In vivo eccentric moment generation is strongly linearly related to isometric activation level, consistent with actomyosin-dependent series elasticity, though maximal voluntary eccentric moments are limited by neural regulatory mechanisms.
No immediate clinical implications for strength assessment; leaves open validation in patient cohorts with neuromuscular impairment.
Muscle series elasticity and its contribution to eccentric moment generation was examined in humans. While subjects [male, n = 30; age 26.3 +/- 4.8 (SD) yr; body mass 78.8 +/- 13.1 kg] performed an isometric contraction of the knee extensors at 60 degrees of knee flexion, a quick stretch was imposed with a 12 degrees -step displacement at 100 degrees /s. The test was performed at 10 isometric activation levels ranging from 1.7 to 95.2% of maximal voluntary contraction (MVC). A strong linear relationship was observed between the peak imposed eccentric moment derived from quick stretch and the isometric activation level (y = 1.44x + 7.08; r = 0.99). This increase in the eccentric moment is consistent with an actomyosin-dependent elasticity located in series with the contractile element of muscle. By extrapolating the linear relationship to 100% MVC, the predicted maximum eccentric moment was found to be 151% MVC, consistent with in vitro data. A maximal voluntary, knee extensor strength test was also performed (5-95 degrees, 3 repetitions, +/-50, 100, 150, 200, and 250 degrees/s). The predicted maximum eccentric moment was 206% of the angle- and velocity-matched, maximal voluntary eccentric moments. This was attributed to a potent neural regulatory mechanism that limits the recruitment and/or discharge of motor units during maximal voluntary eccentric contractions.
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Webber et al. (1997) studied this question.
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