TY - JOUR
T1 - Central excitability contributes to supramaximal volitional contractions in human incomplete spinal cord injury
AU - Thompson, Christopher K.
AU - Lewek, Michael D.
AU - Jayaraman, Arun
AU - Hornby, T. George
PY - 2011/8
Y1 - 2011/8
N2 - Non-technical summary: Individuals with a motor incomplete spinal cord injury (SCI) present clinically with partial control of muscles below the site of the injury, but experience profound weakness which can limit the ability to perform functional tasks such as walking. Interestingly, when individuals with an incomplete SCI are asked to maximally and repeatedly contract their quadriceps muscles, they demonstrate an increase in the peak force generated; individuals without SCI experience a decline in force, or 'fatigue'. Following these repeated maximal efforts, reflex responses to electrical stimulation over the quadriceps muscle elicited amplified and prolonged, involuntary motor activity. Such responses were not observed prior to the maximal contractions, and were not observed in neurologically intact subjects. This finding suggests that increases in spinal excitability following these maximal efforts may enhance force generating capacity, and provides insight into possible novel therapeutic interventions to restore function following SCI. Despite greater muscle fatigue in individuals with spinal cord injury (SCI) when compared to neurologically intact subjects using neuromuscular electrical stimulation (NMES) protocols, few studies have investigated the extent of volitional fatigue in motor incomplete SCI. Using an established protocol of 20 repeated, intermittent, maximal volitional effort (MVE) contractions, we previously demonstrated that subjects with incomplete SCI unexpectedly demonstrated a 15% increase in peak knee extensor torques within the first five MVEs with minimal evidence of fatigue after 20 contraction. In the present study, we investigated potential segmental mechanisms underlying this supramaximal torque generation. Changes in twitch properties and maximum compound muscle action potentials (M-waves) were assessed prior to and following one, three and five MVEs, revealing a significant 17% increase only in maximum twitch torques after a single MVE. Despite this post-activation potentiation of the muscle, use of conventional NMES protocols to elicit repeated muscular contractions resulted in a significant decrease in evoked torque generation, suggesting limited the muscular contributions to the observed phenomenon. To evaluate potential central mechanisms underlying the augmented torques, non-linear responses to wide-pulse width (1 ms), low-intensity, variable-frequency (25-100 Hz) NMES were also tested prior to and following repeated MVEs. When variable-frequency NMES was applied following the repeated MVEs, augmented and prolonged torques were observed and accompanied by sustained quadriceps electromyographic activity often lasting >2s after stimulus termination. Such data suggest a potential contribution of elevated spinal excitability to the reserve in volitional force generation in incomplete SCI.
AB - Non-technical summary: Individuals with a motor incomplete spinal cord injury (SCI) present clinically with partial control of muscles below the site of the injury, but experience profound weakness which can limit the ability to perform functional tasks such as walking. Interestingly, when individuals with an incomplete SCI are asked to maximally and repeatedly contract their quadriceps muscles, they demonstrate an increase in the peak force generated; individuals without SCI experience a decline in force, or 'fatigue'. Following these repeated maximal efforts, reflex responses to electrical stimulation over the quadriceps muscle elicited amplified and prolonged, involuntary motor activity. Such responses were not observed prior to the maximal contractions, and were not observed in neurologically intact subjects. This finding suggests that increases in spinal excitability following these maximal efforts may enhance force generating capacity, and provides insight into possible novel therapeutic interventions to restore function following SCI. Despite greater muscle fatigue in individuals with spinal cord injury (SCI) when compared to neurologically intact subjects using neuromuscular electrical stimulation (NMES) protocols, few studies have investigated the extent of volitional fatigue in motor incomplete SCI. Using an established protocol of 20 repeated, intermittent, maximal volitional effort (MVE) contractions, we previously demonstrated that subjects with incomplete SCI unexpectedly demonstrated a 15% increase in peak knee extensor torques within the first five MVEs with minimal evidence of fatigue after 20 contraction. In the present study, we investigated potential segmental mechanisms underlying this supramaximal torque generation. Changes in twitch properties and maximum compound muscle action potentials (M-waves) were assessed prior to and following one, three and five MVEs, revealing a significant 17% increase only in maximum twitch torques after a single MVE. Despite this post-activation potentiation of the muscle, use of conventional NMES protocols to elicit repeated muscular contractions resulted in a significant decrease in evoked torque generation, suggesting limited the muscular contributions to the observed phenomenon. To evaluate potential central mechanisms underlying the augmented torques, non-linear responses to wide-pulse width (1 ms), low-intensity, variable-frequency (25-100 Hz) NMES were also tested prior to and following repeated MVEs. When variable-frequency NMES was applied following the repeated MVEs, augmented and prolonged torques were observed and accompanied by sustained quadriceps electromyographic activity often lasting >2s after stimulus termination. Such data suggest a potential contribution of elevated spinal excitability to the reserve in volitional force generation in incomplete SCI.
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U2 - 10.1113/jphysiol.2011.212233
DO - 10.1113/jphysiol.2011.212233
M3 - Article
C2 - 21610138
AN - SCOPUS:79960748793
SN - 0022-3751
VL - 589
SP - 3739
EP - 3752
JO - Journal of Physiology
JF - Journal of Physiology
IS - 15
ER -