Eleven healthy subjects repetitively performed maximal cycling movement for 10 s with 20 s rest intervals. The load of the cycling was respectively set to 30% (high frequency task, lIF' task) and 80% (high power task, TIP task) of the optimal load for exerting maximum anaerobic power. Each task was finished when the exerted maximal power was decreased to 80% of the initial value. While performing each task, transcranial magnetic stimulation (TMS) was delivered to the motor cortex which was effectively able to evoke motor evoked potential (MEP) from the thigh muscles. Elec-tromyographic (EMG) activity of the left rectos femoris (RF), vastus lateralis (VL) and the MEP was analyzed.
The maximal power exerted was decreased to 80.6±1.58 % in the HF task, and 77.3±0.77 % in the HP task. The number of repeated sets in each task was 10.1 ± 1.45 (HF task) and 4.1±0.25 sets (HP task) . The MEP area of the RF and VL was not changed significantly in the HF task, though it was significantly increased in the latter half of the HP task. A two-way ANOVA showed that the time course of the changes in the MEP area was significant in the VL (p<0.01), but not in the RF. In both tasks, the duration of the MEP was progressively prolonged in each 10 sec pedaling, and the prolongation was evident in the latter half of the tasks. However, the magnitude of the prolongation was significantly larger during the HP task. The ratio of the integrated amplitude of the EMG and the exerted power at the initial 5 bouts of cycling (EMG/Power ratio) was significantly increased in both the RF and VL, suggesting that peripheral muscular fatigue was induced during at the latter half of each task. Furthermore, the EMG/Power ratio in the VL was significantly higher during the HP task than the HF task.
These results suggest that central fatigue plays a significant role in decreasing the maximum power output, and that it takes place in a muscle-dependent fashion. It was also suggested that during low load, but relatively higher cadence frequency, central fatigue other than that involving the motor cortex accounts for the decreased power output.

Changes in the motor evoked potential (MEP) evoked by transcranial magnetic motor cortex stimulation (TMS) of rectos femoris (RF) and vastus lateralis (VL) was examined during constant cadence cycling tasks for 60 sec. Subjects were 11 normal male volunteers aged between 19 and 25 years. Pedaling load was set at 100% and 80% of the estimated optimal value for maximum anaerobic power output. For the low load task (LL task), the pedaling rate was set at half the value of the maximum pedaling rate with the load set at 80% of the optimal for maximum anaerobic power output. For the high load task (HL task), the pedaling rate was set such that the power was equivalent to the LL task.
The route mean square of the electromyographic (EMG) activity amplitude tended to steeply increase during the latter half of the task. The magnitude of the increase in the RMS was significantly larger in the HL task than the LL task. The area of the MEP also tended to increase in both tasks, though the degree of the increase was significantly larger in the LL task than the HL task. The EMG silent period (SP) after the MEP tended to steeply increase just after the task initiation and to decrease in the latter half of the task in the HL task. However, in the LL task the facilitation of MEP was not found, but it showed a gradual decrease while performing the task. The duration of the MEP tended to increase in both tasks, though the degree of the increase in the VL was significantly larger in the LL task than the HL task. The linear regression analysis between the size of the MEP and the background EMG shows a significant positive correlation coefficient during isometric contraction, but not during the two types of cycling tasks.
These results suggest that the neural circuit responsible for the MEP was controlled differentially during isometric contraction and constant cadence pedaling. Also it is likely that the mechanism of central fatigue differed depending on the cadence and or load in a task-dependent fashion irrespective of the same power output.

The present study investigated how resistance training affects behaviors related to central and peripheral fatigue during a sustained maximal voluntary contraction (MVC) . The subjects were well-trained (TR, n=8) and sedentary untrained (UT, n=6) males. The subjects were asked to repetitively perform 3 sets of MVC (elbow flexion) for 1 min with a rest interval of 1 min. Transcranial magnetic stimulation (TMS) was delivered to the contralateral motor cortex to evoke the motor evoked potential (MEP) and electromyographic (EMG) silent period (SP) after the MEP. Ratio of root mean square (RMS) of the EMG and elbow flexion force (RMS/F) was also calculated.
The time course of the decrease in elbow flexion force that was standardized with respect to the maximal value obtained at the beginning of the first MVC was almost identical in both TR and UT. At the end of the task, the elbow flexion force decreased to around 30 % of the initial value in both groups. Decrease in voluntary activation (VA) estimated by the increment of the force after TMS was significantly larger in UT (77.3%) than in TR (88.2%) at the end of the task. Although the increase in MEP during the first set was significantly greater in UT than in TR, elongation of SP was significantly larger in UT than in TR. Increase in RMS/F, which is a manifestation of peripheral fatigue, was significantly larger in TR than in UT.
These results suggest that decrease in MVC in UT and in TR is respectively more attributable to central and peripheral fatigue, and that inhibitory inputs to motor cortex were larger in UT than in TR. It is concluded that expression of central and peripheral fatigue is affected by resistance training.

The present study investigated an effective method of eliciting medium and long latency cutaneous reflexes in normal human subjects. The effect of changes in stimulus conditions (number of pulse train, duration of electrical pulse and inter-stimulus interval) on cutaneous reflexes in the first dorsal interosseous muscle (FDI) following non-noxious electrical stimulation to the hand digits (digit 1 ; D1, digit 2 ; D2 and digit 5 ; D5) were investigated in seven healthy volunteers. Cutaneous reflexes were elicited while the subjects performed isolated isometric contraction of FDI (D2 abduction). Under all experimental conditions, the level of muscle contraction was set at 10% of the maximal EMG amplitude, which was determined during maximal voluntary contraction. Intensity of the electrical stimulation was set at 2.0 times the perceptual threshold under all experimental conditions.Although the amplitude of E2 (excitatory response, peak latency ∼60∼90 ms) was independent of the number of pulses (1, 2, 3, and 5 pulses, pulse frequency at 333 Hz), that of I1 (inhibitory response, ∼45∼60 ms), I2 (inhibitory response, ∼90∼120 ms) and E3 (excitatory response, ∼120∼180 ms) was significantly increased depending on the number of pulses (p<0.001). Amplitudes of E2 and I2 were significantly affected by the digit stimulated (p<0.01). For all four components of the cutaneous reflexes, there were no significant differences in magnitude even by alternating both the inter-stimulus interval (fixed at 1, 2 and 3 Hz and random between at 0.7 and 2 Hz) and the duration (0.1, 0.5 and 1 ms) of the electrical stimulation.These findings suggest that the susceptibility of responsible interneurons impinging on each reflex pathway to temporal summation of the test impulse differs depending on the digit stimulated. It is also likely that almost the same population of the cutaneous afferent fibers were activated by test stimulation with different durations as far as the same stimulus intensity was utilized. As a practical application, double or more pulses up to 3 Hz without causing pain is recommended to effectively evoke medium and long latency cutaneous reflexes in FDI, which would reduce possible effects arising from fatigue.

It has recently demonstrated that central fatigue during sustained maximal voluntary contraction (MVC) progresses faster in the presence of delayed onset muscle soreness due to eccentric contractions than in normal states (Endoh et al., 2005). However, it remains to be clarified whether these findings are related to muscle damage or muscle pain induced by eccentric contractions. The present study investigated which factor plays a more critical role in the earlier onset of central fatigue during sustained MVC with muscle pain induced by injecting hypertonic saline. Ten healthy male right-handed subjects (age, 21~32 yrs.) were asked to perform brief MVCs (~3 sec) before and after injection of isotonic saline (0.9%, 1.0 ml, ISO) or hypertonic saline (5.25%, 1.0 ml, HYP) into the left biceps brachii. The subjects then performed 1 min MVC (fatigue test) with isometric elbow flexion was done in ISO or HYP condition or intact control condition (CON). During these contractions, transcranial magnetic stimulation was delivered to the contralateral motor cortex to evaluate voluntary activation (VA), the motor evoked potential (MEP) and electromyographic (EMG) silent period (SP). Ratio of root mean square of the EMG and elbow flexion force (EMGrms/F) was also measured.The peak pain induced by the injection of HYP was significantly higher than that of ISO (p<0.01). There was no significant difference in either the maximum size of the M response or the twitch force between ISO and HYP (p>0.05). However, during the brief MVCs, both maximal force (p<0.01) and VA (p<0.05) for HYP were significantly decreased compared to those for ISO. During the fatigue test, although MVC, VA, MEP and SP were significantly altered (p<0.05~0.01), there was no significant difference among CON, ISO and HYP (p>0.05). There was no significant difference in EMGrms during the fatigue test (p>0.05).These results suggest that peripheral force-producing capacity remained intact after the injection of ISO and HYP during sustained MVC, and that progression of central fatigue during sustained MVC was less affected by the increased group III and IV afferent activity induced by HYP.