty This loss of muscle and bone quality, collectively called osteo-sarcopenia, initiate changes in lifestyle, and activity levels that start a sequence of events that lead to significant morbidity and even mortality. The incidence of low impact fractures steeply inclines in the osteo-sarcopenia population, contributing to reduced mobility and independence, increased mortality, and corresponding to increased financial burdens [10,11,12,13] Both men and women experience peak bone mass around 30 years of age, with a steady decline for the rest of life thereafter [14]. Since bone and muscle are known to regularly remodel in response to ever changing mechanical cues, cellular dysfunction caused by aging results in a significant decrease in musculoskeletal formation, favoring catabolic processes leading to osteopenia and sarcopenia (osteo-sarcopenia)
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