Wayne Willis was hired by the ASU Department of Health and Physical Education in August, 1989 to initiate the study of exercise at the cellular and sub-cellular levels. Prior to his arrival at ASU, Dr. Willis carried out his doctoral research with the Membrane Bioenergetics Group at the University of California, Berkeley, and subsequently spent three years doing postdoctoral work on the effects of dietary iron deficiency on the thermodynamics of mitochondrial oxidative phosphorylation at the University of California Medical Center in San Francisco.Research
Since the construction of the Exercise Biochemistry Laboratory was completed in 1991, Dr. Willis and his students have studied the basic mechanisms underlying energy transduction in mitochondria isolated from skeletal muscle, liver, and heart. Recent work supported by the National Science Foundation (NSF) has focused on structure/function differences and associated cost/benefit trade-offs in the mitochondria of slow-twitch (type I) versus fast-twitch (type II) skeletal muscle. In the past mainly animal models have been used, but the recent development of the Metabolic Biology Center, along with new micro-techniques for the functional assessment of mitochondria, have made the study of human skeletal muscle mitochondria possible. Over the past five years Dr. Willis, in collaboration with ASU bioengineers and the Neurobiology/Bioengineering Laboratory at Good Samaritan Medical Center, Phoenix, has also been studying fuel selection during human locomotion (primarily walking) in both disabled and able-bodied populations. These experiments have formed the basis of a recent proposal to NSF, addressing the evolutionary implications of walking at a spontaneously chosen speed and the associated skeletal muscle metabolism.Selected Publications
1. Jackman MR, Willis WT. Characteristics of mitochondria isolated from type I and type IIb skeletal muscle. Am J Physiol 270: C673-C678, 1996.
2. Crowley ME, Willis WT, Matt KS, Donovan CM. A reduced lactate mass explains much of the glycogen sparing associated with training. J Appl Physiol 81: 362-367, 1996.
3. Willis WT, Jackman MR, Bizeau ME, Pagliassotti MJ, Hazel JR. Hyperthermia impairs liver mitochondrial function in vitro. Am J Physiol 278: R1240 - R1246, 2000.
4. Herman R., He J, D'Luzansky S, Willis W, Dilli S. Spinal cord stimulation facilitates functional walking in a chronic, incomplete spinal cord injured. Spinal Cord 40: 65-68, 2002
5. Messer, JI, Jackman MR, Willis WT. Pyruvate and citric acid cycle carbon requirements in isolated skeletal muscle mitochondria. Am J Physiol 286: C565-C572, 2004
6. Ganley KJ, Willis WT, Carhart MR, He J, Herman RM. Epidural spinal cord stimulation improves locomotor performance in low ASIA C wheelchair dependent spinal cord injured individuals: Insights from metabolic response. Top Spinal Cord Inj Rehab 50-63, 2005.
7. Willis WT, Ganley KJ, Herman RM. Fuel oxidation during human walking. Metabolism 54:793-9, 2005
8. Glancy B, Barstow T, Willis W. Linear relation between time constant of oxygen uptake kinetics, total creatine, and mitochondrial content in vitro Am J Physiol (In Review)