Velocity Recovery Function Research Articles

Time‐dependent effects of pre‐conditioning activation on muscle fiber conduction velocity and twitch torque

In this study we investigate the range of interstimulus intervals influencing the recovery functions for conduction velocity (velocity recovery function, or VRF) and twitch torque (twitch torque recovery function, or TRF) of muscle fibers. We studied the tibialis anterior muscle of 8 healthy men by varying the time interval between a pair of stimuli in the range of 4-1000 ms, with (triplet) and without (doublet) a preconditioning stimulus. For triplet stimulations, the interval between the first and second stimulus or between the second and third stimulus was fixed, and the other interval was varied. VRF and TRF were influenced by a preconditioning stimulus only when it was delivered within 125 ms and 30 ms, respectively, before the doublet stimulation. The results provide evidence of the range of preconditioning intervals influencing the VRF and TRF; this is relevant for understanding the mechanisms of force generation and for standardizing compound action potential measurements.

Effect of muscle‐fiber velocity recovery function on motor unit action potential properties in voluntary contractions

Measurements of muscle-fiber conduction velocity during voluntary contractions have been used in the diagnosis of neuromuscular diseases. However, the velocity of propagation of action potentials depends on the interspike interval of activation due to the velocity recovery function (VRF) of muscle fibers. The comparison of muscle-fiber conduction velocity estimates between individuals may thus be influenced by differences in motor unit discharge rate. This study investigates action potential properties of motor units of the sternocleidomastoid muscle during voluntary modulation of discharge rate with the purpose of assessing the effect of the VRF on motor unit properties in voluntary contractions. Nineteen healthy men trained to control a target motor unit with feedback of surface multichannel electromyographic (EMG) signals. The subjects performed three 30-s contractions of cervical flexion/rotation modulating the discharge rate of the target motor unit from 6.6 +/- 1.6 pps to 28.0 +/- 6.4 pps. Action potential conduction velocity was correlated to instantaneous discharge rate (R = 0.38 +/- 0.21). Action potential conduction velocity, peak-to-peak amplitude, and duration varied between minimum and maximum discharge rate (P < 0.01; percent change 12.3 +/- 5.0, -11.8 +/- 9.9, and -12.9 +/- 7.3). Thus, the properties of surface motor unit action potentials vary with modulation of discharge rate. This has implications for the use of conduction velocity values measured during voluntary contractions to differentiate patient populations from healthy individuals and for the development of normative data.

Motor unit discharge pattern and conduction velocity in patients with upper motor neuron syndrome

Motor unit properties were analyzed in patients with upper motor neuron syndrome (UMNS). Multi-channel surface electromyographic (EMG) signals were recorded for 300 s from the biceps brachii muscle of seven male subacute patients (time from lesion, mean ± SE, 4.9 ± 1.0 months). In three patients, both arms were investigated, leading to 10 recorded muscles. Patients were analyzed in rest-like condition with motor units activated due to pathological muscle overactivity. For a total of 12 motor units, the complete discharge pattern was extracted from EMG decomposition. Interpulse interval variability was 7.8 ± 0.9%. At minimum discharge rate (6.4 ± 0.4 pulses per second, pps), conduction velocity was smaller than at maximum discharge rate (12.0 ± 0.9 pps) in all motor units (3.60 ± 0.21 m/s vs. 3.84 ± 0.20 m/s). Conduction velocity changed by 1.35 ± 0.48% (different from zero, P < 0.01) for each increase of 1 pps in discharge rate. It was concluded that conduction velocity of low-threshold motor units in subacute patients with UMNS had similar values as reported in healthy subjects and was positively correlated to instantaneous discharge rate (velocity recovery function of muscle fibers).

Velocity recovery function of the compound muscle action potential assessed with doublet and triplet stimulation

Normative values of muscle fiber conduction velocity depend on the conditions in which conduction velocity is measured due to the velocity recovery function (VRF) of muscle fibers. In this study the VRF of the compound muscle action potential (CMAP) was assessed following doublet and triplet stimulation in order to investigate the effect of repetitive muscle activation on muscle fiber conduction velocity. The VRF from doublet and triplet activation showed a peak of 4.6%-15.0% and 6.4%-25.9%, respectively, which is not significantly different. The VRF of the CMAP with doublet stimulation had a plateau between 25-75 ms, similar to that reported for single muscle fibers, and changed as a consequence of previous activation. The VRFs with doublet and triplet stimulation were different for interstimulus intervals in the range of 12-250 ms, where the triplet resulted in a plateau of supernormal conduction velocity. The VRF of the triplet could be explained by linear summation of the effects from doublet stimulations only for small distances between the two conditioning stimuli. These results provide new information on the adaptation of membrane properties of muscle fibers to repetitive activation. Changes in CMAP properties due to repeated activation may influence the accuracy of techniques based on CMAP recordings, such as collision methods.

Conduction block in one-dimensional heart fibers.

We present a nonlinear dynamical systems analysis of the transition to conduction block in one-dimensional cardiac fibers. We study a simple model of wave propagation in heart tissue that depends only on the recovery of action potential duration and conduction velocity. If the recovery function has slope >or=1 and the velocity recovery function is nonconstant, rapid activation causes dynamical heterogeneity and finally conduction block away from the activation site. This dynamical mechanism may play a role in the initiation and breakup of spiral waves in excitable media.

Muscle fiber conduction velocity changes with length

While recording activity from individual muscle fibers by single fiber EMG (SFEMG), stimulated either through their axons or directly, the length of the recorded muscle fiber was changed--stretched or made shorter--by manipulating the recording needle or by passive joint movements. This resulted in significant changes of latency corresponding to an increase in propagation velocity on shortening of the muscle fiber and to a slowing of its lengthening. The maximum increase in velocity was estimated to 33% and slowing to about 22%. These length-dependent changes of muscle fiber propagation velocity are suggested to contribute to the supernormal phase of propagation velocity recovery function and to be responsible for an important part of the myogenic, interdischarge interval-dependent, jitter.

Jitter in the muscle fibre.

Direct stimulation of muscle fibres with a regular 10 Hz rate, three computer generated random rhythms and a sequence of voluntary discharges was used to quantify the interdischarge interval (IDI) dependent jitter due to velocity recovery function (VRF). This jitter was found to depend on conduction time and strength of VRF, but not on propagation velocity. The results suggest that in the usual jitter study in voluntarily activated muscle fibre pairs, with moderately irregular discharge rate and interpotential intervals below 3 ms the IDI dependent jitter contributes on average less than 10 microseconds, but can be so large as to produce false abnormal values at more irregular rates, longer interpotential intervals and pronounced differences in VRF. It can be effectively removed by mathematical algorithms or, better still, by using electrical stimulation.

Improving electromyographic jitter measurements by analysis of the firing pattern

A new model for predicting the jitter from the firing pattern is presented. The jitter is decomposed into two components: 1) variation explained by the firing pattern, 2) random variation. The first component reflects the velocity recovery function of the muscle fiber. The second component reflects the neuromuscular transmission. Two methods are deduced from the model. Method I predicts the jitter from the most recent discharge. Method II can take any period of firing pattern into consideration. Model parameters can be given a physiological interpretation. Measures describing the velocity recovery function are derived. An improved estimate of the neuromuscular jitter is obtained compared to traditional jitter measures under simulated conditions.

Effect of electrical stimulus parameters on the development and propagation of action potentials in short excitable fibres

Intracellular action potentials (IAPs) produced by short fibres in response to their electrical stimulation were analysed. IAPs were calculated on the basis of the Hodgkin-Huxley (1952) model by the method described by Joyner et al. (1978). Principal differences were found in processes of activation of short (semilength L < 5 λ) and long fibres under near-threshold stimulation. The shorter the fibre, the lower was the threshold value (I thr). Dependence of the latency on the stimulus strenght (I st) was substantially non-linear and was affected by the fibre length. Both fibre length and stimulus strength influenced the IAP amplitude, the instantaneous propagation velocity (IPV) and the site of the first origin of the IAP (and, consequently, excitability of the short fibre membrane). With L ⩽ 2 λ and I thr ⩽ I st ⩽ 1·1I thr, IPV could reach either very high values (so that all the fibre membrane fired practically simultaneously) or even negative values. The latter corresponded to the first origin of the propagated IAP, not at the site of stimulation but at the fibre termination or at a midpoint. The characters of all the above dependencies were unchanged irrespective of the manner of approaching threshold (variation of stimulus duration or its strength). Reasons for differences in processes of activation of short and long fibres are discussed in terms of electrical load and latency. Applications of the results to explain an increased jitter, velocity recovery function and velocity-diameter relationship are also discussed.

Jitter correction: a computer algorithm for reduction of the velocity recovery function artifact.

The measurement of neuromuscular jitter in single fiber electromyography may be artifactually raised by a component of interdischarge interval (IDI)-dependent jitter caused by the velocity recovery function (VRF) in muscle fibers. We have developed a computer algorithm for on-line mathematical correction for this artifact, thus improving the reliability of neuromuscular jitter estimates. The method, based on a modeling technique, was validated using intramuscular stimulation in order to either exclude an IDI-dependent component (using regular stimulation) or to include an IDI-dependent component (using pseudorandom stimulation). In 10 normal subjects the distribution of 106 corrected jitter values obtained using voluntary activity showed no difference from the measured values. This finding implies that previously published values for normal jitter are not likely to have been influenced by the VRF effect.

The ‘velocity Recovery Function’ in directly activated human muscle fibers

The ‘velocity Recovery Function’ in directly activated human muscle fibers

PROPAGATION VELOCITY DURING ISCHEMIA

SUMMARYThe effect of ischemia on propagation velocity and on the velocity recovery function was studied.1. The extensor digitorum communis muscle was made ischemic by means of a blood‐pressure cuff with or without previous application of an Esmarch roller.2. During ischemia the velocity could decrease (5 out of 23 cases), increase (3 out o f 23 cases) or be unchanged (15 out of 23 cases) in relation t o the pre‐ischemic slopc of the velocity curve.3. The velocity recovery function was unchanged in 4 out of 20 cases. It lost the supernormal phase in 10 out of 20 cases and in 6 out of 20 cases the supernormal phase changed to a subnormal.3. The influence of the innervation frequency upon the propagation velocity became continotisly more pronounced during the period of ischemia.

PROPAGATION VELOCITY AT DIFFERENT TEMPERATURES

SUMMARY1. The intramuscular temperature of the brachial biceps muscle was changed between 22.1 and 39.0°C by alteration of the external temperature of the upper arm.2. In relation to the normal change in propagation velocity during activity, an increase in temperature up to 39°C seemed to increase the propagation velocity in all of 6 cases. When the temperature was decreased by 9°C significant changes were seen in 2 out of 5 cases. When the temperature was decreased by 4°C in 3 cases no change was seen.3. An increase in temperature from normal did not alter the Velocity Recovery Function in the one case where this was studied. A decrease of the normal temperature below 30°C made the supernormal phase disappear in the 3 cases where this was studied.4. The variation in intramuscular temperature when the environmental conditions were reasonably constant were small and does not appreciably influence the propagation velocity or the Velocity Recovery Function.

SOME FINDINGS IN MUSCULAR DISORDERS

SUMMARY1. The mean value of propagation velocity was lower than normal in one case of disuse atrophia and in two cases of dystrophia myotonica.2. The propagation velocity was within the normal range in 5 cases of myxoedema.3. In one of two cases of acromegalia the mean velocity was significantly higher than in healthy subjects.4. The mean propagation velocity seemed to decrease during thyroid therapy in a case of myxoedema.5. The Velocity Recovery Function was shown to be changed in myxoedema but seemed to be normal in dystrophia myotonica and myasthenia gravis.

VARIABILITY IN PROPAGATION VELOCITY FOR CONSECTIVE DISCHARGES IN A FIBER

SUMMARY1. The interspike interval dependent variability in the propagation velocity was studied.2. The experiments were performed with voluntary activation or with electrical stimulation of intramuscular nerve‐twigs.3. The general appearance of the interval velocity curve was obtained with double pulse stimulation. For the time interval of about 3–10 msec after a preceding impulse the velocity was subnormal. For a longer time interval the velocity was supernormal with maximum (112.5–124%) at the interval 8–50 msec. After the maximum there was an asymptotic decay. After 500 msec some supernormality still remained. This curve is called the Velocity Recovery Function (VRF).4. When stimulating with a train of pulses the effect of cach impulse was added to the remaining effect of the preceding impulses.5. At voluntary contraction where the innervation frequency was irregular this effect causes an interval dependent variability of the propagation velocity.6. A method has been developed for calculating the descending part of the VRI from the interval dependent velocity variations.