| Summary: | The stopping of an earlier intended action is best explained in a race between a go process and a
stop process (Logan & Cowan, 1984). The finish line, to which each process races, has been likened
to a point of no return, specifically one that marks the onset of a final ballistic (unstoppable) process.
Of note is the typical relation of reduced go probabilities and faster go latencies at shorter signal
onset asynchronies (SOAs). (The SOA is the time interval between presentation of the go signal and
presentation of the stop signal.) We report, in some cases, sub-maximal surface electromyograms
(EMGs) at onset when trying to stop a maximal speeded action. These data indicate reduced
synaptic drive to reach the motor pools as a result of earlier stopping effects and, as such, hold
important implications for a theory of control. First, we interpret these data to suggest that the point
of no return is phantom. Sub-maximal EMGs indicate a point in the control stream beyond which
some EMG will be later observed but, importantly, they fail to mark the onset of a final ballistic
process if, once breached, the same process remains subject to further effects of stopping. The
alternative interpretation, however, that of a final ballistic process that receives sub-maximal input
which results in sub-maximal output (i.e., EMG onset) cannot be ruled out from these data. We used
the Hoffmann (H) reflex to probe further the mechanism of control for stopping a voluntary action.
The H-reflex, an involuntary reflex that is taken as an index of spinal control, is relevant to the
control of stopping because it is typically facilitated a short time before EMG onset. In other words,
it provides a window of control within which a final ballistic process would otherwise be expected
to locate. Thus, we interpret the effects of stopping on the H-reflex before EMG onset as strong
evidence against a final ballistic process. Second, while the race model can explain the relation
between the go probabilities, the go latencies and the SOAs, it fails to explain the sub-maximal EMG
onsets that describe that same action in some cases. We submit a mechanism of excitatory-inhibitory
interaction at all times up to the motor pool to explain both sets of empirical data. The viability of
this theory is demonstrated using computer analyses.
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