Gregory Frye

Mentor: Dr. Leonardo Ferreira
College of Health and Human Performance
"I got involved with research to further expand on my education.  I realized that learning can not just be from classroom, but one's endeavors out of the classroom.  The ability to conduct research has allowed me to further expand on my education with emphasis on the newest science and on a more individualized basis."


Applied Physiology and Kinesiology



Research Interests

  • Skeletal Muscle Function
  • Congestive Heart Failure
  • Skeletal Muscle Atrophy

Academic Awards

  • David S. Bruce Abstract Awardee
  • Lee McCachren Endowed Scholarship


  • Phi Epsilon Kappa
  • Golden Key Honor Society
  • Microfinance Organization


  • Buchholz High School Cross Country and Track Coach

Hobbies and Interests

  • Personal Training
  • Running
  • Weightlifting
  • Surfing

Research Description

Norepinephine accelerates diaphragm fatigue independent of blood flow
Sympathetic nervous activity is increased during exercise, chronic diseases, aging, and psychological stress. Muscle sympathetic nerve endings release norepinephrine, which stimulates primarily alpha-adrenergic receptors, to regulate vascular conductance and blood pressure. However, little is known about norepinephrine effects on skeletal muscle function that are independent of blood flow.  To address this issue, we assessed the contractile properties of diaphragm bundles exposed to buffer solution and norepinephrine  for 60 minutes in vitro (i.e., free of blood flow).  NE accelerated fatigue in vitro. Specifically, NE-treated muscles generated lower forces than control from 45 s until the end of the fatigue trial (300 s). The rate of force development and relaxation were also slower in NE-treated muscles during the fatigue trial. In subsequent studies, we found that the α1-adrenergic receptor agonist phenylephrine exerted effects nearly identical to those of norepinephrine. Our preliminary studies suggest that norepinephrine accelerates skeletal muscle fatigue through activation of α1-adrenergic receptors, and these responses are independent of blood flow.