Discussion in 'Hypertrophy Research' started by dkm1987, Dec 6, 2008.

  1. dkm1987

    dkm1987 New Member

    J Physiol. 2007 Aug 15;583(Pt 1):365-80. Epub 2007 Jun 21.  
    Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction.

    Crameri RM, Aagaard P, Qvortrup K, Langberg H, Olesen J, Kjaer M.

    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.

    Exercise protocol
    Two exercise protocols were used. One leg was randomly assigned to perform a voluntary (VOL; heterogenic myofibre activation) exercise bout. A total of four subjects used their dominant kicking leg for this exercise protocol. The exercise protocol consisted of two exercise phases: (i) 100 maximal eccentric quadriceps contractions (10 sets of 10 repetitions) at slow contraction speed (knee joint angular velocity 30 deg s−1); followed by (ii) 110 maximal eccentric quadriceps contractions (11 sets of 10 repetitions) at high contraction speed (180 deg s−1) using an isokinetic dynamometer (KinCom KC125AP, Chattanooga group Inc., Harrison, TN, USA). Range of motion was from 90 to 10 deg (0 deg = full extension). At the completion of each eccentric contraction, the leg was immediately returned passively to the starting position (10 deg) by the motor of the dynamometer (angular velocity, 60 deg s−1), and another eccentric contraction was immediately initiated. A 30 s rest phase was used between each set, and a 5 min rest period was used between exercise phases (i) and (ii). A total of 210 maximal eccentric muscle contractions were performed. A similar protocol has previously been used in our laboratory, and resulted in significant DOMS (Crameri et al. 2004c).
    The contralateral leg was exercised using percutanous electrical stimulation (ES). Impulse trains (300 μs single pulse duration; 35 Hz; maximal current, 300 mA) were delivered under microprocessor control over the motor points of the vastus lateralis using a constant-bicurrent stimulator (ELFA 2000, Biofina, Odense, Denmark; Crameri et al. 2004a). After careful preparation of the skin, two electrodes (Bio-Flex, 50 mm × 89 mm, Biofina A/S, Odense, Denmark) were placed over the vastus lateralis muscle. The subjects were carefully instructed not to produce any voluntary muscle contraction during this phase of the exercise protocol. Electrical stimulation was commenced at the initiation of downward movement of the dynamometer lever arm (i.e. at 10 deg knee joint angle), and it was turned off at the end of this downward movement (i.e. at 90 deg knee joint angle). The exercise protocol consisted of two exercise phases, identical to that described above for the voluntary exercise leg. Thus, a total of 210 eccentric muscle contractions were also performed in the electrically stimulated leg. Mechanical muscle output was analysed in all eccentric loading contractions (see ‘Force measurements’ below). The stimulation pulse train was similar to that previously used in both able-bodied and spinal cord-injured individuals (Crameri et al. 2004a). The stimulation pulse train was chosen to reduce any unpleasant sensory input from the electrical impulse that would limit the intensity of the muscle contraction that was tolerable by the subjects.

    Myofibre proteins
    No evidence of desmin-negative, dystrophin-negative or vimentin-positive myofibres was evident in the voluntarily activated leg at any time point tested (Figs 7 and 8). Furthermore, no positive staining of CD68+ reactive macrophages was noted within the myofibres of the VOL leg (data not shown). In contrast, the stimulated leg showed gross myofibre protein changes, with significant increases in desmin-negative, dystrophin-negative and vimentin-positive myofibres. Figures 7 and 8 show changes in desmin staining only; however, the dystrophin and vimentin staining provided identical results and are therefore not shown in detail. In addition, myofibre necrosis was evident in the ES leg but not in the VOL leg, as reflected by an increase in CD68+ reactive macrophages within the desmin-negative myofibres of the ES leg (data not shown).

    The present study is the first to examine the magnitude of eccentric contraction-induced muscle damage during electrical muscle stimulation (representing that of previous animal studies) in comparison to that evoked by maximal voluntary muscle activation. Several notable findings emerged. Firstly, it was demonstrated that significant damage to the Z-lines and myofibre proteins was present in the skeletal muscle biopsies taken from the ES leg but not the VOL leg. Secondly, acute eccentric muscle loading can activate myogenic satellite cells (both ES and VOL); however, it appears that a degeneration–regeneration process is required for amplified terminal differentiation of these activated satellite cells (ES leg). Thirdly, the present study showed that despite differences in the response of the myofibre proteins to the electrical stimulation and voluntary exercise, no significant differences were noted in the expression of tensacin C within the extracellular matrix. This adds further evidence to the existing literature of a potential role for the extracellular matrix in inducing symptoms associated with the delayed onset of muscle soreness observed after unaccustomed intense eccentric exercise.

    <span style='color:blue'>So why post this study?
    1. It adds to the mounting evidence pool that DOMS is not indicative of muscle damage. Something that still seems to permeate the internet bodybuilding lore.

    2. As I've said previously the response seen with this study shows us that the satellite cell activation is more atuned to a repairing type response that soley a purely hypertrophic response (conferred from other work).

    3. In light of 2 above I still have to wonder if indeed damage is a prerequisite to hypertrophy.</span>

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