This is the first study to examine corticospinal excitability (CSE) to antagonistic muscle groups during arm cycling. Transcranial magnetic stimulation (TMS) of the motor cortex and transmastoid electrical stimulation (TMES) of the corticospinal tract were used to assess changes in supraspinal and spinal excitability, respectively. TMS induced motor evoked potentials (MEPs) and TMES induced cervicomedullary evoked potentials (CMEPs) were recorded from the biceps and triceps brachii at two positions, mid-elbow flexion and extension, while cycling at 5% and 15% of peak power output. While phase-dependent modulation of MEP and CMEP amplitudes occurred in the biceps brachii, there was no difference between flexion and extension for MEP amplitudes in the triceps brachii and CMEP amplitudes were higher during flexion than extension. Furthermore, MEP amplitudes in both biceps and triceps brachii increased with increased workload. CMEP amplitudes increased with higher workloads in the triceps brachii, but not biceps brachii, though the pattern of change in CMEPs was similar to MEPs. Differences between changes in CSE between the biceps and triceps brachii suggest that these antagonistic muscles may be under different neural control during arm cycling. Putative mechanisms are discussed.

In quadrupeds, special circuity located within the spinal cord, referred to as central pattern generators (CPGs), is capable of producing complex patterns of activity such as locomotion in the absence of descending input. During these motor outputs, the electrical properties of spinal motoneurones are modulated such that the motoneurone is more easily activated. Indirect evidence suggests that like quadrupeds, humans also have spinally located CPGs capable of producing locomotor outputs, albeit descending input is considered to be of greater importance. Whether motoneurone properties are reconfigured in a similar manner to those of quadrupeds is unclear. The purpose of this review is to summarize our current state of knowledge regarding the modulation of motoneurone excitability during CPG-mediated motor outputs using animal models. This will be followed by more recent work initially aimed at understanding changes in motoneurone excitability during CPG-mediated motor outputs in humans, which quickly expanded to also include supraspinal excitability.

Lockyer EJ, Benson RJ, Hynes AP, Alcock LR, Spence AJ, Button DC, Power KE. Intensity matters: effects of cadence and power output on corticospinal excitability during arm cycling are phase and muscle dependent. The present study investigated the effects of cadence and power output on corticospinal excitability to the biceps (BB) and triceps brachii (TB) during arm cycling. Supraspinal and spinal excitability were assessed using transcranial magnetic stimulation (TMS) of the motor cortex and transmastoid electrical stimulation (TMES) of the corticospinal tract, respectively. Motor-evoked potentials (MEPs) elicited by TMS and cervicomedullary motor-evoked potentials (CMEPs) elicited by TMES were recorded at two positions during arm cycling corresponding to mid-elbow flexion and mid-elbow extension (i.e., 6 and 12 o'clock made relative to a clock face, respectively). Arm cycling was performed at combinations of two cadences (60 and 90 rpm) at three relative power outputs (20, 40, and 60% peak power output). At the 6 o'clock position, BB MEPs increased~11.5% as cadence increased and up to~57.2% as power output increased (P Ͻ 0.05). In the TB, MEPs increased~15.2% with cadence (P ϭ 0.013) but were not affected by power output, while CMEPs increased with cadence (~16.3%) and power output (up to~19.1%, P Ͻ 0.05). At the 12 o'clock position, BB MEPs increased~26.8% as cadence increased and up to~96.1% as power output increased (P Ͻ 0.05), while CMEPs decreased~29.7% with cadence (P ϭ 0.013) and did not change with power output (P ϭ 0.851). In contrast, TB MEPs were not different with cadence or power output, while CMEPs increased 12.8% with cadence and up to~23.1% with power output (P Ͻ 0.05). These data suggest that the "type" of intensity differentially modulates supraspinal and spinal excitability in a manner that is phase-and muscle dependent. NEW & NOTEWORTHYThere is currently little information available on how changes in locomotor intensity influence excitability within the corticospinal pathway. This study investigated the effects of arm cycling intensity (i.e., alterations in cadence and power output) on corticospinal excitability projecting to the biceps and triceps brachii during arm cycling. We demonstrate that corticospinal excitability is modulated differentially by cadence and power output and that these modulations are dependent on the phase and the muscle examined.

Measures of walking such as the timed 25-ft walk test (T25FWT) may not be able to detect subtle impairment in lower limb function among people with multiple sclerosis (MS). We examined bipedal hopping to determine to what extent people with mild (Expanded Disease Severity Scale ≤ 3.5) MS (n = 13) would differ compared to age-, gender-, and education-matched controls (n = 9) and elderly participants (n = 13; ≥ 70 years old). We estimated lower limb power (e.g., hop length, velocity), consistency (e.g., variability of hop length, time), and symmetry (ratio of left to right foot). Participants completed the T25FWT and, after a rest, they then hopped using both feet 4 times along the walkway. We found that although all groups scored below the 6 -s cutoff for T25FWT, the elderly group had significantly shorter hop lengths, more variability, and more asymmetry than the controls. The results of the MS group were not significantly different from the elderly or controls in most measures and most of their values fell between the control and elderly groups. Hop length, but not measures of walking predicted Expanded Disease Severity Scale score (R = .38, p = .02). Bipedal hopping is a potentially useful measure of lower limb neuromuscular performance.

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