Muscles paralyzed by chronic (>1 yr) spinal cord injury fatigue readily. Our aim was to evaluate whether the fatigability of paralyzed thenar muscles (n = 10) could be reduced by the repeated delivery of variable versus constant frequency pulse trains. Fatigue was induced in four ways. Intermittent supramaximal median nerve stimulation (300-ms-duration trains) was delivered at 1) constant high frequency (13 pulses at 40 Hz each second for 2 min); 2) variable high frequency (each second for 2 min). The first two intervals of each variable frequency train were 5 and 20 ms. The remaining pulses were evenly distributed in time across 275 ms. The number of pulses varied for each subject such that the force time integral in the unfatigued state matched that evoked by a constant 40-Hz train; 3) constant low frequency (7 pulses at 20 Hz each second for 4 min); and 4) variable low frequency (each second for 4 min). The pulse pattern was the same as that for variable high frequency except that the force-time integral was matched to that produced by the constant low-frequency stimulation. These same experiments were performed on the thenar muscles of five able-bodied control subjects. The variable high-frequency trains used to fatigue paralyzed and control muscles had an average (+/- SE) of 12 +/- 2 and 10 +/- 1 pulses, respectively. Variable low-frequency trains had 7 +/- 1 and 6 +/- 1 pulses, respectively. Significant mean force declines of comparable magnitude (to 20-25% initial fatigue force or to 13-21% initial 50 Hz force) were seen in paralyzed muscles with all four stimulation protocols. The force reductions in paralyzed muscles were always accompanied by significant increases in half-relaxation time and decreases in force-time integral, irrespective of the stimulation protocol. Significant force decreases also occurred in control muscles during each fatigue test. Again, these force declines were similar whether constant or variable pulse patterns were used at high or low frequencies (to 40-60% initial fatigue force or to 29-36% initial 50 Hz force). The force reductions in control muscles were significantly less than those seen in paralyzed muscles, except when constant high-frequency stimulation was used. The variations in stimulation frequency, pulse pattern, and pulse number used in this study therefore had little influence on thenar muscle fatigue in control subjects or in spinal cord-injured subjects with chronic paralysis.

The pattern of seven pulses that elicited maximal thenar force was determined for control muscles and those that have been paralyzed chronically by spinal cord injury. For each subject group (n = 6), the peak force evoked by two pulses occurred at a short interval (5-15 ms; a "doublet"), but higher mean relative forces were achieved in paralyzed versus control muscles (41.4 +/- 3.9% vs. 22.7 +/- 2.0% maximal). Thereafter, longer intervals evoked peak force in each type of muscle (mean: 35 +/- 1 ms, 36 +/- 2 ms, respectively). With seven pulses, paralyzed and control muscles reached 76.4 +/- 5.6% and 57.0 +/- 2.6% maximal force, respectively. These force differences resulted from significantly greater doublet/twitch and doublet/tetanic force ratios in paralyzed (2.73 +/- 0.08, 0.35 +/- 0.03) compared with control muscles (2.07 +/- 0.07, 0.25 +/- 0.01). The greater force enhancement produced in paralyzed muscles with two closely spaced pulses may relate to changes in muscle stiffness and calcium metabolism. Peak force-time integrals were also achieved with an initial short interpulse interval, followed by longer intervals. The postdoublet intervals that produced peak force-time integrals in paralyzed and control muscles were longer than those for peak force, however (77 +/- 3 ms, 95 +/- 4 ms, respectively). These data show that the pulse patterns that maximize force and force-time integral in paralyzed muscles are similar to those that maximize these parameters in single motor units and various whole muscles across species. Thus the changes in neuromuscular properties that occur with chronic paralysis do not strongly influence the pulse pattern that optimizes muscle force or force-time integral.

Muscles paralyzed by injury or disease fatigue excessively when stimulated. This study examined whether the first few paralyzed thenar motor units recruited by electrical stimulation of the median nerve were more fatigue resistant than the total thenar motor unit population. The paralyzed thenar muscles of four subjects with chronic cervical spinal cord injury were fatigued by a 2-min intermittent 40-HZ protocol on 2 days. One experiment involved submaximal stimulation, the other supramaximal stimulation. These stimuli resulted in activation of part and all of the thenar muscles, respectively. Relative force loss, force-time integral decline, and slowing of half-relaxation time were always significantly less when only part rather than all of the muscles was fatigued. The part of the paralyzed muscles that was activated was also relatively fatigue resistant compared with control single thenar motor units. Thus, a reversal of recruitment order from fatigable to fatigue-resistant units cannot explain the extreme fatigability of paralyzed muscles. Use of submaximal stimulation during functional electrical stimulation may therefore help to reduce muscle fatigue because it recruits the more fatigue-resistant units.

No abstract

Involuntary muscle contractions are common after spinal cord injury (SCI). Increased sensitivity to Ia muscle afferent input may contribute to the development of these spasms. Since tendon vibration results in a period of postactivation depression of the Ia synapse, we sought to determine whether Achilles tendon vibration (80 HZ for 2 s) altered involuntary contractions evoked by superficial peroneal nerve (SPN) stimulation (5 pulses at 300 HZ) in paralyzed leg muscles of subjects with chronic (>1 year) SCI. Responses to SPN stimulation that were conditioned by vibration were reduced in 66% of trials (by 33+/-12% in tibialis anterior and 40+/-16% in soleus). These reductions in electromyographic activity are unlikely to be mediated by changes at the Ia synapse or motoneuron because vibration did not alter the magnitude of the soleus H reflex. The electromyographic reductions may involve long-lasting neuromodulatory effects on spinal inhibitory interneurons or synapses involved in the flexor reflex pathway. Vibration-evoked depression of electromyographic activity may be clinically useful in controlling involuntary muscle contractions after SCI.

Whether interlimb reflexes emerge only after a severe insult to the human spinal cord is controversial. Here the aim was to examine interlimb reflexes at rest in participants with chronic (>1 year) spinal cord injury (SCI, n = 17) and able-bodied control participants (n = 5). Cutaneous reflexes were evoked by delivering up to 30 trains of stimuli to either the superficial peroneal nerve on the dorsum of the foot or the radial nerve at the wrist (5 pulses, 300 Hz, approximately every 30 s). Participants were instructed to relax the test muscles prior to the delivery of the stimuli. Electromyographic activity was recorded bilaterally in proximal and distal arm and leg muscles. Superficial peroneal nerve stimulation evoked interlimb reflexes in ipsilateral and contralateral arm and contralateral leg muscles of SCI and control participants. Radial nerve stimulation evoked interlimb reflexes in the ipsilateral leg and contralateral arm muscles of control and SCI participants but only contralateral leg muscles of control participants. Interlimb reflexes evoked by superficial peroneal nerve stimulation were longer in latency and duration, and larger in magnitude in SCI participants. Interlimb reflex properties were similar for both SCI and control groups for radial nerve stimulation. Ascending interlimb reflexes tended to occur with a higher incidence in participants with SCI, while descending interlimb reflexes occurred with a higher incidence in able-bodied participants. However, the overall incidence of interlimb reflexes in SCI and neurologically intact participants was similar which suggests that the neural circuitry underlying these reflexes does not necessarily develop after central nervous system injury.