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Updated: Jun 22, 2026

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI
Published on: April 18, 2011
Repeated maximal volitional effort contractions in human spinal cord injury: initial torque increases and reduced
T George Hornby1, Michael D Lewek, Christopher K Thompson
1Department of Physical Medicine and Rehabilitation, Northwestern University Medical School, Chicago, Illinois 60612, USA. tgh@uic.edu
Background:
Substantial data indicate greater muscle fatigue in individuals with spinal cord injury (SCI) compared with healthy control subjects when tested by using electrical stimulation protocols. Few studies have investigated the extent of volitional fatigue in motor incomplete SCI.
Methods:
Repeated, maximal volitional effort (MVE) isometric contractions of the knee extensors (KE) were performed in 14 subjects with a motor incomplete SCI and in 10 intact subjects. Subjects performed 20 repeated, intermittent MVEs (5 seconds contraction/5 seconds rest) with KE torques and thigh electromyographic (EMG) activity recorded.
Results:
Peak KE torques declined to 64% of baseline MVEs with repeated efforts in control subjects. Conversely, subjects with SCI increased peak torques during the first 5 contractions by 15%, with little evidence of fatigue after 20 repeated efforts. Increases in peak KE torques and the rate of torque increase during the first 5 contractions were attributed primarily to increases in quadriceps EMG activity, but not to decreased knee flexor co-activation. The observed initial increases in peak torque were dependent on the subject's volitional activation and were consistent on the same or different days, indicating little contribution of learning or accommodation to the testing conditions. Sustained MVEs did not elicit substantial increases in peak KE torques as compared to repeated intermittent efforts.
Conclusions:
These data revealed a marked divergence from expected results of increased fatigability in subjects with SCI, and may be a result of complex interactions between mechanisms underlying spastic motor activity and changes in intrinsic motoneuron properties.
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