Effects of acute exercise and training on insulin binding to monocytes and insulin sensitivity in vivo

Insulin binding to monocytes was studied in well-trained long distance runners and in sedentary control subjects in the resting state and after 3 h cycle ergometer exercise at 40% of maximal aerobic power. In addition, in previously untrained subjects we examined the effect of 6 weeks of training on insulin binding to monocytes and insulin sensitivity in vivo. In the athletes at rest, insulin binding to monocytes was 69% higher than in controls (p less than 0.01), and correlated with maximal aerobic power (r = 9.63, p less than 0.05). The rise in insulin binding in the athletes was due to an increase in binding capacity rather than a change in binding affinity. During exercise, insulin binding fell in athletes by 31% (p less than 0.025) in contrast to a 35% rise observed in control subjects (p less than 0.01). As compared to controls, the athletes had a lower respiratory exchange ratio and a smaller decline in plasma glucose during exercise. In previously untrained subjects, physical training resulted in a 35% rise in insulin binding to monocytes (p less than 0.02). The rise in binding was due mainly to an increase in binding capacity. Insulin mediated glucose uptake (as measured by insulin clamp technique) also rose by 30% after physical training (p less than 0.01). The rise in insulin sensitivity was proportional to the improvement in physical fitness (r = 0.81, p less than 0.05). These findings indicate that (a) elevated insulin binding may contribute to the enhanced insulin sensitivity observed after physical training, (b) a fall in insulin binding in athletes during acute exercise may contribute to a greater shift from carbohydrate to fat utilization during exercise in athletes as compared to sedentary controls. These data suggest that physical training may provide a means of reversing or ameliorating abnormalities in insulin binding and sensitivity in insulin resistant states, such as obesity or maturity onset diabetes.