THE INTERACTIVE EFFECTS OF GREEN TEA EXTRACT SUPPLEMENTATION AND EXERCISE ON METABOLISM AND GLYCEMIC CONTROL IN HUMANS

Abstract

Green tea contains high concentrations of polyphenolic compounds known as catechins. Studies in animal models suggest several potential mechanisms for specific metabolic effects at rest and during exercise, including improved glycemic control, altered activity of several glucose transporter proteins and improved endurance capacity. In humans, green tea extract (GTE) supplementation has been associated with improved glycemic control under resting conditions and increased fat oxidation during exercise. This dissertation examined the potential interactive effects of GTE supplementation and exercise on metabolism in humans with a focus on glycemic control. In Study 1, we demonstrated that GTE increased lipolysis and reduced heart rate during steady-state exercise in recreationally active men. Although substrate oxidation was not affected, GTE appeared to lower postprandial glucose under resting conditions. We hypothesized that the effects of GTE on exercise metabolism and glycemic control would be more apparent in humans with reduced exercise tolerance and impaired glucose tolerance. Thus, in Study 2, we examined the effects of GTE in sedentary overweight men. There were no differences in any metabolic or physiological responses during exercise; however, following exercise, GTE supplementation reduced [glucose] and insulinemia in response to an oral glucose load. Based on the findings of Study 2, the aim of Study 3 was to elucidate potential mechanisms for the alterations in glycemic response. Through the use of a dual-glucose tracer method, we demonstrated that GTE did not affect the rate of appearance of glucose in plasma in sedentary men; however, GTE supplementation allowed for the same glucose clearance rate despite a reduced insulinemia. We also observed lower carbohydrate oxidation during exercise with GTE. These findings suggest that GTE has an insulin-sensitizing effect during recovery from exercise, possibly due to enhanced glucose transporter activity; however, this hypothesis warrants further investigation in humans.