During rhythmic arm cycling soleus H-reflex amplitudes are reduced by modulation of group Ia presynaptic inhibition (Frigon et al, 2004). This reflex suppression is graded with the frequency of arm cycling (Loadman & Zehr 2007; Hundza & Zehr 2009) and 0.8 Hz is the minimum frequency to significantly reduce the soleus H-reflex (Hundza & Zehr 2009). Despite the data on modulation of the soleus H-reflex amplitude induced by rhythmic arm cycling, comparatively little is known about the modulation of stretch reflexes due to remote limb movement. Therefore, the present study was intended to explore the effect of arm cycling on stretch and H-reflex amplitudes in the soleus muscle. In so doing, additional information on the mechanism of action during rhythmic arm cycling would be revealed. Although both reflexes share the same afferent pathway, we hypothesized that stretch reflex amplitudes would be less suppressed by arm cycling because they are less inhibited by presynaptic inhibition (Morita et al, 1998). Failure to reject this hypothesis would add additional strength to the argument that Ia presynaptic inhibition is the mechanism modulating soleus H-reflex amplitude during rhythmic arm cycling. Participants were seated in a customized chair with feet strapped to footplates. Three motor tasks were performed: static control trials and arm cycling at 1 and 2 Hz. Soleus H-reflexes were evoked using single 1 ms pulses of electrical stimulation delivered to the tibial nerve at the popliteal fossa. A constant M-wave and ~6% MVC activation of soleus was maintained across conditions. Stretch reflexes were evoked using a vibratory shaker (ET-126; Labworks Inc). The shaker was placed over the triceps surae tendon and controlled by a custom written LabView program (single sinusoidal pulse at 100Hz). Results demonstrated that rhythmic arm cycling that was effective for conditioning soleus H-reflexes did not show a suppressive effect on the amplitude of the soleus stretch reflex. We suggest this indicates that stretch reflexes are less sensitive to conditioning by rhythmic arm movement, as compared to H-reflexes, due to the relative insensitivity of Ia presynaptic inhibition. / Graduate

Training locomotor pattern generating networks (CPGs) with body weight supported treadmill training or through arm and leg cycling improves walking in chronic stroke. These outcomes are presumed to result from enhanced interlimb connectivity and CPG function. The extent to which rhythmic arm training activates interlimb CPG networks for locomotion remains unclear and was assessed by studying chronic stroke participants before and after 5-weeks of arm cycling training. Strength was assessed bilaterally via maximal voluntary isometric contractions in the legs and hands. Muscle activation during arm cycling and transfer to treadmill walking were assessed in the more affected (MA) and less affected (LA) sides via surface electromyography. Changes to interlimb coupling during rhythmic movement were evaluated using modulation of cutaneous reflexes elicited by electrical stimulation of the superficial radial nerve at the wrist. Bilateral soleus stretch reflexes were elicited at rest and during 1Hz arm cycling. Clinical function tests assessed walking, balance and motor function. Results show significant changes in function and neurophysiological integrity. Training increased bilateral grip strength, force during MA plantarflexion and muscle activation. ‘Normalization’ of cutaneous reflex modulation was found during arm cycling. There was enhanced activity in the dorsiflexor muscles on the MA side during swing phase of walking. Enhanced interlimb coupling was shown by increased modulation of MA soleus stretch reflexes amplitudes during arm cycling after training. Clinical evaluations showed enhanced walking ability and balance. These results are consistent with training-induced changes in CPG function and interlimb connectivity and underscore the need for arm training in the functional rehabilitation of walking after neurotrauma. / Graduate

In common with animal species, evidence in humans suggests that similar neural mechanisms (e.g. locomotor central pattern generator (CPG)) regulate rhythmic movements in both arm and leg and that interlimb neural connections coordinate movement between upper and lower limbs ; however, by comparison the evidence in humans is limited. This thesis focused upon exploring the neural control of rhythmic arm cycling and the influence of the neural control of arm cycling on the neural circuits controlling the legs. Specifically, the effect of five different arm cycling paradigms on EMG and reflex responses in arm and leg muscles were explored. First, the pattern of muscle activity and cutaneous reflex modulation evoked with electrical stimulation to the superficial radial (SR) nerve were evaluated during forward and backward arm cycling. Irrespective of the cycling direction, background electromyographic (bEMG) and cutaneous reflex patterns were similarly modulated suggesting similar neural control mechanisms for both forward and backward cycling. These bEMG and reflex findings provide further evidence of contributions from CPG activity to the neural regulation of rhythmic arm movement. Second, bEMG and cutaneous reflex (SR nerve) modulation were evaluated during three dissimilar bilateral rhythmic arm cycling tasks created by unilaterally manipulating crank length (CL). The neural regulation of arm cycling was shown to be insensitive to asymmetrical changes in arm crank length suggesting that the neural control was equivalent across the three dissimilar rhythmic arm cycling tasks and that differences in peripherally generated inputs between the dissimilar rhythmic tasks had limited effect on the neural control. Third, the neural control of arm movements was evaluated between those with unstable shoulders and control participants. The alterations of bEMG and the cutaneous reflex patterns suggest that the neural control is compromised in those with shoulder instabilities during rhythmic arm movement. Fourth, inhibition of the soleus H-reflex in stationary legs induced by rhythmic arm cycling was shown to be graded with arm cycling frequency. A minimum threshold arm cycling frequency of .8Hz was required to produce a significant interlimb effect. Fifth, the degree of the soleus H-reflex suppression induced by arm cycling was independent of afferent feedback associated with arm cycling at different crank loads. In combination the latter two studies suggest that central motor commands related to the frequency of arm cycling is the major signal responsible for the soleus H-reflex suppression in stationary legs, while afferent feedback related to upper limb loading during arm cycling is not. Collectively, the data contained in this thesis contribute to the evidence suggesting that CPG activity contributes to neural regulation of rhythmic arm movement, alterations in sensory feedback associated with arm cycling have limited influence on the observed reflex modulation and that the neural control can be disrupted in the presence of prolonged orthopaedic injury. Taken together with our previous findings, the current results also suggests that central motor command (e.g. CPGs) for rhythm generation of the rhythmic arm movement is the primary source of the signal responsible for the observed interlimb neural communication.

Plasticity in spinal networks has been proposed as a means to permit motor skill learning and recovery after central nervous system disorders. This plasticity is significantly driven by input from the periphery (Wolpaw & Carp, 2006). For instance, attenuation of soleus Hoffmann (H) reflex can last beyond the period of different types of conditioning via putative presynaptic inhibition (Brooke et al., 1997). Interestingly, rhythmic arm cycling can also attenuate soleus H-reflex via interlimb connections and presynaptic pathways (Frigon, Collins, & Zehr, 2004). However, it remains to be studied if this attenuation is maintained beyond the period of arm cycling. In this study, we hypothesized that excitability of H-reflex pathway would remain suppressed after cessation of arm cycling. Subjects were seated with their trunk and feet fixed at a neutral position. Using an arm ergometer, they cycled at 1Hz for 30min. H-reflexes were evoked via stimulation of the tibial nerve in the popliteal fossa at 5 minute intervals. These intervals began prior to the cycling and continued during cycling and up to 30 minutes iv after termination of cycling (n=12). Besides soleus muscle, electromyography was recorded from tibialis anterior, vastus lateralis and biceps femoris. Stimulation was set to evoke an M-wave which evoked an H-reflex on the ascending limb of the recruitment curve (size was 75% Hmax) obtained prior to cycling. The M-wave amplitude was maintained throughout all trials by monitoring and adjusting the level of stimulation intensity. All H-reflex and M-wave data were normalized to the averaged Mmax to reduce inter –subject variability. The main result was that the suppression of H-reflex amplitude persisted beyond the period of arm cycling. H-reflex amplitudes were significantly (p<0.05) smaller up to 20 min after arm cycling had stopped. This suggests that arm cycling can induce plastic adaptation in the soleus H-reflex pathway that persists well beyond the period of conditioning. Also, in an additional experiment (n=8), the prolonged effect of arm cycling combined with superficial radial (SR) nerve stimulation was investigated. Interestingly, this cutaneous nerve stimulation cancelled out the prolonged suppression of H-reflex amplitude induced by arm cycling. Since SR nerve stimulation facilitates soleus H-reflex via reductions in the level of Ia presynaptic inhibition (Zehr, Hoogenboom, Frigon, & Collins, 2004), persistence in presynaptic inhibitory pathways is suggested as an underlying neural mechanism. These results have relevance for optimizing rehabilitation techniques in the treatment of spasticity which is known to be related to the H-reflex size (Levin & Hui-Chan, 1993).

Rhythmic arm cycling suppresses the soleus H-reflex amplitude in stationary legs in neurologically intact (NI) participants. It has been suggested that interlimb pathways connecting cervical and lumbosacral spinal cord are responsible for modulating the reflex excitability. After stroke, stretch reflex and its electrical analogue the H-reflex become hyperactive. The purpose of this study was to examine the effect of arm cycling on the H-reflex amplitude in the stationary legs after stroke. It was hypothesized that rhythmic arm movement would suppress the H-reflex amplitudes in the Iegs after stroke. Sixteen stroke participants performed bilateral arm cycling at 1Hz and at the highest frequency possible they could maintain. Additionally, thirteen age-matched neurologically intact individuals participated as a control group. Tibial nerves were stimulated to evoke H-reflexes simultaneously in both legs. M-wave, H-reflex (M-H) recruitment curves (RC) were collected during arm cycling and with arms stationary. Four variables (i.e.. M-H slope, H at threshold. Hmax, and 50% Hmax] obtained from the ascending limb of the M-H RC were compared across conditions. Results showed that the general effects of arm cycling in suppressing H-reflex size are preserved after stroke. However, effects after stroke were limited in that arm cycling did not affect the whole recruitment curve similarly, as it does in the NI population. Overall the results suggest that incorporation of rhythmic arm movement in rehabilitation paradigms after stroke might be helpful in suppression of hyperactive reflexes in the legs and therefore assist in locomotion.