The relationship between physical inactivity, obesity and chronic diseases has been widely investigated over the last decades. Several research and review papers have been published on the topic [1][2][3][4]. Even though this area still requires further research, one thing is clear: chronic exercise exerts a positive effect on our body's immune system by decreasing the prevalence of chronic diseases. These illnesses -cardiovascular diseases, cancers, chronic respiratory diseases and dementia -not only compose over 80% of global deaths from noncommunicable diseases [5,6], but all have the same predictor of risk: a chronic low grade inflammatory state.According to the World Health Organization statistics 2012 [6] 13% of global deaths can be attributed to raised blood pressure, 6% to raised blood glucose, 6% to physical inactivity and 5% to being overweight/obese. Physical activity can be considered a medicine because it can reverse all of the above [5], not to mention the other health benefits of being fit [7,8]. Nevertheless, obesity and inactivity continues to increase all over the world. Obesity alone is a lesser risk factor compared to physical inactivity; studies have shown that some beneficial effects of physical activity are achieved even without changes in body mass or body composition [4]. The benefits are mainly due to the anti-inflammatory effects of exercise, which have been shown to be responsible for decreasing the prevalence of chronic diseases via, for example:
Reduction of Toll-Like Receptor (TLR) Expression on Monocytes and MacrophagesTLRs are trans-membrane proteins that provide important functions both for the innate and the adaptive immune system [9][10][11]. Their main role includes recognizing and responding to a variety of Pathogen-Associated Molecular Patterns (PAMPS) via intracellular signaling and the recognition of endogenous signals following tissue damage. Over the last decade, it has been shown that acute and chronic exercise can lead to a down regulation of TLRs expression on monocytes and macrophages cell surfaces and also a shift in macrophage phenotype (from M1-type which produces inflammatory cytokines to M2-type which produces anti-inflammatory cytokines); thus, leading to an increase in the anti-inflammatory milieu [12][13][14].