Osmotic engine drives shortening in passive skeletal muscle


Meeting Abstract

75-3  Monday, Jan. 6 08:30 – 08:45  Osmotic engine drives shortening in passive skeletal muscle WOLD, ES*; ROBERTS, TJ; SLEBODA, DA; Brown University, Providence RI; Brown University, Providence RI; Brown University, Providence RI ethan_wold@brown.edu

Skeletal muscle, like most biological tissues, is primarily made up of fluid. This fluid is rarely considered a mechanical component of muscle, but recent work suggests that it may be a determinant of basic muscle properties. We have shown previously that an isolated muscle bathed in dilute solution takes on water and swells. If held at constant length during this process, it develops greater passive tension over time. This phenomenon can be replicated by a model of a fluid-filled cylinder surrounded by a fiber-wound matrix, and we have proposed that a similar interaction of fluid pressure and the collagenous extracellular matrix influences passive force development in muscle. We explore this hypothesis further by measuring shape changes in isolated bullfrog semimembranosus muscle held at constant tension by a servomotor. When bathed in hypotonic solution 20% of isotonic, muscles swelled (as measured by an increase in muscle width) and shortened. Over time, shortening was proportional to the increase in width. Although the work done was small compared to an active muscle, the forceful shortening demonstrates that passive skeletal muscle is capable of acting as an osmotic engine, converting osmotic potential to mechanical work. Returning muscle to an isotonic solution reduced muscle width and was associated with re-lengthening. Length changes observed in muscle that was held at a low force were greater than those at high force, and a mathematical model inspired by human-engineered McKibben pneumatic actuators yields similar outcomes. These results suggest another parallel between biological muscle and McKibben actuators, and give support for the notion that muscle shape change is influenced interactions between extracellular matrix collagen and intracellular fluid.

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