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UBC Theses and Dissertations

Generation of the triphasic electromyographic pattern accompanying targeted ballistic movements Forgaard, Christopher James


Muscles involved in rapid, targeted movements about a single-joint often display a triphasic (agonist – antagonist – agonist) electromyographic (EMG) pattern. Early work using movement perturbations suggested that for short movements, the entire EMG pattern was prepared and initiated in advance (Wadman et al., 1979), whereas more recent TMS evidence indicates that the ANT may be programmed separately (MacKinnon & Rothwell, 2000) with execution of the bursts occurring serially (Irlbacher et al., 2006). The purpose of this thesis was to investigate the generation of triphasic EMG bursts for movements of different amplitudes. In Experiment 1, participants performed rapid elbow extension movements to 20˚ and 60˚ targets and on some trials, a startling acoustic stimulus (SAS), which is thought to trigger prepared motor commands at short latency, was delivered at the onset of AG1. For short movements, this perturbation elicited ANT and AG2 early, suggesting the agonist and antagonist bursts may have been programmed separately and were sufficiently prepared (for SAS trigger) at the time of AG1 onset. In contrast, the same manipulation did not disrupt EMG timing parameters for the long movement, where the ANT and AG2 bursts normally occurred later. The inability to trigger these bursts separate from AG1 raised the possibility that for a longer movement, ANT and AG2 were not fully prepared in advance of movement onset. In Experiment 2, generation of the ANT (and AG2) bursts underlying a longer movement was examined in more detail. We presented a SAS later in movement, relative to each participant’s expected ANT onset (70 ms before). This perturbation produced an early onset of both the ANT and AG2 bursts. Similar to recent TMS findings, our findings suggest that the triphasic pattern is executed serially. By manipulating movement amplitude, and thus specific EMG timing characteristics, we have shown the trigger signal for initiating the ANT burst occurs not in direct relation to the AG1 burst, but rather in close temporal proximity to the expected onset of ANT.

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