Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction

Abstract

Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n = 8, range 22-27 years) performed 210 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

“…Different from previous reports (Armstrong et al, 1983;Smith, 1991;Pyne, 1994), signs of inflammation and muscle damage were minimal (almost absent) in our DOMS model (Fujii et al, 2008), but mechanical hyperalgesia was clear. Furthermore, Crameri et al (2007) Figure 7. Effects of intramuscular injection of bradykinin (BK), and the combination of bradykinin and shortening contraction.…”

“…They include lactic acid, spasm, connective tissue damage, muscle damage, inflammation, and oxidative stress (Armstrong, 1984;Smith, 1991;Cheung et al, 2003). The most widely supported mechanisms are muscle damage and inflammation induced by it, but reports suggesting other causes are emerging (Malm et al, 2004;Crameri et al, 2007).…”

Prostaglandin synthesis can be inhibited locally by infusion of NSAIDS through microdialysis catheters in human skeletal muscle

“…The subjects performed an eccentric exercise protocol that has previously been used by our laboratory (2). It is important to note that both legs were exercising, and comparisons were made between the blocked (NSAID) and unblocked leg.…”

Assessment of Muscle Pain Induced by Elbow-Flexor Eccentric Exercise

“…4,5 Damage to contractile proteins, intermediate filaments, and the connective tissue surrounding muscle fibers and the subsequent inflammatory processes are associated with DOMS. 2,6 Malm et al 7 and others [8][9][10] reported that DOMS could be associated more with increased inflammation in the epimysium or perimysium than with the muscle fibers. However, the mechanisms underpinning DOMS have not yet been fully elucidated.…”