Voluntary contraction impairs the refractory period of transmission in healthy human axons

Citation
S. Kuwabara et al., Voluntary contraction impairs the refractory period of transmission in healthy human axons, J PHYSL LON, 531(1), 2001, pp. 265-275
Citations number
50
Categorie Soggetti
Physiology
Journal title
JOURNAL OF PHYSIOLOGY-LONDON
ISSN journal
00223751 → ACNP
Volume
531
Issue
1
Year of publication
2001
Pages
265 - 275
Database
ISI
SICI code
0022-3751(20010215)531:1<265:VCITRP>2.0.ZU;2-S
Abstract
1. Voluntary contraction of a muscle causes substantial hyperpolarization o f the active motor axons due to activation of the electrogenic Na+-K+ pump. The present study was undertaken to determine whether voluntary effort pro duces a significant impairment in impulse transmission in normal axone and whether mechanisms other than membrane hyperpolarization contribute to the changes in axonal excitability. 2. The compound muscle action potential (CMAP) was recorded after median ne rve stimulation at the wrist using sub- and supramaximal stimuli, delivered singly and in pairs at conditioning-test intervals of 2-15 ms. Axonal exci tability parameters (threshold, refractoriness, supernormality, and strengt h-duration time constant (tau (SD))) were measured using threshold tracking . Impulse transmission was assessed using supramaximal stimuli. 3. Maximal voluntary contractions of the abductor pollicis brevis for 1 min produced a substantial increase in threshold, an increase in supernormalit y and a decrease in tau (SD), all of which lasted similar to 10 min and ind icate axonal hyperpolarization. However, immediately after the contraction there was an unexpected increase in refractoriness. The post-contraction in crease in refractoriness could mot be mimicked by an imposed ramp of hyperp olarization that produced changes in the other indices to an extent that wa s similar to voluntary contraction. 4. The contraction had relatively little effect on the size of the uncondit ioned maximal CMAP. However, there was failure of transmission of supramaxi mal conditioned volleys when the conditioning-test interval was short. 5. The relationships between axonal excitability and supernormality and tau (SD) following voluntary contraction differed significantly from those rec orded during the hyperpolarization produced by DC current. It is argued tha t these differences probably result from extra-axonal K+ accumulation with the voluntary contraction but not with the DC polarization. 6. It is concluded that, following maximal voluntary contraction of a norma l muscle, the refractory period of transmission is impaired distal to the s timulus site sufficient to cause transmission failure of the second of a pa ir of closely spaced impulses. The site of transmission failure is: likely to be the terminal axon, presumably at branch points, possibly in the unmye linated pre-terminal segment.