Substantial effects of epimuscular myofascial force transmission on muscular mechanics have major implications on spastic muscle and remedial surgery.
The specific aim of this paper is to review the effects of epimuscular myofascial force transmission on muscular mechanics and present some new results on finite element modeling of non-isolated aponeurotomized muscle in order to discuss the dependency of mechanics of spastic muscle, as well as surgery for restoration of function on such force transmission. The etiology of the effects of spasticity on muscular mechanics is not fully understood. Clinically, such effects feature typically a limited joint range of motion, which at the muscle level must originate from altered muscle length-force characteristics, in particular a limited muscle length range of force exertion. In studies performed to understand what is different in spastic muscle and what the effects of remedial surgery are, muscle is considered as being independent of its surroundings. Conceivably, this is because the classical approach in muscle mechanics is built on experimenting with dissected muscles. Certainly, such approach allowed improving our understanding of fundamental muscle physiology yet it yielded implicitly a narrow point of view of considering muscle length-force characteristics as a fixed property of the muscle itself. However, within its context of its intact connective tissue surroundings (the in vivo condition) muscle is not an isolated and independent entity. Instead, collagenous linkages between epimysia of adjacent muscles provide direct intermuscular connections, and structures such as the neurovascular tracts provide indirect intermuscular connections. Moreover, compartmental boundaries (e.g., intermuscular septa, interosseal membranes, periost and compartmental fascia) are continuous with neurovascular tracts and connect muscular and non-muscular tissues at several locations additional to the tendon origins and insertions. Epimuscular myofascial force transmission occurring via this integral system of connections has major effects on muscular mechanics including substantial proximo-distal force differences, sizable changes in the determinants of muscle length-force characteristics (e.g. a condition dependent shift in muscle optimum length to a different length or variable muscle optimal force) explained by major serial and parallel distributions of sarcomere lengths. Therefore, due to epimuscular myofascial force transmission, muscle length-force characteristics are variable and muscle length range of force exertion cannot be considered as a fixed property of the muscle. The findings reviewed presently show that acutely, the mechanical mechanisms manipulated in remedial surgery are dominated by epimuscular myofascial force transmission. Conceivably, this is also true for the mechanism of adaptation during and after recovery from surgery. Moreover, stiffened epimuscular connections and therefore a stiffened integral system of intra- and epimuscular myofascial force transmission are indicated to affect the properties of spastic muscle. We suggest that important advancements in our present understanding of such properties, variability in the outcome of surgery and considerable recurrence of the impeded function after recovery cannot be made without taking into account the effects of epimuscular myofascial force transmission.
Yucesoy
Can A
CA
Biomedical Engineering Institute, Boğaziçi University, 34342 Bebek, Istanbul, Turkey. can.yucesoy@boun.edu.tr
Huijing
Peter A
PA
D001696:Biomechanical Phenomena; D005205:Fascia / Q000473:pathology / Q000503:physiopathology*; D020342:Finite Element Analysis; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology*; D018485:Muscle Fibers, Skeletal / Q000473:pathology / Q000502:physiology; D009128:Muscle Spasticity / Q000503:physiopathology* / Q000601:surgery; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology*; D016059:Range of Motion, Articular / Q000502:physiology; D012518:Sarcomeres / Q000473:pathology / Q000502:physiology; D013710:Tendons / Q000473:pathology / Q000503:physiopathology