Steven L. Britton, Ph.D. ~Professor of Physical Medicine and Rehabilitation ~Professor of Molecular & Integrative Physiology 6649 Kresge I 1500 E. Medical Center Drive Ann Arbor, Michigan 48109-0718 office phone: 734 615 5969 cell phone: 419 283 5866 fax: 734 615 1722 brittons@med.umich.edu

Current Research: 

Two billion years of evolution in an oxygen environment has determined that oxygen metabolism occupies a central feature of our biology. It appears evolution followed the increased free energy transfer afforded by the widened redox potential when oxygen is the final electron acceptor in oxidation reactions. Obligatory for using oxygen in energy
transfer pathways, was the simultaneous co-evolution of enzymes that detoxify the reactive oxygen species that are by-products of oxidation reactions. Thus, the pathways that mediate both oxidation reactions and oxygen detoxification reactions constitute a large part of our biology. As an extension, it is not surprising that maximal oxygen consumption (VO2max) has emerged as a clinical reference point. In aggregate, these ideas suggest this unified hypothesis:

"Aerobic capacity is the major determinant of the continuum between health and disease."

If true, then general models of low and high health should emerge from artificial selection for low and high aerobic capacity.

In 1996 Koch and Britton started large-scale artificial selection (two-way) for low and high aerobic capacity (Physiological Genomics, 2001). Aerobic capacity was estimated from a speed-ramped treadmill run to exhaustion to create lines of Low Capacity Runners (LCR) and High Capacity Runners (HCR). Our work involves testing the validity of the above unified hypothesis. If the hypothesis is true, the low line will
manifest many diseases and the high line will be largely resistant to disease. Current data support the view that LCR manifest many of the complexes associated with metabolic syndrome (Science, 2005).

Selected Publications:

Koch LG, Britton SL. Artificial selection for intrinsic aerobic endurance running capacity in rats. Physiological Genomics 5:45-52, 2001.

Chen J, Feller GM, Barbato JC, Periyasamy S, Xie Z-J, Koch LG, Shapiro JI,
Britton SL. Cardiac performance in inbred rat genetic models of low and high running capacity. Journal of Physiology: London 535.2:611-617, 2001.

Koch LG, Britton SL. Genetic component of sensorimotor capacity in rats. Physiological Genomics 13:241-247, 2003.

Wisloff U, Najjar SM, Ellingsen O, Haram PM, Swoap S, Al-Share Q, Fernström M, Rezaei K, Lee SJ, Koch LG, Britton SL. Cardiovascular risk factors emerge from artificial selection for low aerobic capacity. Science 307:418-420, 2005.

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