Effects of Exercise Training on Chronic Inflammation in Obesity

Abstract

Chronic, systemic inflammation is an independent risk factor for several major clinical diseases. In obesity, circulating levels of inflammatory markers are elevated, possibly due to increased production of pro-inflammatory cytokines from several tissues/cells, including macrophages within adipose tissue, vascular endothelial cells and peripheral blood mononuclear cells. Recent evidence supports that adipose tissue hypoxia may be an important mechanism through which enlarged adipose tissue elicits local tissue inflammation and further contributes to systemic inflammation. Current evidence supports that exercise training, such as aerobic and resistance exercise, reduces chronic inflammation, especially in obese individuals with high levels of inflammatory biomarkers undergoing a longer-term intervention. Several studies have reported that this effect is independent of the exercise-induced weight loss. There are several mechanisms through which exercise training reduces chronic inflammation, including its effect on muscle tissue to generate muscle-derived, anti-inflammatory 'myokine', its effect on adipose tissue to improve hypoxia and reduce local adipose tissue inflammation, its effect on endothelial cells to reduce leukocyte adhesion and cytokine production systemically, and its effect on the immune system to lower the number of pro-inflammatory cells and reduce pro-inflammatory cytokine production per cell. Of these potential mechanisms, the effect of exercise training on adipose tissue oxygenation is worth further investigation, as it is very likely that exercise training stimulates adipose tissue angiogenesis and increases blood flow, thereby reducing hypoxia and the associated chronic inflammation in adipose tissue of obese individuals.

Effects of a multi-component camp-based intervention on inflammatory markers and adipokines in children: A randomized controlled trial

“…However, no intervention effects on CRP were observed at 52 weeks, although the intervention effects on body fatness persisted at 52 weeks (Larsen et al, 2015). Studies suggest that regular exercise may improve low-grade inflammation by reducing body fat mass and local inflammation in fat tissue (Gleeson et al, 2011;You et al, 2013). However, in this study, the reduction in CRP at 6 weeks was not mediated by the changes in total body fat mass or regional fat mass.…”

“…One explanation for the disproportional changes in fat mass and CRP may be that exercise exerted its anti-inflammatory effects by other mechanisms. Evidence has suggested some potential mechanisms underlying the anti-inflammatory effects of exercise, including effects on muscle tissue to produce anti-inflammatory myokines, effects on endothelial cell to reduce leukocyte adhesion, and reducing pro-inflammatory cytokines (Gleeson et al, 2011;You et al, 2013). Nonetheless, the visceral fat mass was not quantified in our study.…”

Physical activity and health: Shifting focus from modern era to Stone Age life style

“…Chronic systemic inflammation is associated with the development of obesity and metabolic dysfunction. During obesity, increased secretion of pro-inflammatory cytokines (adipokines) from adipocytes (fat cells) [20] is accompanied by insulin resistance and glucose intolerance. Mild to chronic exercise have shown to ameliorate both dyslipidemia and systemic inflammation [21].…”

Anti-Inflammatory Effects of Physical Exercise on Obesity

“…Over the years, this simplistic point of view has been studied and it is now known that this tissue is able to synthesize substances that regulate vascular tone and hemostasis, beyond its additional essential functions to the organism [3] [4]. The literature has indicated the proinflammatory action of adipocytokines in mechanisms of vascular injury, insulin resistance and endothelial dysfunction, which accelerate and increase the appearance of atherosclerosis [5] [6]. The authors highlight tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP) as key markers of inflammatory response [4] [5] [6].…”

“…The literature has indicated the proinflammatory action of adipocytokines in mechanisms of vascular injury, insulin resistance and endothelial dysfunction, which accelerate and increase the appearance of atherosclerosis [5] [6]. The authors highlight tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP) as key markers of inflammatory response [4] [5] [6].…”