John Faulkner's research focuses on the contractile properties of whole skeletal muscles, motor units, and single skeletal muscle fibers from mice and rats and single fibers from muscle biopsies of humans. In particular, he and his associates are interested in the changes that occur in the contractile properties of skeletal muscle fibers during and following injury, fatigue and regeneration. Skeletal muscle fibers are injured by a variety of diseases; local anesthetics; direct injury, such as crushing and cutting, or puncturing; extremes of temperature; ischemia; and development of high forces during contractions. Regardless of the cause of injury, skeletal muscle fibers regenerate by the same process of activation and division of satellite cells. The models concentrate on are contraction-induced injury, denervation, stress and damage by reactive oxygen species, contraction-induced conditioning, age-related changes, and the muscle deseases of Duchenne and upper-limb girdle muscular dystrophy. Dependent upon the number of fibers injured, the magnitude of the injury to independent fibers and to the vasculature, the skeletal muscle or individual fibers will incur a transient or permanent functional deficit of some magnitude. The major functional deficits are in maximum force development, rate and magnitude of displacement, and consequently power output. Experimental protocols of free whole muscle grafting with and without neurovascular repair, contraction-induced injury, and genetic modifications are employed to induce functional deficits. The long-term goal is to devise techniques to reduce functional deficits. The age of the animals involved in the experimental protocols is a significant factor in the magnitude of the injury, the rate of recovery, and the permanent deficits incurred. Hypotheses have been formulated and experiments designed to investigate the physiological mechanisms responsible for these age effects.
The hypotheses, that skeletal muscle fibers in aged animals are more susceptible to injury and when injured, regenerate less well than skeletal muscle fibers in young animals, has been supported and underlying mechanisms are now under investigation. Current research protocols are designed to clarify the relationship among aging, skeletal muscle fatigue, injury, and regeneration. Experiments have also been implemented to determine the mechanisms responsible for the 20% to 30% loss in the development of maximum force in the muscles of aged animals. Faculty collaborators in these studies include James Ashton-Miller, Susan Brooks, Bruce Carlson, Jeffrey Chamberlain, Lisa Larkin, Daniel Goldman, William Kuzon, and Richard Miller at the UM and Kevin Campbell from the University of Iowa and Malcolm Jackson from the University of Liverpool (UK).