Department of Exercise and Health Sciences, College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125, USA.
Sports Med. 2013 Apr;43(4):243-56. doi: 10.1007/s40279-013-0023-3.
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.
慢性系统性炎症是几种主要临床疾病的独立危险因素。在肥胖症中，循环炎症标志物水平升高，可能是由于脂肪组织、血管内皮细胞和外周血单核细胞等几种组织/细胞中促炎细胞因子的产生增加所致。最近的证据支持脂肪组织缺氧可能是一种重要机制，通过该机制，增大的脂肪组织引发局部组织炎症，并进一步导致全身炎症。目前的证据支持运动训练，如有氧运动和抗阻运动，可以减轻慢性炎症，尤其是在肥胖症患者中，这些患者炎症生物标志物水平较高，并进行了更长时间的干预。有几项研究报告称，这种效果独立于运动引起的体重减轻。运动训练通过多种机制减轻慢性炎症，包括其对肌肉组织产生肌肉源性抗炎“肌因子”的影响、改善缺氧和减少局部脂肪组织炎症的影响、减少白细胞黏附和全身细胞因子产生的内皮细胞影响，以及降低促炎细胞数量和减少每个细胞促炎细胞因子产生的免疫系统影响。在这些潜在机制中，运动训练对脂肪组织氧合的影响值得进一步研究，因为运动训练很可能刺激脂肪组织血管生成并增加血流量，从而减轻肥胖个体脂肪组织的缺氧和相关慢性炎症。
