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Previous research has shown that an acute bout of passive muscle stretching can diminish performance in certain movements where success is a function of maximal force and/or power output. Two possible mechanisms that might account for such findings are a change in active musculotendinous stiffness and a depression of muscle activation. To investigate the likelihood of these two mechanisms contributing to a post-stretch reduction in performance, we examined the acute effects of stretching on the active stiffness and muscle activation of the triceps surae muscle group during maximal single-joint jumps with movement restricted to the ankle joint. Ten males performed both static (SJ) and countermovement (CMJ) jumps before and after passively stretching the triceps surae. Electrical activity of the triceps surae during each jump was determined by integrating electromyographic recordings (IEMG) over the course of the movement. Triceps surae musculotendinous stiffness was calculated before and after stretching using a technique developed by Cavagna (1970). Following stretching, a significant decrease [mean (SD) 7.4 (1.9)%; P<0.05] in jump height for the CMJ occurred, but for the SJ, no significant ( P>0.05) change in jump height was found. A small but significant decrease [2.8 (1.24)%; P<0.05] in stiffness was noted, but the magnitude of this change was probably not sufficient for it to have been a major factor underlying the decline in CMJ performance. Paradoxically, after stretching, the SJ exhibited a significant ( P<0.05) decrease in IEMG, but the IEMG for the CMJ remained unchanged ( P>0.05). It appears that an acute bout of stretching can impact negatively upon the performance of a single-joint CMJ, but it is unlikely that the mechanism responsible is a depression of muscle activation or a change in musculotendinous stiffness.

Recent research has shown that a regimen of stretching provides an acute inhibition of maximal force production by the stretched muscle group. To further characterize this phenomenon, the effect of an acute stretching regimen on maximal isokinetic knee-extension torque at 5 specific movement velocities (1.05, 1.57, 2.62, 3.67, and 4.71 rad x s(-1)) was examined in 10 men and 5 women (22-28 years). Each person's 5 baseline maximal isokinetic knee-extension torques (dominant leg) were measured on a Cybex NORM dynamometer. Following the baseline torque measurements, the participants stretched the dominant quadriceps for 15 minutes using 1 active and 3 passive stretching exercises. Once the stretching exercises were completed, the maximal torque measurements were repeated. Poststretch maximal torque at 1.05 rad x s(-1) was significantly reduced (p < 0.05) from 218 +/- 47 Nm (mean +/- SD) to 199 +/- 49 Nm (7.2% decrease). At 1.57 rad x s(-1), a similar decrease (p < 0.05) was also seen (204 +/- 48 Nm vs. 195 +/- 47 Nm; 4.5% decrease), but at the other velocities (2.62, 3.67, and 4.71 rad x s(-1)), poststretch maximal torque was unaltered (p > 0.05). It appears, therefore, that the deleterious impact of stretching activities on maximal torque production might be limited to movements performed at relatively slow velocities.

No abstract

Functional electrical stimulation (FES), the coordinated electrical activation of multiple muscles, has been used to restore arm and hand function in people with paralysis. User interfaces for such systems typically derive commands from mechanically unrelated parts of the body with retained volitional control, and are unnatural and unable to simultaneously command the various joints of the arm. Neural interface systems, based on spiking intracortical signals recorded from the arm area of motor cortex, have shown the ability to control computer cursors, robotic arms and individual muscles in intact non-human primates. Such neural interface systems may thus offer a more natural source of commands for restoring dexterous movements via FES. However, the ability to use decoded neural signals to control the complex mechanical dynamics of a reanimated human limb, rather than the kinematics of a computer mouse, has not been demonstrated. This study demonstrates the ability of an individual with long-standing tetraplegia to use cortical neuron recordings to command the real-time movements of a simulated dynamic arm. This virtual arm replicates the dynamics associated with arm mass and muscle contractile properties, as well as those of an FES feedback controller that converts user commands into the required muscle activation patterns. An individual with long-standing tetraplegia was thus able to control a virtual, two-joint, dynamic arm in real time using commands derived from an existing human intracortical interface technology. These results show the feasibility of combining such an intracortical interface with existing FES systems to provide a high-performance, natural system for restoring arm and hand function in individuals with extensive paralysis.