Muscle residual force enhancement has been observed in different muscle preparations for more than half a century. Nonetheless, its mechanism remains unclear; to date, there are three generally accepted hypotheses: 1) sarcomere length non-uniformity, 2) engagement of passive elements, and 3) an increased number of crossbridges. The first hypothesis uses sarcomere non-homogeneity and instability to explain how "weak" sarcomeres would convey the higher tension generated by an enhanced overlap from "stronger" sarcomeres, allowing the whole system to produce higher forces than predicted by the force-length relationship; nonuniformity provides theoretical support for a large amount of the experimental data. The second hypothesis suggests that passive elements within the sarcomeres (i.e., titin) could gain strain upon calcium activation followed by stretch. Finally, the third hypothesis suggests that muscle stretch after activation would alter crossbridge kinetics to increase the number of attached cross-bridges. Presently, we cannot completely rule out any of the three hypotheses. Different experimental results suggest that the mechanisms on which these three hypotheses are based could all coexist. © 2013 CLINICS.
CITATION STYLE
Minozzo, F. C., & de Lira, C. A. B. (2013). Muscle residual force enhancement: A brief review. Clinics. https://doi.org/10.6061/clinics/2013(02)R01
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