Abstract
Skeletal muscle and bone share common embryological origins from mesodermal cell populations and also display common growth trajectories early in life. Moreover, muscle and bone are both mechanoresponsive tissues, and the mass and strength of both tissues decline with age. The decline in muscle and bone strength that occurs with aging is accompanied in both cases by an accumulation of adipose tissue. In bone, adipocyte (AC) accumulation occurs in the marrow cavities of long bones and is known to increase with estrogen deficiency, mechanical unloading, and exposure to glucocorticoids. The factors leading to accumulation of intra- and intermuscular fat (myosteatosis) are less well understood, but recent evidence indicates that increases in intramuscular fat are associated with disuse, altered leptin signaling, sex steroid deficiency, and glucocorticoid treatment, factors that are also implicated in bone marrow adipogenesis. Importantly, accumulation of ACs in skeletal muscle and accumulation of intramyocellular lipid are linked to loss of muscle strength, reduced insulin sensitivity, and increased mortality among the elderly. Resistance exercise and whole body vibration can prevent fatty infiltration in skeletal muscle and also improve muscle strength. Therapeutic strategies to prevent myosteatosis may improve muscle function and reduce fall risk in the elderly, potentially impacting the incidence of bone fracture.
Highlights
Osteoporosis affects ~10 million people in the U.S and results in over 1.5 million bone fractures per year
The processes driving the accumulation of bone marrow adipocytes (ACs) are becoming more well understood [3, 4]; the factors leading to the accumulation of fat in skeletal muscle with age are not yet as well defined
Androgen deprivation therapy increases fatty infiltration of skeletal muscle in men with prostate cancer, CT imaging does not enable a distinction between IMC or intermuscular lipid accumulation and so the actual site of lipid deposition is not clear in this case [54]. These findings indicate that many of the conditions that induce marrow adipogenesis and bone loss in men and women such as disuse, sex steroid deficiency, altered leptin signaling, and glucocorticoid treatment stimulate the accumulation of ACs and IMC lipid in skeletal muscle (Figure 2)
Summary
Osteoporosis affects ~10 million people in the U.S and results in over 1.5 million bone fractures per year. Loss of muscle and bone mass with age is a significant public health problem, as the morbidity that accompanies fractures in the elderly is costly both in terms of financial burden and quality of life. The mechanisms underlying loss of muscle and bone strength with age are complex and multifactorial in nature, but evidence suggests that common factors regulate the integrated growth, development, and degeneration of these two tissues. The decline in muscle and bone strength that occurs with aging is accompanied in both cases by an accumulation of adipose tissue. The processes driving the accumulation of bone marrow adipocytes (ACs) are becoming more well understood [3, 4]; the factors leading to the accumulation of fat in skeletal muscle (myosteatosis) with age are not yet as well defined. We review these findings to highlight potential therapeutic strategies for the prevention of age-related myosteatosis as an approach for reducing fall risk and the likelihood of bone fracture
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