I obtained my M.D. at the University of Mexico, Mexico City in 1957 and my Ph.D. at London University, England in 1967. I was a post-doc with Professor Sir Andrew Huxley at Universitty College, London and did a second postdoc in the Department of Physiology at the University of Rochester, NY. I have been in UMB since 1997.

My laboratory conducts three areas of research on skeletal muscle physiology.

1. Excitation contraction (e-c) coupling in normal muscles and during fatigue development. We are studying calcium release regulatory mechanisms, calcium homeostatic regulatory mechanisms and the biological role of inward Ca currents and the ontogenic evolution of e-c coupling. We have shown that during tetanic isometric contractions Ca2+ release is not homogeneous but, that it is composed of spikes of very significant and slow fluctuations which form gradients within the cross section area of the cell. Presently we are investigating the mechanism of this stochastic-like type of calcium release from the intracellular Ca stores. We have found that during fatigue development, groups of myofibrils become inactive due to a decrease of maximal Ca2+ release which become sporadic. When this muscle fibers are exposed to caffeine they develop contractures of maximal force while inactive myofibrils become active again. We are investigating what causes Ca2+ release inhibition under these circumstances. Since there is a continuous influx of Ca2+ into muscle cells, a homeostatic mechanism must exist to maintain a long term intracellular low level Ca2+ concentration. The Na/Ca exchanger is being studied as this possible mechanism. Since inward ionic calcium currents (ICa)have no obvious e-c coupling role in mature skeletal muscles, the biological role of Ica and e-c coupling in embryonic myocytes from Xenopus Laevis before the T-system and SR develop are being investigated.

2. Skeletal muscle calcium handling and mechanical alterations during chronic heart failure. We have found that EDL muscle from rats with chronic heart failure develop half of the specific force as SR calcium release is decreased. In addition the cells show no atrophy. We are currently investigating what causes these alterations which are similar to the ones in the failing heart.

3. Membrane healing and restoration of contractility after mechanical injury. We are investigating a method to heal large (>30 μm) sarcolemmal damages. If a cell is provided with lecithin after the damage, its membrane integrity and contractility recovers. Currently we are investigating the most efficient chemical compound combination to produce healing and functional recovery of large Sarcolemmal damages and if this method can applied to other excitable cells including cardiac myocytes.

The main biological preparations that we use in my laboratory are either intact, skinned or split open isolated single amphibian muscle cells, small bundles of mammalian skeletal muscle and diaphragm cells, embryonic skeletal myocytes. The main technics that we use in my laboratory are: mechanical recordings, electrophysiology, ordinary light microscopy, cine microphotography, imaging.