Technical noteForce output during and following active stretches of rat plantar flexor muscles: effect of velocity of ankle rotation
Introduction
The production of extra force during and following stretches of activated skeletal muscles has been described for undamaged muscles (Abbott and Aubert, 1952; Cook and McDonagh, 1995; Edman et al., 1978) but not for muscles in which prior stretching produced force deficits indicative of muscle injury (Hesselink et al., 1996). For normal (undamaged) skeletal muscles, there is a relationship between velocity of stretching and the extra force produced during the stretch at low velocities of stretch such that the faster the stretch the greater the extra force produced. At higher velocities of stretching, no such relationship exists as force remains constant with increasing stretching velocity. In addition to velocity, the magnitude of the extra force depends on initial length, length changes and final muscle length (Edman et al., 1978). The magnitude of the extra force produced by stretching also correlates with the force deficit produced. The force deficit caused by exposure of muscle to unaccustomed stretches is taken as indirect evidence of muscle injury (e.g. McCully and Faulkner, 1986) because there is no correlation between the amount of structural damage (e.g. sarcomere disruption) and the force deficit.
For the extra force recorded after the stretch (i.e. stress-relaxation), velocity of stretching was without effect for undamaged muscles (Edman et al., 1978). Stress-relaxation has not been studied in muscles exposed to repeated stretching or following other types of muscle injury. For injured muscles where structural and functional parameters are changing, the response to subsequent stretching could be quite different than for undamaged muscles. Since repeated stretches with and without muscle damage are common during sports and occupational tasks, knowledge of any altered biomechanics would be useful in predicting functional outcomes.
Using velocity-controlled joint rotations to produce the stretches, the extra force during and following stretches was monitored as a function of repetition number to determine the effects of angular velocity of repeated stretches on the capacity for extra force production and stress-relaxation. It was found that stress-relaxation following stretches became sensitive to the angular velocity with repeated fast but not slow stretches.
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Animal care and preparation
Experiments were performed on plantar flexor muscles of female Sprague–Dawley rats (body weight 264.9±5.0 g) and approved by the West Virginia University Animal Care and Use Committee (WVU-ACUC #9511-05). Animal requests for this study complied with Animal Welfare Act P.L. 91-579 and DHHS Guidelines governing the care and use of laboratory animals. Rats were kept anaesthetized with sodium pentobarbital (75 mg kg−1 intraperitoneal) and euthanized by an intracardial injection of sodium pentobarbital
Results
The increased force due to the stretches (i.e. Fpeak/Fpre, see Fig. 1) was not velocity sensitive [Fig. 2, slopes of regression lines were not different (p=0.44)] but the relative relaxation following stretches (i.e. Fpeak/Fpost300) was velocity sensitive [Fig. 3, slopes of regression lines were different (p=0.02)]. Fast stretches resulted in a greater increased relative force during stress-relaxation at 300 ms compared to slow stretches (Fig. 3). All force data for fast stretches showed larger
Discussion
Repeated stretches of active skeletal muscles produce force deficits indicative of injury (Hesselink et al., 1996). Injury itself could alter the active force developed during and following subsequent repeated stretches. Velocity may play a role. Contractile parameters such as absolute isometric force and the rate of force development have been studied following unaccustomed stretches (Lieber and Fridén, 1993; Warren et al., 1993). We examined in this study the force during and following
Acknowledgements
This work was supported in part by the National Institute of Occupational Safety and Health of the Centers for Disease Control (R01-0HAR-02918).
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