The influence of exercise, smoking cessation and ageing on the level of advance glycation endproducts

Advanced glycation endproducts (AGEs) play a crucial role in the pathogenesis of diabetes and its complications such as retinopathy, nephropathy, neuropathy and atherosclerosis. AGEs may also contribute to the age-related debilitation of skeletal muscles. Glycation of myosin, for instance, does reduce myosin function. Moreover, glycation is accompanied by the generation of free radicals through autoxidation of glucose and glycated proteins. The accumulation of AGEs can be caused by various factors including diet, obesity and smoking, while regular physical activity and altered diet may reduce the levels of AGEs. The aim of this research was to study the effect of 8 weeks aerobic exercise, smoking and 2 weeks of smoking cessation on the level of serum AGEs in healthy participants and the effects of ageing on glycation of skeletal muscle fibers. Serum AGEs were determined using an enzyme-linked immunosorbent assay (ELISA) and by their autofluorescence. Oxidative stress biomarkers were measured using a colometric method. Circulating inflammatory cytokines were examined using flow cytometry. In vivo glycation of muscles from young (5 months), old rats (25 months) and very old rats (32 months) were evaluated by immunohistochemistry. There were no changes in serum AGEs and oxidative stress biomarkers after 8 weeks aerobic exercise. Smokers, however, had elevated serum AGEs, oxidative stress biomarkers and levels of the cytokines IL-2 and TNF-α. Although 2 weeks of smoking cessation had a negligible effect on the level of AGEs and oxidative stress biomarkers, it returned the levels of TNF-α and IL-2 to normal levels. We showed for the first time glycation was increased with age in gastrocnemius muscle. The age-related increase in muscle glycation may contribute to the slowing of the muscle in old age.