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.

Telomeres protect the integrity of information-carrying DNA by serving as caps on the terminal portions of chromosomes. Telomere length decreases with aging, and this contributes to cell senescence. Recent evidence supports that telomere length of leukocytes and skeletal muscle cells may be positively associated with healthy living and inversely correlated with the risk of several age-related diseases, including cancer, cardiovascular disease, obesity, diabetes, chronic pain, and stress. In observational studies, higher levels of physical activity or exercise are related to longer telomere lengths in various populations, and athletes tend to have longer telomere lengths than non-athletes. This relationship is particularly evident in older individuals, suggesting a role of physical activity in combating the typical age-induced decrements in telomere length. To date, a small number of exercise interventions have been executed to examine the potential influence of chronic exercise on telomere length, but these studies have not fully established such relationship. Several potential mechanisms through which physical activity or exercise could affect telomere length are discussed, including changes in telomerase activity, oxidative stress, inflammation, and decreased skeletal muscle satellite cell content. Future research is needed to mechanistically examine the effects of various modalities of exercise on telomere length in middle-aged and older adults, as well as in specific clinical populations.

Our results support that aerobic exercise training could improve severe obesity-related hypogonadism in male Zucker rats. The underlying mechanism needs to be further clarified.

The purpose of this investigation was to study the effects of obesity and chronic exercise on sex organ testosterone levels in male rats. Lean and obese male Zucker rats were randomly assigned to a sedentary group and an exercise training group (lean sedentary: n=7, lean exercise: n=8, obese sedentary: n=7, obese exercise: n=7). The exercise group walked on a rat treadmill for 8 weeks. Testicular testosterone was extracted and total testosterone levels were measured by using radioimmunoassay. Compared to lean sedentary rats, obese sedentary rats had lower levels of testicular testosterone (concentration: 17.2±11.0 vs. 61.5±21.2 ng/g; total content: 50.8±29.4 vs. 191.5±80.3 ng; both P<0.001). There were no group differences between lean sedentary and lean exercise rats in testicular testosterone levels. However, compared to obese sedentary rats, obese exercise rats had higher testicular testosterone levels (concentration: 40.6±20.0 vs. 17.2±11.0 ng/g; total content: 119.6±52.4 vs. 50.8±29.4 ng, both P<0.05). These results support our previous findings that chronic exercise attenuated obesity‐related hypogonadism. Further studies are needed to clarify the underlying mechanisms.