Altered responses of human elbow flexors to peripheral-nerve and cortical stimulation during a sustained maximal voluntary contraction

The short-latency electromyographic response evoked by transcranial magneti c stimulation (MEP) increases in size during fatigue, but the mechanisms ar e unclear. Because large changes occur in the muscle action potential, we t ested whether changes in the response to stimulation of the peripheral moto r nerve could fully account for the increase in the MEP. Subjects (n=8) per formed sustained maximal voluntary contractions (MVCs) of the right elbow f lexors for 2 min. During the contraction, the MEP and the response to supra maximal stimulation of motor-nerve fibres in the brachial plexus were alter nately recorded. During the contraction, responses to motor-nerve stimulati on increased in area by 87+/-35% (mean+/-SD) in the biceps brachii and 74+/ -30% in the brachioradialis, but the area of the MEPs increased by 153+/-86 % and 175+/-122%, respectively. Thus, the increase in the MEP was greater t han the increase in the peripheral M-wave. The onset latency of the MEP in the biceps brachii increased by 0.7+/-0.6 ms (range: -0.2 to 1.9 ms) during the sustained contraction. A smaller increase occurred in response to peri pheral nerve stimulation (0.3+/-0.3 ms; from -0.3 to 0.9 ms). In the contra lateral elbow flexors, neither responses to transcranial magnetic stimulati on nor responses to motor-nerve stimulation changed in size or latency. Dur ing the sustained contraction, the shea silent period after stimulation of the peripheral nerve (48+/-5 ms in biceps brachii and 48+/-4 ms in brachior adialis) increased in duration by about 12 ms (to 61+/-12 ms and 60+/-9 ms, respectively), whereas the silent period following transcranial magnetic s timulation increased from 238+/-39 ms in biceps brachii and 243+/-34 ms in brachioradialis to 325+/-41 ms and 343+/-42 ms, respectively. During a sust ained MVC, while the motor responses to peripheral and to cortical stimulat ion grow concurrently, growth of the MEP cannot be entirely accounted for b y changes in the muscle action potential. Hence, some of the increase in ME P size during fatigue must reflect changes in the central nervous system. I ncreased latency of the MEPs and lengthening of the peripherally evoked sil ent period are consistent with decreased excitability of the alpha motoneur one pool. Thus, an increased response from the motor cortex to the magnetic stimulus remains a likely contributor to the increase in the size of the M EP in fatigue.