Electrical characteristics of human ankle dorsi- and plantar-flexor muscles. Comparative responses during fatiguing stimulation and recovery.

Changes in muscle excitability were investigated during fatigue and the recovery of human dorsi- and plantar-flexor isometric contractions. The indirectly evoked muscle compound action potentials [tibialis anterior (TA) and soleus (SOL) M-waves] were used as an index of excitability. Ten subjects successfully completed five experiments, spaced at least 1 week apart, in which intermittent tetanic trains at different frequencies of stimulation (0-30 Hz) were used to fatigue the ankle dorsi-flexors. Muscles were rendered ischaemic via a thigh cuff inflated above mean arterial pressure. The effects of ischaemia were examined by repeating the 20-Hz stimulation protocol under non-ischaemic conditions. Five of those subjects also participated in one further session in which the ischaemic plantar-flexors were also fatigued. It was hypothesized that muscle excitability would be preferentially retained in the SOL. Maintenance of excitability in both muscles was possible for 1 min regardless of stimulus frequency; thereafter, stimulation at the highest frequencies induced the greatest decline [30 Hz stimulation; 95.4 (0.5)%, P < 0.01) in the amplitude of the M-wave. The decline in M-wave amplitude was always greater than the decline in M-wave area and occurred at firing rates not normally associated with neuromuscular blockade, implying propagation failure along the sarcolemma. The presence of ischaemia significantly accelerated the decline in both amplitude (78% versus 12%, P<0.01) and area (45% versus no decline, P<0.01) of the M-wave. Recovery was limited when tetanic stimulation ceased but progressed rapidly after circulation was restored. Twitch and tetanic torque declines were significantly different between SOL and TA (fall between rest and fatigue -SOL: 77%, 75.2%; TA: 95.5%, 96.9%, P<0.01, respectively). M-wave changes between the two muscles were not significantly different although the onset of the decline was delayed in the SOL. It is proposed that the observed delay in fatiguing decline was due to the early potentiation in muscle excitability observed in the SOL but not in the TA.