Insulin Responsiveness in Metabolic Syndrome after Eight Weeks of Cycle Training

Abstract

Introduction Insulin resistance in obesity is decreased after successful diet and exercise. Aerobic exercise training alone was evaluated as an intervention in subjects with the metabolic syndrome. Methods Eighteen non-diabetic, sedentary subjects, eleven with the metabolic syndrome, participated in eight weeks of increasing intensity stationary cycle training. Results Cycle training without weight loss did not change insulin resistance in metabolic syndrome subjects or sedentary control subjects. Maximal oxygen consumption (VO2max), activated muscle AMP-dependent kinase, and muscle mitochondrial marker ATP synthase all increased. Strength, lean body mass, and fat mass did not change. Activated mammalian target of rapamycin was not different after training. Training induced a shift in muscle fiber composition in both groups but in opposite directions. The proportion of 2x fibers decreased with a concomitant increase in 2a mixed fibers in the control subjects, but in metabolic syndrome, 2x fiber proportion increased and type 1 fibers decreased. Muscle fiber diameters increased in all three fiber types in metabolic syndrome subjects. Muscle insulin receptor expression increased in both groups and GLUT4 expression increased in the metabolic syndrome subjects. Excess phosphorylation of insulin receptor substrate-1 (IRS-1) at Ser337 in metabolic syndrome muscle tended to increase further after training in spite of a decrease in total IRS-1. Conclusion In the absence of weight loss, cycle training of metabolic syndrome subjects resulted in enhanced mitochondrial biogenesis, and increased expression of insulin receptors and GLUT4 in muscle, but did not decrease the insulin resistance. The failure for the insulin signal to proceed past IRS-1 tyrosine phosphorylation may be related to excess serine phosphorylation at IRS-1 Ser337 and this is not ameliorated by eight weeks of endurance exercise training.

Interactions of exercise training and high-fat diet on adiponectin forms and muscle receptors in mice

“…These observations corroborated the results of Gomes et al, showing that exercise ameliorated insulin hypersecretion from pancreatic islets of HF diet rats [38]. An increased GLUT4 expression was also observed in trained subjects with MetS [39, 40] and could participate to the decreased glucose intolerance. These studies coupled with our results confirmed that physical activity provides numerous health-related benefits that prevent the development of MetS, whether directly through its effect on skeletal muscle and energy expenditure or indirectly by changing nutrition behavior.…”

Exercise Training Reverses the Deleterious Effect of Sucrose Intake on Insulin Resistance and Visceral Fat Mass Deposition on Mice

“…Furthermore, the present results are also somewhat similar to those showing that physical exercise causes weight-loss and reduces the incidence of Type 2 diabetes in overweight men with impaired glucose tolerance (Stuart et al, 2013).…”

“…The results are essentially similar to those from human studies in which physical exercise has invariable beneficial effects causing decreased in body weight and visceral fat accumulation in relatively short time intervals (Henriksen, 2002;Stuart et al, 2013). Furthermore, the present results are also somewhat similar to those showing that physical exercise causes weight-loss and reduces the incidence of Type 2 diabetes in overweight men with impaired glucose tolerance (Stuart et al, 2013).…”

“…Physical exercises have been reported as an important factor that can increase insulin responsiveness by tissues (Snel et al, 2012;Stuart et al, 2013;Hecksteden et al, 2013). The results of the present investigation clearly demonstrated that exercise re-established all the alterations caused by a high sucrose diet and returned to control levels the abdominal fat, glucose and insulin in a mice model of diet-induced insulin resistance.…”

“…In fact, training induced enhancement of insulin action is associated with up regulation of specific components of the glucose transport system in insulinresistant muscle and includes increased protein expression of GLUT-4 and insulin receptor substrate-1 (Henriksen, 2002;Stuart et al, 2013).…”