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Obesity-linked insulin resistance is mainly due to fatty acid overload in non-adipose tissues, particularly skeletal muscle and liver, where it results in high production of reactive oxygen species and mitochondrial dysfunction. Accumulating evidence indicates that resistance and endurance training alone and in combination can counteract the harmful effects of obesity increasing insulin sensitivity, thus preventing diabetes. This review focuses the mechanisms underlying the exercise role in opposing skeletal muscle insulin resistance-linked metabolic dysfunction. It is apparent that exercise acts through two mechanisms: (1) it stimulates glucose transport by activating an insulin-independent pathway and (2) it protects against mitochondrial dysfunction-induced insulin resistance by increasing muscle antioxidant defenses and mitochondrial biogenesis. However, antioxidant supplementation combined with endurance training increases glucose transport in insulin-resistant skeletal muscle in an additive fashion only when antioxidants that are able to increase the expression of antioxidant enzymes and/or the activity of components of the insulin signaling pathway are used.
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At present, obesity is one of the most important public health problems in the world because it causes several diseases and reduces life expectancy. Although it is well known that insulin resistance plays a pivotal role in the development of type 2 diabetes mellitus (the more frequent disease in obese people) the link between obesity and insulin resistance is yet a matter of debate. One of the most deleterious effects of obesity is the deposition of lipids in non-adipose tissues when the capacity of adipose tissue is overwhelmed. During the last decade, reduced mitochondrial function has been considered as an important contributor to ‘toxic’ lipid metabolite accumulation and consequent insulin resistance. More recent reports suggest that mitochondrial dysfunction is not an early event in the development of insulin resistance, but rather a complication of the hyperlipidemia-induced reactive oxygen species (ROS) production in skeletal muscle, which might promote mitochondrial alterations, lipid accumulation and inhibition of insulin action. Here, we review the literature dealing with the mitochondria-centered mechanisms proposed to explain the onset of obesity-linked IR in skeletal muscle. We conclude that the different pathways leading to insulin resistance may act synergistically because ROS production by mitochondria and other sources can result in mitochondrial dysfunction, which in turn can further increase ROS production leading to the establishment of a harmful positive feedback loop.
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We investigated whether swim training modifies the effects of tri-iodothyronine (T3) treatment on the metabolic response and oxidative damage of rat liver. Respiratory capacities, oxidative damage, levels of antioxidants, and susceptibility to oxidative challenge of liver homogenates were determined. Mitochondrial respiratory capacities, rates of H2O2 release, and oxidative damage were also evaluated. Training modified most of the measured parameters in both thyroid states, although the extent of changes was higher in hyperthyroid preparations. T3 treatment enhanced homogenate respiratory capacity, which was further enhanced by training despite the decrease in mitochondrial respiratory capacity. Hormonal treatment also induced liver oxidative damage and glutathione depletion, and increased tissue susceptibility to oxidative challenge. These effects were lower in trained animals. The extensive oxidative damage found in liver homogenates from hyperthyroid sedentary rats was due to low tissue antioxidant protection and high mitochondrial H2O2 production rate, which were increased and decreased respectively by animal training. The training effect on H2O2 production was associated with lower oxidative damage and susceptibility to Ca2 +-induced swelling of mitochondria. Measurements with respiratory inhibitors indicated that the differences in H2O2 release in hyperthyroid groups were due to differences in mitochondrial content of autoxidizable electron carrier located at Complex III. We conclude that moderate training is able to reduce hyperthyroid state-linked cellular and subcellular oxidative damage in liver increasing its antioxidant defenses and decreasing the mitochondrial generation of reactive oxygen species.
