Meeting Abstract

S2-4  Thursday, Jan. 4 09:30 - 10:00  Muscle function from molecule to organism NISHIKAWA, K; Northern Arizona University

There is a wide gap between our understanding of muscle contraction at the molecular level and our ability to predict in vivo muscle forces in animals during natural movements. We know that animal muscles can function as motors, springs, brakes, or struts, but we have little idea how muscle sarcomeres produce these different behaviors. During a work loop, a change in the phase of activation relative to the phase of length oscillations can convert a muscle from a motor into a spring. Current theories also fail to predict the increase in muscle force with stretch. They also fail to explain why a single stimulus added to a train of stimuli doubles the rate of force development. When stretch and doublet stimulation are combined in a work loop, muscle force doubles and work increases by 50% per cycle, yet we have no theory that explains why this occurs. Early studies circa 1970 suggested that all of the instantaneous elasticity of muscle sarcomeres resides in the cross bridges. In the 1990s, cross bridge models were developed that explained the increase in force during active stretch, but required assumptions now known to be unreasonable. Recent estimates suggest that cross bridges account for only ~12% of the energy stored by muscles during active stretch, and it is now apparent that the very small size of cross bridges and their cyclical behavior limits their ability to store energy. It was apparent much earlier that cross bridges were unable to account for the increase in force that persists after active stretching, leading to development of the sarcomere inhomogeneity theory. Most predictions of this theory fail, yet the theory persists. Based on these considerations, it is increasingly apparent that we need to consider structures other than cross bridges to understand the contributions of muscle to animal movement and motor control.