Excess visceral fat tissue leads to chronic inflammation via a range of mechanisms that include the creation of more senescent cells than would otherwise exist. Senescent cells secrete a potent mix of inflammatory and other signals that degrade tissue function in many ways. Since the accumulation of lingering senescent cells is a cause of aging, being overweight doesn't just increase risk and severity of age-related disease, and shorten life expectancy, but also literally accelerates aging. The more fat tissue, the worse the outcome over the long term. As this paper points out, however, this is only the case for excess visceral fat tissue. When lean, the normal, smaller amounts of this tissue are actually anti-inflammatory and beneficial.
Adipose tissue is host to various immune cells and it is well established that during obesity, the amount of inflammatory macrophages increase in adipose tissue. Visceral adipose tissue (VAT), surrounding the inner organs, has been shown to be more inflammatory active than subcutaneous adipose tissue (SAT), as increased amounts of visceral/abdominal fat associates with high levels of circulating inflammatory markers and a high number of pro-inflammatory cells in their adipose tissue.
Interestingly, in human and rodent studies, ageing is associated with an increase in the amount of visceral adipose tissue and/or level of inflammation. It is, however, unclear to what extent these age-related changes are a result of ageing per se or rather the result of changes in life-style with e.g. reduced levels of physical activity without a corresponding reduction in caloric intake. A human cross sectional study reported that whereas ageing is associated with increased inflammation, life-long endurance training resulted in lower circulating levels of inflammatory markers in both young and elderly individuals.
In the current study, we wanted to investigate the inflammatory status and tissue integrity of VAT in an exercise-training model of lean adult and old mice. We randomized adult (11 months; n = 21) and old (23 months; n = 27) mice to resistance training or endurance training, or to a sedentary control group. Strikingly, we observed an anti-inflammatory phenotype in the old mice, consisting of higher accumulation of anti-inflammatory M2 macrophages and IL-10 expression, compared to the adult mice. In concordance, old mice also had less VAT mass and smaller adipocytes compared to adult mice. In both age groups, exercise training enhanced the anti-inflammatory phenotype. In conclusion, in the absence of obesity, visceral adipose tissue possesses a pronounced anti-inflammatory phenotype during aging which is further enhanced by exercise.