Scott Powers, Ed.D., Ph.D.

UAA Endowed Professor, Distinguished Professor of Applied Physiology and Kinesiology

College of Health and Human Performance

2015 Awardee

Scott Powers’ research focuses upon the effects of muscular exercise and inactivity on redox signaling, gene expression, and contractile function of both cardiac and skeletal muscle. Specifically, the Powers laboratory has focused on two major topics. First, Powers has investigated the mechanisms responsible for exercise-induced cardioprotection against ischemia-reperfusion induced cardiac injury. Myocardial ischemia-reperfusion injury (i.e., heart attack) remains the leading cause of morbidity and mortality associated with cardiovascular disease. Powers’ work reveals that endurance exercise training promotes phenotypic changes in heart muscle that resist damage during a heart attack. Using this strategy, Powers’ research has provided the knowledge necessary to develop a pharmacological approach to protect the heart during a heart attack. Importantly, two different drugs have been shown to provide cardioprotection against ischemia-reperfusion injury and are now in phase II clinical trials. Second, Powers is developing a therapeutic approach to protect respiratory muscles against ventilator-induced weakness. Mechanical ventilation is a life-saving intervention for patients unable to breathe on their own, due to respiratory failure or other problems. Although mechanical ventilation can be a life-saving intervention, prolonged mechanical ventilation results in respiratory muscle weakness which translates to problems in removing patients (i.e., weaning) from a ventilator. Failure to wean patients from the ventilator results in prolonged hospital stays and greatly increases the risk of patient mortality and morbidity. Powers’ studies have revealed the importance of protecting respiratory muscles against both oxidative stress and protease activation during prolonged mechanical ventilation. These discoveries have led to the development of new drugs that have the potential to protect respiratory muscles against ventilator-induced weakness.