Metabolic actions of estradiol: significance for acute and chronic exercise responses

Abstract

Although estradiol (E2) is considered primarily for its role in reproduction, it can exert numerous physiological actions on a variety of tissues. However, there are several difficulties in isolating these actions and determining its impact for in vivo situations. Despite the limitations, it does appear that E2 can alter, under certain conditions, resting and acute exercise metabolism and blood glucose regulation. Specifically, E2 can increase lipid availability and utilization and decrease gluconeogenesis and glycogenolysis. Development of glucose intolerance as a result of insulin insensitivity has also been documented. The mechanisms of E2 may be through direct alterations in key enzyme activity and membrane permeability or indirectly via changes in insulin:glucagon, cortisol, hGH, and catecholamine levels or sensitivity. Future research should focus on understanding the effects of exercise and diet on chronic E2 status and the resulting impact for a variety of conditions that include reproductive and skeletal integrity and predisposing metabolic risk factors for CAD and diabetes. In order to make meaningful correlations between E2 levels and physiological measurements such as bone mineral content, lipid profiles, glucose intolerance, etc., there needs to be a standard guideline for determining and defining one's "estrogen status." Finally, in order to identify underlying mechanisms, an understanding of and appreciation for the interrelationships among the numerous compositional, metabolic, and (neuro)endocrine factors involved is needed. A general model is presented, along with specific applications, to study these interactions.