Exercise and Chronic Low-Grade Inflammation

A common characteristic of ageing is an increased chronic low-grade systemic inflammation which contributes to a number of diseases including diabetes, cardiovascular disease, Alzheimer’s and cancer [80, 81]. Termed ‘inflammageing’ it is characterized by increased concentrations of pro-inflammatory cytokines and reduced concentrations of anti-inflammatory cytokines [81]. Although the cause of inflammation is multifactorial, immunesenescence and obesity are thought to contribute significantly [82]. Both ageing and a positive energy balance are associated with metabolic and physiological changes leading to increased adiposity. The result is an increased production of cytokines leading to catabolic effects in muscle and deprives tissue of nutrients through altering insulin signaling leading to chronic damage [83]. Couple this with a dysfunctional immune system prone to producing increased inflammatory cytokines and the effects on health are potentially great [6, 78, 84]. Moreover, the anti-inflammatory effect of exercise is associated with a reduced risk of chronic metabolic and cardiorespiratory diseases [66]. Three possible mechanisms have been suggested: the reduction in visceral fat mass, synthesis and secretion of anti-inflammatory cytokines from skeletal muscle and modification of immunesenescence (discussed previously) [31, 66, 85].

This anti-inflammatory effect of exercise may be mediated by the release of the typically pro-inflammatory cytokine IL-6 from working muscle [86 ] . IL-6 is a pleiotropic cytokine that signals differently depending on its origins and target cells [85]. Subsequently, during exercise there is a transient increase in muscle derived IL-6 which promotes the synthesis of anti-inflammatory cytokines such as IL-10 and IL-1 receptor agonist (RA) from immune cells [87]. Immune cell infiltration into adipose tissue is also reduced by exercise. Subsequently, reduced adipocyte infiltration by neutrophils, macrophages and perhaps T-cells has been shown with exercise [13,43]. Furthermore, exercise promotes increases in the adrenal hormones cortisol and adrenaline which have anti-inflammatory effects on immune cell production of TNFa and IL-ip [88-90].

Cross-sectional studies are often used to determine associations with physical activity and systemic inflammation. It remains unclear whether exercise alone reduces fat mass, however with exercise there is a shift in energy balance which is associated with reduced visceral fat mass [91]. Critically, the metabolism of adipocytes is altered and they become sensitive to insulin and glucose metabolism which is associated with increased adiponectin, a metabolic hormone responsible for fatty acid metabolism [92]. Therefore, reduced inflammatory cytokines such as CRP, IL-6 and TNFa coincide with elevated concentrations of adiponectin in physically active older individuals [93-96]. Similarly, exercise interventions ranging from 12 weeks to 6 months of aerobic and/or resistance exercise in older individuals resulted in reduced markers of inflammation and increased anti-inflammatory markers [97,98].

Taken together exercise appears to promote an anti-inflammatory response which is mediated by altered adipocyte function and improved energy metabolism leading to suppression of pro-inflammatory cytokine production in immune cells. Although others have shown no effects of exercise and physical activity on inflammation [11, 99, 100], these studies are atypical and the majority report exercise as anti-inflammatory.

 
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