The major research focus of the lab is skeletal muscle atrophy and dysfunction, which we are currently studying with respect to both disuse and disease. Mechanical unloading of skeletal muscle, which may be associated with prolonged bed rest, immobilization, a sedentary lifestyle, or exposure to microgravity, is known to cause a reduction in fiber cross sectional area, muscle weakness, and increased fatigability. Likewise, patients with Peripheral Arterial Disease (PAD) also show significant muscle atrophy and weakness, which appears to be independent of a reduction in peripheral blood flow. Although muscle disuse and PAD are clearly independent initiators of muscle atrophy, there may be some overlap in the molecular signaling pathways triggering protein catabolism in each condition. One such group of signaling molecules may be reactive oxygen species (ROS), and we have previously shown significant oxidative damage in skeletal muscle following disuse and in the muscles of PAD patients. Ongoing research projects in our lab are using genetic, pharmacological, and nutritional tools to determine if inhibition of oxidative damage prevents muscle atrophy in each condition.
In addition, we are also testing the effects of several formulations of Botulinum
Neurotoxin A on skeletal muscle function, and subsequent recovery of afferent
motor action. Botulinum Neurotoxin A prevents neuromuscular transmission by
binding to, and entering the motor nerve terminals. Here, the neurotoxin cleaves
SNAP-25, a protein essential to the successful docking and release of acetylcholine
from synaptic vesicles.
© Applied Physiology & Kinesiology
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Updated: July 5, 2007