Sunday, February 19, 2012
Exhibit Hall A-B1 (VCC West Building)
Presynaptic inhibition (PSI) of Ia afferent terminals is one of the major reflex control mechanisms associated with soleus H-reflex modulation during remote rhythmic arm movement. Although forearm H-reflexes are suppressed by rhythmic leg cycling, comparatively little is known about mechanisms subserving effects from leg to arm. The purpose of this study was to test the hypothesis that changes in Ia PSI using a conditioning stimulation technique was the mechanism behind the suppression of FCR H-reflexes during leg rhythmic movement. Surface electromyograms (EMG) were recorded from arm muscles flexor carpi radialis (FCR), extensor carpi radialis (ECR), biceps (BB) and triceps (Tri) brachii and leg muscle soleus (Sol) of neurologically intact subjects. Subjects performed two tasks: 1) leg cycling at 1Hz; and, 2) static leg positioning. For each trial, subjects maintained a consistent low-level (~ 10% of max) tonic contraction of FCR. H-reflexes in FCR were evoked by stimulating the median nerve at the elbow (control reflex size: 70-90 % of Hmax). The somatosensory conditioning stimuli were applied to either the radial nerve in the spiral groove at 1.0 times the motor threshold of ECR (condition-test (C-T) interval: 20ms) or to the superficial radial (SR) nerve with train of five pulses delivered at 300 Hz at 3 times the radiating threshold (C-T interval: 37 - 47 ms). While stationary, FCR H-reflex amplitudes were significantly suppressed by radial nerve conditioning and facilitated by SR nerve conditioning. Leg cycling reduced FCR H-reflex amplitudes (unconditioned H-reflex) and the amount of suppression was increased with the addition of radial nerve conditioning. Furthermore, SR conditioning stimulation removed the suppression of H-reflex resulting from leg cycling. Interestingly, these effects during leg cycling were also observed by using subthreshold conditioning stimulus intensities without evoking FCR reflex responses on the rectified and averaged EMG (Radial: 0.8-0.5 x motor threshold, SR: 0.8-0.41 x radiating threshold). In addition, FCR EMG responses, evoked by stimulating Radial and SR nerves, were not significantly altered by rhythmic leg cycling. Based on these results, we conclude that the interaction between leg cycling and somatosensory conditioning on the forearm H-reflex amplitudes is mediated by modulation of Ia PSI. As such, this study confirms a parallel organization of effects of leg cycling on H-reflex excitability in the arms and legs.