10 and 11 After exercising, increased adenosine triphosphate synthesis and, later, increased mitochondrial biogenesis via activation of peroxisome-proliferator activated receptor-γ coactivator 1α, increases muscle insulin sensitivity in the post-exercise period.12 Another proposed mechanism is increased membrane permeability accompanied by elevated insulin-stimulated microvascular perfusion in the post-exercise state which could favor glucose uptake.12 The cellular mechanisms of acute resistance-type exercise are less clear. An increase in muscle mass over time has been thought to account for the

benefits of resistance exercise on glycaemic control and the associated expansion of glucose disposal capacity.13 The study by van Dijk et al.7 showed

that a single bout of resistance exercise reduced the prevalence of hyperglycaemia by about 36% during the CHIR99021 24-h post-exercise period. The authors ascribed these acute improvements in glycaemic control following resistance exercise to direct improvements in insulin-dependent and insulin-independent glucose uptake, similar to the effects generally observed after endurance exercise. However, it remains to be established whether resistance exercise can also modulate glycaemic control throughout subsequent day/s, and whether the acute glucoregulatory KU-55933 mouse effects of resistance exercise remain at lower intensities.7 More studies are needed to determine whether strength or endurance type training should be recommended to improve glycaemic control. The effects of training on skeletal muscle and glucose metabolism may be also modulated by variants

in genes. A recent study conducted by Barres et al.14 showed that acute aerobic exercise alters global and gene-specific promoter methylation in skeletal muscle suggesting that DNA hypomethylation is an early event in contraction-induced gene activation. Florfenicol Further, they found that exercise-induced effects on DNA methylation are dependent on exercise intensity. These findings provide further evidence that the epigenetic marks across the genome are subject to more dynamic variations than previously appreciated.14 Both in-depth mechanistic studies and long-term trials are needed to clarify the overall long term effects of different types of training on disease progression, occurrence of related cardio-vascular diseases, complications and mortality. One of the novel mechanisms needing further study is microRNAs and their regulation in the context of insulin resistance.15 Furthermore, adipose tissue has an important role as an energy store and dysregulation of its function also predicts cardio-metabolic diseases. Recently, the importance and interaction of muscle and adipose tissues for disease risk has received much attention.