TY - JOUR
T1 - Load- and cadence-dependent modulation of somatosensory evoked potentials and Soleus H-reflexes during active leg pedaling in humans
AU - Sakamoto, Masanori
AU - Nakajima, Tsuyoshi
AU - Wasaka, Toshiaki
AU - Kida, Tetsuo
AU - Nakata, Hiroki
AU - Endoh, Takashi
AU - Nishihira, Yoshiaki
AU - Komiyama, Tomoyoshi
PY - 2004/12/17
Y1 - 2004/12/17
N2 - Modulation of transmission in group I muscle afferent pathways to the somatosensory cortex and those to the α-motoneuron were investigated during active leg pedaling. Cerebral somatosensory evoked potentials (SEPs) and Soleus (Sol) H-reflexes following posterior tibial nerve stimulation were recorded at four different pedaling phases. The subjects were asked to perform pedaling at three different cadences (30, 45 and 60 rpm with 0.5 kp, cadence task; C-task) and with three different workloads (at 45 rpm with 0.0, 0.5 and 1.0 kp, load task; L-task). In both C- and L-tasks, Sol H-reflexes were modulated in a phase-dependent manner, showing an increase in the power phase and a decrease in the recovery phase. In contrast, the early SEP (P30-N40) components were modulated in a phase-dependent manner when the cadence and load were low. When focusing on the power phases, significant cadence- and load-dependent modulations of the P30-N40 were found, and inversely graded with the cadence and load. The H-reflex was found to be significantly decreased at the highest cadence, i.e., cadence-dependent modulation. In contrast, the H-reflex during the L-task was found to be proportional to the load. The correlation analysis between the size of H-reflex and the amount of background (BG) electromyographic (EMG) activity demonstrated that the H-reflex in the power phase did not depend on the BG EMG in either C- or L-task. These findings suggested that transmission of muscle afferents along the ascending pathways to the cerebral cortex and the spinal cord is independently controlled in accordance with the biomechanical constraints of active pedaling.
AB - Modulation of transmission in group I muscle afferent pathways to the somatosensory cortex and those to the α-motoneuron were investigated during active leg pedaling. Cerebral somatosensory evoked potentials (SEPs) and Soleus (Sol) H-reflexes following posterior tibial nerve stimulation were recorded at four different pedaling phases. The subjects were asked to perform pedaling at three different cadences (30, 45 and 60 rpm with 0.5 kp, cadence task; C-task) and with three different workloads (at 45 rpm with 0.0, 0.5 and 1.0 kp, load task; L-task). In both C- and L-tasks, Sol H-reflexes were modulated in a phase-dependent manner, showing an increase in the power phase and a decrease in the recovery phase. In contrast, the early SEP (P30-N40) components were modulated in a phase-dependent manner when the cadence and load were low. When focusing on the power phases, significant cadence- and load-dependent modulations of the P30-N40 were found, and inversely graded with the cadence and load. The H-reflex was found to be significantly decreased at the highest cadence, i.e., cadence-dependent modulation. In contrast, the H-reflex during the L-task was found to be proportional to the load. The correlation analysis between the size of H-reflex and the amount of background (BG) electromyographic (EMG) activity demonstrated that the H-reflex in the power phase did not depend on the BG EMG in either C- or L-task. These findings suggested that transmission of muscle afferents along the ascending pathways to the cerebral cortex and the spinal cord is independently controlled in accordance with the biomechanical constraints of active pedaling.
KW - Active pedaling
KW - H-reflex
KW - Load- and cadence-dependent modulation
KW - Phase-dependent modulation
KW - Somatosensory evoked potential
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UR - http://www.scopus.com/inward/citedby.url?scp=7944232370&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2004.09.054
DO - 10.1016/j.brainres.2004.09.054
M3 - Article
C2 - 15542082
AN - SCOPUS:7944232370
SN - 0006-8993
VL - 1029
SP - 272
EP - 285
JO - Brain Research
JF - Brain Research
IS - 2
ER -