• Directly between two adjacent muscles (occurring exclusively within a muscle group: synergistic muscles). We call this specific case intermuscular myofascial force transmission.

• Between a muscle and some extramuscular structures, such as the neurovascular tract (i.e., the collagen-reinforced structure in which blood vessels, lymphatics and nerves are embedded), intermuscular septa between muscle groups, interosseal membrane, periosteum, general (or deep) fascia, etc. We call this extramuscular myofascial force transmission to emphasize the role of extramuscular tissues. Forces exerted this way may play a role in stabilizing joints, or be exerted on bones and other extramuscular structures, but may also be exerted at other muscles.

Proximo-distal force differences

Due to additional myofascial loading, forces exerted at the origin and insertion of muscle are not equal (Huijing & Baan 2001). The net myofascial load (i.e., the vector sum of all such loads, involving size and direction) will keep sarcomeres at one end of myofibers within muscle longer than at other locations within the same myofibers, i.e., different active forces exerted locally (Fig. 3.2.1A). A force equal to the additional load is integrated into the force exerted at the opposite end of the muscle. Active force of several muscles may appear also at the insertion of another muscle, as long as myofascial connections to the extratendinous tissues are intact (Rijkelijkhuizen et al. 2005, 2009).

Distributions of sarcomere lengths within muscle and its myofibers

Myofascial loading will cause a distribution of lengths of sarcomeres arranged in series within myofibers (serial distribution). Most of such additional force is borne by active sarcomeres (since they are very stiff), but may also be borne by the connective tissue stroma of muscle and will be added to the active force exerted.

If the point of application of myofascial loads on myofibers and their size and direction were identical, sarcomere length distributions would be limited to serial ones. However, a simple test illustrates that the situation is more complex. If one suspends equal masses from the tendon of a (horizontal) muscle, the muscle is pulled down exposing the extramuscular neurovascular tract (Plate 3.2.1A), but this tract is pulled down more at the distal tendon than at the proximal tendon. This indicates that the tract is stiffer at the proximal side of the muscle. As a consequence, myofibers located proximally within muscle will, on average, be longer than more distal ones. Therefore, parallel distributions of sarcomere lengths will be present as well. The nature of both types of distributions will vary with the specific conditions of myofascial loading. It is hard to measure such distributions, but finite element modeling (Ch. 8.5) allows the study of such principles even in quite complex conditions of loading.

Myofascial interaction between muscles

Dissection experiments (Maas et al. 2005) indicate that intermuscular transmission plays a role, but extramuscular myofascial force transmission is the more important mechanism for muscular interaction. Intermuscular mechanical effects are present through two coupled events of extramuscular myofascial force transmission (muscle to extramuscular tissues to another muscle). Myofascial interaction was shown for synergistic muscles involving both intermuscular and extramuscular transmission (Huijing & Baan 2001; Huijing 2003). During experiments this is apparent as follows: After the agonistic muscle is lengthened at its distal tendon while its synergistic muscle is kept at constant length (Plate 3.2.1B), distal force of the isometric synergistic muscle is decreased (compared to the unconnected case) with increasing lengths of its adjacent muscle. The lengthened muscle creates, or enhances, a distally directed myofascial load on the isometric synergistic muscle. At its proximal tendon, this load is integrated into force exerted by the muscle (as in Plate 3.2.1A). In contrast, distally exerted force is decreased because of such loading conditions.

Myofascial force transmission between antagonistic muscles is (by definition) only possible via extramuscular mechanisms, as such muscles are separated by compartment walls. Stiff connections are made between compartments by neurovascular tracts, but also other extramuscular fascial structures are expected to play a role. The effects and explanation of myofascial interaction between two muscle groups located at opposite sides of an intermuscular septum or interosseal membrane (Plate 3.2.1B) are similar to those described for synergistic muscles (Huijing 2007; Huijing et al. 2007; Meijer et al. 2007, Rijkelijkhuizen et al. 2007). In a series of experiments in rats, we have shown that such mechanisms and effects are active between all muscles of the lower leg (for an overview of results, see Rijkelijkhuizen et al. 2009). So, even antagonistic muscles located at opposite sides of the leg interact (e.g., m. tibialis anterior and triceps surae muscles, see Ch. 5.8 for similar physiological results in mice), and cannot be considered as fully independent entities. It should be realized that this means that part of the force exerted by active sarcomeres within a muscle may be exerted at the tendon of its antagonistic muscle. In fact, the proximal sarcomeres of myofibers are in series not only with more distal sarcomeres of the same myofiber, but via myofascial loading also with distal sarcomeres (and their adjacent endomysia) in the lengthened antagonistic muscle(s). It is evident that the classical concept of antagonistic muscles (as having opposite mechanical effects) and the nomenclature used to describe them is due for a fundamental update… that, however, is beyond the scope of the present chapter.