Contractile and cellular remodeling in rabbit skeletal muscle after cyclic eccentric contractions

Abstract

The time course of muscle contractile and cellular properties was studied in rabbit ankle flexor muscles after injury produced by eccentric exercise. Cyclic eccentric exercise was produced by increasing the tibiotarsal angle of the rabbit while activating the peroneal nerve by use of transcutaneous electrodes. Muscle properties were measured 1, 2, 3, 7, 14, and 28 days after exercise to define the time course of muscle changes after injury. A control group receiving only isometric contraction was used to study the effect of cyclic activation itself. The magnitude of the torque decline after 1 day was the same with use of isometric or eccentric exercise, but eccentric exercise resulted in a further decrease in torque after 2 days, at which time isometrically exercised muscles had fully recovered. The most prominent morphological changes in the injured muscle fibers were the loss of antibody staining for the desmin cytoskeletal protein and deposition of intracellular fibronectin, even when the injured muscle fibers retained their normal complement of contractile and enzymatic proteins. The presence of fibronectin inside the myofibers indicated a loss of cellular integrity. Invasion by inflammatory cells was apparent on the basis of localization of embryonic myosin. Thus eccentric exercise initiates a series of events that results in disruption of the cytoskeletal network and an inflammatory response that could be the mechanism for further deterioration of the contractile response.

Mesenchymal Stem Cells Improve Muscle Function Following Single Stretch Injury: A Preliminary Study

“…Despite these limitations, mechanical assessment of function through isometric peak torque revealed an improvement in the MSC treated group at seven days, while the saline treated group experienced a further decline. This further reduction in function has been well documented in the literature and characterized by inflammatory changes within the muscle [34,35]. Peak isometric torque deficits in both groups were similar at 14 days, suggesting that the protection provided by MSCs was no longer evident.…”

Contractile function, sarcolemma integrity, and the loss of dystrophin after skeletal muscle eccentric contraction-induced injury

“…Dystrophin's binding partners, such as ␤-dystroglycan or ␤-spectrin, may form the next link in the putative pathway of radial force transmission, but our data suggest that they are not as vulnerable as dystrophin to either mechanical disruption or protein degradation. Desmin is an intracellular protein thought to link individual myofibrils laterally to each other and is lost after repeated eccentric contractions (31). In that study, the extensor digitorum longus (EDL) had an immediate loss of desmin, and it was only after 15 min of repeated contractions that the TA showed a significant loss in desmin, indicating that anatomical and biomechanical variables are likely important.…”

“…muscle injury; dystrophin; cytoskeleton; sarcolemma SKELETAL MUSCLE INJURY is characterized by an immediate loss of the ability to produce force. The cause of this force loss has been attributed to such factors as a defect in excitationcontraction (EC) coupling (55), disruption or loss of forcegenerating structures such as actin and myosin (49), and disruption or loss of force-transmitting structures, such as desmin (6,31). Perhaps the best evidence that disruption of force-bearing structures contributes to strength loss after injury comes from single-fiber studies, where reduction in single-fiber maximal force is observed immediately after eccentric injury (32,33).…”

The efficacy of manual versus local vibratory massage in promoting recovery from post-exercise muscle damage – A systematic review

“…Lieber et al (1994) reported that in the rabbit model, cytoskeletal disruption including a loss of immunostaining of desmin, was followed by increased membrane permeability. In 1996 this laboratory reported that the sarcolemmal proteins including dystrophin and laminin were also completely disrupted following EIMD (Lieber et al , 1996).…”