Thomas L. Clanton, Ph.D.
Professor of Applied Physiology and Kinesiology
College of Health and Human Performance
2014 AwardeeThomas Clanton’s research focuses on the effects of stressful environments such as hypoxia, hyperthermia and fatiguing exercise on skeletal muscles.
When normal skeletal muscles move from conditions of rest to intense exercise, they are exposed to physical challenges like hypoxia and hyperthermia that most other tissues could not withstand. For example, skeletal muscles can tolerate long periods of near complete obstruction of blood flow for many minutes without long term damage. Therefore, compared to other excitable tissues like heart and brain, they are literally “born to survive,” which makes them a very interesting tissue to study from a biological standpoint.
However, in chronic disease states, like heart disease, cardiopulmonary failure, or obstructive pulmonary disease, the respiratory and limb muscles are under additional mechanical and biochemical constraints that begin to reduce their function and, thus, limit the ability of patients to perform daily activities. Therefore, understanding the origins of muscle dysfunction in disease and developing ways to reverse the problem have been long term goals of Clanton’s research. One approach in humans has been to reverse the effects of disease on the respiratory muscles through muscle training. He developed testing and training methods for the respiratory muscles which have resulted in a patented device that is used extensively in pulmonary rehabilitation.
From a basic science standpoint, Clanton has focused on how disease or extreme stress exposures induce the production of reactive oxygen and nitrogen species in muscle and how these interact with the muscle contractile machinery. Clanton has found that, in most cases, these reactive products play protective roles in promoting the necessary signaling pathways to withstand the stress and initiate survival mechanisms. However, in disease states, or in extreme conditions, the reactive oxygen and nitrogen signals are often out of regulation and then contribute to protein and membrane damage and long term dysfunction.
Recent work has focused on the observation that, when skeletal muscles are exposed to stress signals, they respond by secreting cytokines and other proteins that have endocrine effects on other organ systems like liver or intestine. Most of these endocrine responses function to lower inflammation and initiate survival mechanisms in remote tissues. This endocrine role of skeletal muscles is emerging as a candidate to explain why performing regular exercise and maintaining a healthy musculature has many unexpected health benefits that improve resistance to disease and to environmental exposure and reduce rates of mortality by all causes.