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Tendon organs as monitors of muscle damage from eccentric contractions

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Abstract

Eccentric contractions, where the active muscle is stretched, can lead to muscle damage. One of the signs of damage is a rise in the whole-muscle passive tension. Here we have asked, how many eccentric contractions are necessary to produce a measurable rise in passive tension and can this be detected by the muscle's tension sensors, the tendon organs? Responses of tendon organs of the medial gastrocnemius muscle of the anaesthetised cat were recorded during and after a series of eccentric contractions. The contractions were arranged so that the length change to which the muscle was subjected lay symmetrically about the optimum length for active tension. Tendon organ responses were measured as a mean rate, calculated over a 1-mm length change during a slow stretch of the muscle. Progressive increases in passive tension and tendon organ response were measured after each of a series of 1–100 eccentric contractions of the whole muscle, bundles of motor units and single motor units. One to two eccentric contractions of a single motor unit were sufficient to produce measurable rises in passive tension and tendon organ response. After a series of eccentric contractions had been completed, passive tension and tendon organ response were seen to continue rising with similar time-courses over the next 50 min. Both tension and afferent response could be reduced by large passive stretches. There was also a large increase in the responses of tendon organs to combined stretch and vibration at 100 Hz after the eccentric contractions. All of this indicates that tendon organs are able to monitor the passive tension changes in the muscle, thought to result from muscle damage produced by the eccentric contractions. The findings are relevant to known changes in proprioception and motor control after eccentric exercise.

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Correspondence to U. Proske.

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Gregory, J.E., Morgan, D.L. & Proske, U. Tendon organs as monitors of muscle damage from eccentric contractions. Exp Brain Res 151, 346–355 (2003). https://doi.org/10.1007/s00221-003-1508-3

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