Can physical activity prevent the age-related ectopic fat accumulation and decline in mitochondrial function or at least mitigate the negative effects of an unfavourable body composition?
Age-related changes in body composition, including loss of lean mass, increase in fat mass and preferential redistribution of adipose tissue to ectopic stores, are some of the insidious aspects of ageing.
The physiology and pathophysiology of adipose tissue is complex for many reasons. First, adipose tissue is distributed in several metabolically distinct depots (e.g., subcutaneous, visceral, intramuscular, hepatic) throughout the body. Second, adipose tissue is composed of many cell types (e.g., adipocytes, immune cells, vascular cells). Furthermore, in addition to serving as a primary energy reservoir, adipose tissue is recognized as an important endocrine organ. In short, the various stores of adipose tissue differ in their composition, function, and effects in health and disease.
The accumulation of adipose tissue in ectopic depots, such as visceral and intramuscular depots, is closely associated with the metabolic syndrome, as ectopic adipose tissue appears to be more insidious than subcutaneous adipose tissue.
In fact, due to the inflammatory nature of ectopic adipose tissue, its secretion can have particularly harmful effects on both local and distant tissues. For example, it has been shown that the secretion of intramuscular adipose tissue weakens insulin signalling in skeletal muscle.
Recent data suggest that the loss of muscle mass due to age, the increase in intramuscular adipose tissue and the impairments in the mitochondrial bioenergetic function of skeletal muscle are associated with deterioration in mobility and the subsequent development of frailty.
However, whether this ectopic adipose tissue is causally linked to metabolic changes remains unclear, as do the ways to prevent or reverse the accumulation of this potentially harmful adipose tissue accumulation.
A recent study sought to elucidate the mechanisms by which different adipose tissue depots may contribute to metabolic dysfunction by assessing the associations between different adipose tissue depots and skeletal muscle mitochondrial bioactivity in a large cohort of elderly men and women.
This study sheds important light on the potential metabolic consequences of ectopic fat accumulation during ageing, suggesting that physical activity may play an important role in preventing ectopic fat accumulation and metabolic decline.
One of the findings was that, in ex vivo measurements of mitochondrial bioenergetic function, adipose tissue in thighs and visceral adipose tissue were associated with worse carbohydrate-supported mitochondrial bioenergetic function in skeletal muscle, while total abdominal adipose tissue and visceral adipose tissue were associated with worse fatty acid-assisted mitochondrial bioenergetic function of skeletal muscle.
Although these correlations do not prove causality, they are enough to lead to speculation and reflection. Fat-derived proteins, cytokines and free fatty acids have been implicated in many aspects of age- and obesity-related metabolic dysfunction, including reduced mitochondrial function and insulin resistance.
As we seek to identify the mechanistic determinants of these potentially interrelated age-related physiological changes in adipose tissue and skeletal muscle, we also hope to identify ways to prevent or reverse these age-related declines. The physical inactivity that often accompanies aging is likely to be an important factor.
In this study, the addition of physical activity to the statistical models reversed the correlation between all adipose tissue depots and peak in vivo ATP production, suggesting that physical activity may be a factor of better mitochondrial function, even mitigating the negative effects of an unfavourable body composition.
Therefore it appears that, ATP production rates are a function of both mitochondrial bioenergetic function and microvascular perfusion, which can be affected by ageing, changes in body composition and physical activity.
Taken together, these results suggest that physical activity may inhibit age-related ectopic fat accumulation and decline in mitochondrial function or at least mitigate the negative effects of adipose tissue accumulation in ectopic depots.
The findings of this study add to a growing body of literature suggesting that physical activity can prevent many age-related changes in adipose tissue and skeletal muscle.
For example, a recent study found that the mitochondrial oxidative capacity of skeletal muscle was at preserved levels in elderly subjects whose daily activity levels were similar to those of a comparison group of young people.
Interestingly, studies also suggest that cardiorespiratory fitness affects visceral obesity, regardless of physical activity.
As we can conclude from the above, physical activity can act as a powerful countermeasure for many age-related changes in fat and skeletal muscle, reducing fat mass and ectopic fat deposition, increasing muscle mass, strength and mitochondrial content, improving mitochondrial function and insulin sensitivity.
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