Exercise for the management of type 2 diabetes: A review of the evidence

The aim is to critically review the more relevant evidence on the interrelationships between exercise and metabolic outcomes. The research questions addressed in the recent specific literature with the most relevant randomized controlled trials, meta-analysis and cohort studies are presented in three domains: aerobic exercise, resistance exercise, combined aerobic and resistance exercise. From this review appear that the effects of aerobic exercise are well established, and interventions with more vigorous aerobic exercise programs resulted in greater reductions in HbA1c, greater increase in VO2max and greater increase in insulin sensitivity. Considering the available evidence, it appears that resistance training could be an effective intervention to help glycemic control, especially considering that the effects of this form of intervention are comparable with what reported with aerobic exercise. Less studies have investigated whether combined resistance and aerobic training offers a synergistic and incremental effect on glycemic control; however, from the available evidences appear that combined exercise training seems to determine additional change in HbA1c that can be seen significant if compared with aerobic training alone and resistance training alone.

Xanthine oxidase pathway and muscle damage: Insights from McArdle disease

The intent of this review is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.