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B Bigland-Ritchie

Publications and source records attributed to B Bigland-Ritchie.

At least 37 records · Page 2Linked to original sources
PubMed1990

A comparison of human thenar motor-unit properties studied by intraneural motor-axon stimulation and spike-triggered averaging.

1. Measurements of twitch contractile properties of human motor units recorded by spike-triggered averaging may be distorted by partial fusion between twitches, because motor units seldom fire at rates below 8-10 Hz. The effects of this fusion were examined by comparing the responses of 27 human thenar motor units when their motor axons were stimulated at 1, 8, and 10 Hz. 2. Resultant forces were calculated from the abduction and flexion force components, together with various contraction and relaxation rate indexes as reported previously. Values for single twitches were compared to measurements made from the unfused force fluctuations ("apparent twitches") of the same units recorded during 8 and 10 Hz stimulation. 3. For all units, stimulation at 8 and 10 Hz caused partial twitch fusion. At 10 Hz, mean values for "apparent twitch" forces, contraction times (CT), and one-half relaxation times (1/2RT) were reduced to 44, 76, and 52% of the corresponding values measured from separate twitches evoked by 1 Hz stimulation. Similar but smaller reductions were seen at 8 Hz. 4. Slow units, with initial twitch CT greater than 60 ms, showed significantly more distortion of all "apparent twitch" parameters when stimulated at both 8 and 10 Hz, compared to fast units (less than 50 ms). 5. The potentiated abduction force component data were compared with abduction forces obtained previously by spike-triggered averaging from the same muscle group. Mean force obtained by spike-triggered averaging ("STA twitch" force: 21 mN) was significantly larger than that measured in abduction in response to either 1 or 10 Hz motor-axon stimulation (14 mN, 6 mN, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Axons↗
PubMed1989

Impulse propagation and muscle activation in long maximal voluntary contractions.

With fatigue, force generation may be limited by several factors, including impaired impulse transmission and/or reduced motor drive. In 5-min isometric maximal voluntary contraction, no decline was seen in the peak amplitude of the tibialis anterior compound muscle mass action potential (M wave) either during or immediately after the voluntary effort, provided maximal nerve stimulation was retained. For first dorsal interosseous (FDI) muscle, M wave amplitudes declined by 19.4 +/- 1.6% during the first 2 min but did not change significantly thereafter, despite the continued force reduction (up to 94% in 5 min for both muscles). The duration of the FDI M waves increased (greater than 30%), suggesting that the small decline in amplitude was the result of increased dispersion between the responses of different motor units. Some subjects kept FDI maximally activated throughout, but when they used tibialis anterior, twitch occlusion and tetanic muscle stimulation showed that most subjects were usually only able to do so for the first 60 s and thereafter only during brief "extra efforts." Thus force loss during isometric voluntary contractions sustained at the highest intensities results mainly from failure of processes within the muscle fibers.

Electric Stimulation↗
PubMed1988

Motor drive and metabolic responses during repeated submaximal contractions in humans.

Contractile failure during various types of exercise has been attributed to intramuscular metabolic changes. We examined the temporal changes in force-generating capacity and metabolic state during intermittent isometric contractions in humans. One-legged quadriceps contractions at 30% maximum voluntary contraction (MVC) were executed for 6 s, with 4 s of rest between. The decrease in force-generating capacity was tested from brief MVC's and short bursts of 50-Hz stimulation applied at 5-min intervals. After 1 min of exercise, the MVC force declined linearly and in parallel to the 50-Hz stimulation force, indicating that the contractile failure was due to intramuscular processes. After 30 min of exercise the MVC force had declined by approximately 40% compared with the value obtained after 1 min. In separate experiments the same contraction protocol was followed, but two-legged contractions were used. Muscle biopsies taken after 5, 15, and 30 min of exercise showed only minor changes in the concentrations of glycogen, lactate, creatine phosphate (CrP), and ATP. However, at exhaustion, defined as loss of ability to sustain the target force, the concentrations of CrP and glycogen were reduced by 73 and 32%, and muscle lactate concentration had increased to 4.8 mmol/kg wet wt. Thus the gradual decline in force-generating capacity was not due to lactacidosis or lack of substrates for ATP resynthesis and must have resulted from excitation/contraction coupling failure, whereas exhaustion was closely related to phosphagen depletion, without significant lactacidosis.

Adenosine Triphosphate↗
PubMed1987

Central components of diaphragmatic fatigue assessed by phrenic nerve stimulation.

The extent to which diaphragmatic fatigue results from failure of neural drive has been investigated using twitch occlusion. Fatigue was induced by repeatedly generating transdiaphragmatic pressures (Pdi) of either 50 or 75% maximum Pdi (Pdimax) until approximately 10 min after the target Pdi could no longer be reached (Tlim). Maximal bilateral shocks delivered periodically to the phrenic nerves elicited Pdi twitches between breaths (Tr) and superimposed on the voluntary contractions (Ts). The ratio [1 - Ts/Tr], which provides an index of the degree of central nervous system muscle activation, increased as fatigue developed. However, superimposed twitches were still detectable at and beyond Tlim when all contractions involved maximal efforts. They were not seen in maximal contractions of the unfatigued muscle. Initially, the diaphragm electromyogram increased, but then declined. No impairment of neuromuscular transmission was seen. We conclude that at and beyond Tlim about one-half of the reduction in Pdimax resulted from reduced central motor drive; the remainder resulted from peripheral muscle contractile failure. No fatigue was evident during 50% Pdimax dynamic contractions.

Adult↗
PubMed1987

Evidence for a fatigue-induced reflex inhibition of motoneuron firing rates.

1. In previous studies on the adductor pollicis and biceps brachii muscles we suggested that motoneuron firing rates are inhibited by a reflex from the muscle during fatigue, since: the firing rates decline during a sustained maximal voluntary contraction (MVC); recovery of MVC firing rates is prevented if the fatigued state of the muscle is preserved for 3 min by local occlusion of its blood supply; and full recovery occurs during this time once the blood supply to the peripheral muscle is restored. These findings were confirmed in the present study for quadriceps contractions. 2. These results do not necessarily imply an inhibitory reflex. The lower firing rates recorded from the muscle fibers during an MVC following 3 min of postfatigue ischemia may have been caused by either reduced subject effort (decreased muscle activation by the CNS) or impaired peripheral impulse transmission under these conditions. The present experiments, carried out on the quadriceps and adductor pollicis muscles, were designed to test this alternative explanation. 3. For both muscles, MVC contractions were sustained for 40 s with a blood pressure cuff inflated to 200 mmHg. This was followed by 3 min ischemic rest and a second 20-s MVC before cuff release. Three minutes after the blood supply to the muscle was restored a third 20-s MVC was made. Single shocks were delivered to the muscle throughout to record twitches from the relaxed muscle (Tr) before and after each MVC, and any twitches super-imposed on the voluntary contractions (Ts). The degree to which the muscle could be activated by voluntary effort was assessed from the ratio [1 - Ts/Tr]. For adductor pollicis, changes in the amplitude of the evoked M-waves were also measured. 4. Spike frequencies were only recorded during quadriceps experiments. These declined by 30% during the initial 40-s MVC. No recovery was seen in the second MVC following 3 min ischemic rest, but full recovery occurred within 3 min of cuff release. 5. Failure to retain full muscle activation was frequently seen in all three MVCs. However, for many well-motivated subjects twitch occlusion showed no reduction in the degree to which either the adductor pollicis or quadriceps muscles could be activated voluntarily during the MVC executed after 3 min of ischemic rest compared with that performed 3 min after the blood supply had been restored.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Fatigue of intermittent submaximal voluntary contractions: central and peripheral factors.

Central and peripheral factors were studied in fatigue of submaximal intermittent isometric contractions of the human quadriceps and soleus muscles. Subjects made repeated 6 s, 50% maximal voluntary contractions (MVC) followed by 4 s rest until the limit of endurance (Tlim). Periodically, a fatigue test was performed. This included a brief MVC, either a single shock or 8 pulses at 50 Hz during a rest period and a shock superimposed on a target force voluntary contraction. At Tlim, the MVC force had declined by 50%, usually in parallel with the force from stimulation at 50 Hz. The twitches superimposed on the target forces declined more rapidly, disappearing entirely at Tlim. In similar experiments on adductor pollicis, no reduction of the evoked M wave was seen. The results suggest that, during fatigue of quadriceps and adductor pollicis induced by this protocol, no central fatigue was apparent, but some was seen in soleus. Thus the reduced force-generating capacity could result mainly or entirely from failure of the muscle contractile apparatus.

Adolescent↗
PubMed1986

Contractile properties of the human diaphragm in vivo.

The mechanical properties of the human diaphragm have been studied at fractional residual capacity in normal seated subjects with closed glottis. The transdiaphragmatic pressure (Pdi) developed in response to single shocks or to trains of stimuli at increasing frequency was approximately 3 times greater during bilateral than unilateral stimulation. During unilateral phrenic nerve stimulation the Pdi twitches increased as the interval (0-200 ms) of a preceding conditioning stimulus to the contralateral phrenic nerve was decreased suggesting that the two hemidiaphragms are mechanically coupled in series. The contraction time and half-relaxation time of single bilateral twitches as well as the Pdi-frequency relationship (5-35 Hz) during bilateral tetanic stimulation indicate that the contractile properties of the human diaphragm are intermediate between those of fast- and slow-twitch muscle fibers. The results suggest that the contractile properties of the human diaphragm are well illustrated by single bilateral twitches recorded from the relaxed muscle, but that the responses to unilateral stimulation are misleading due to distortion by abnormal changes in the muscle geometry.

Adult↗
PubMed1986

Fatigue of submaximal static contractions.

Experiments are described which suggest that the loss of force generating capacity seen during fatigue from intermittent, submaximal voluntary contractions of the quadriceps muscle cannot be explained by any of the usual factors thought to be responsible for fatigue. During the first 30 min of intermittent contractions at 30% MVC the force generated periodically by a brief test train of 50 Hz stimulation and by brief maximal voluntary contractions both declined by 50%. Yet no significant changes were seen in the muscle lactate, ATP or phosphocreatine. Glycogen depletion was confined only to the type I and type IIA fibres, with less than 10% totally depleted. The depletion patterns indicated that the type IIAB and type IIB motor units were not recruited during the first 30 min. The central nervous system appeared to remain capable of generating full muscle activation since the force from maximal voluntary efforts declined in parallel with that from 50 Hz stimulation. We suggest that, in this type of fatigue, the loss of force may be largely due to impaired excitation/contraction coupling. This possibility is supported by the disproportionate depression of the twitches recorded between contractions compared with that from 50 Hz stimulation (low frequency fatigue). The single unit EMG recordings suggest that, in sustained and repeated submaximal contractions, muscle contractile failure is compensated by recruitment of additional motor units rather than by rate coding of those already active. During intermittent contractions large increases in the surface EMG were associated with only modest increases in firing rates. In sustained contractions when the EMG was held constant the discharge rates declined in parallel with the force. In constant force contractions involving about 35% muscle contractile failure no changes in discharge rates were seen despite substantial increases in EMG.

Central Nervous System↗
PubMed1984

Assessment of human diaphragm strength and activation using phrenic nerve stimulation.

The phrenic nerves were stimulated bilaterally in human subjects with supermaximal shocks and the transdiaphragmatic pressure (Pdi) twitches recorded at end-expiratory lung volume with glottis closed. Stimulus maximality was monitored by the evoked muscle potentials. The highly reproducible twitch amplitudes elicited from the relaxed diaphragm were greater with bound (48 +/- 13 cm H2O) than unbound (34.6 +/- 10 cm H2O) abdomen in sitting position. With bound abdomen, the twitch amplitudes were similar in sitting and supine positions. When the same stimuli were applied during voluntary contractions the superimposed twitch amplitude declined almost linearly with the voluntary Pdi exerted, reflecting a progressively increasing activation by the CNS. From this relationship both the maximal Pdi (Pdimax) and the relative degree of diaphragm activation (% Pdimax) can be estimated for any type of breathing effort. Generally no twitch could be detected during maximal efforts (Pdimax: 218 +/- 34 cm H2O) indicating that all stimulated motor units were already fully activated. The Pditwitch/Pdimax ratio of 0.21 +/- 0.04 was similar to the twitch/tetanus ratios of isolated mammalian muscle, suggesting that bilateral stimulation can activate all phrenic motor neurons.

Adult↗
PubMed1984

Muscle fatigue and the influence of changing neural drive.

Fatigue of respiratory muscles is currently receiving much attention because of the critical role it may play in various pathologic conditions. This article attempts to provide physicians with some additional insights into the physiologic factors thought to underlie the development in general, and how these may be influenced by changing patterns of neural activity.

Action Potentials↗
PubMed1983

Changes in motoneurone firing rates during sustained maximal voluntary contractions.

Tungsten micro-electrodes have been used to record the electrical activity of single motor units in the human adductor pollicis during maximal voluntary contractions. The potentials were characteristic of those from single muscle fibres. In brief maximal contractions, the firing rates of over 200 motor units were obtained from five normal subjects. Four subjects had a similar range (mean 26.4 +/- 6.5 Hz) while the fifth was slightly higher (35 +/- 7.4 Hz). When maximal voluntary force was sustained for 40-120 s, there was a progressive decline in the range and mean rate of motor-unit discharge. In the first 60 s, mean rates fell from about 27 Hz to 15 Hz. There was some evidence to suggest that those units with the highest initial frequencies changed rate most rapidly. It is suggested that this decline in motor unit discharge rates is not responsible for force loss, but that it may enable effective modulation of voluntary strength by rate coding to continue during fatigue.

Action Potentials↗
PubMed1983

Contractile speed and EMG changes during fatigue of sustained maximal voluntary contractions.

Measurements were made from the human adductor pollicis muscle of force, contractile speed, and electromyographic activity (EMG) before, during, and after maximal isometric voluntary contractions sustained for 60 s. The use of brief test periods of maximal nerve stimulation with single shocks or trains of shocks enabled various muscle mechanical properties to be studied throughout each contraction. Electrical activity was measured after rectification and smoothing of the surface potentials and also by counting the total number of potentials per unit time from a population of motor units using fine wire intramuscular electrodes. During a 60-s maximal voluntary contraction, the force fell by 30-50%. Throughout the experiment the voluntary force matched that produced by supramaximal tetanic nerve stimulation. This indicated that, with sufficient practice, full muscle activation could be maintained by voluntary effort. However, the amplitude of the smoothed, rectifed EMG and the rate of spike counts declined. Since no evidence for neuromuscular block was found, the decline in EMG and spike counts was attributed to a progressive reduction of the neural drive from the central nervous system, despite maintained maximum effort. After the prolonged voluntary contractions twitch duration was prolonged, mainly as a result of slowing in relaxation rate. Twitch summation in unfused tetani increased. Both the maximum rate of relaxation and the time course of force decay declined by 50-70%. Similar changes were seen in both voluntary contractions and in test periods of stimulation. The percentage change in muscle contractile speed measured by these parameters approximately equaled the percentage change in the surface EMG measured simultaneously. It is concluded that 1) during a 60-s sustained maximal voluntary contraction there is a progressive slowing of contraction speed such that the excitation rate required to give maximal force generation is reduced, 2) the simultaneous decline in EMG may be due to a continuous reduction in motoneuron discharge rate, and 3) the EMG decline may not necessarily contribute to force loss.

Adult↗
PubMed1983

Motor-unit discharge rates in maximal voluntary contractions of three human muscles.

Single motor-unit firing rates have been recorded during maximal voluntary contractions using tungsten microelectrodes. Over 300 units from four subjects were sampled from each of three muscles. These were the biceps brachii, adductor pollicis, and soleus, chosen because of known differences in their fiber-type composition and contractile properties. In all cases the contraction maximality was assured by delivering single supramaximal shocks during the voluntary contractions. All motor units were deemed to have already been fully activated if no additional force resulted. Thus for each muscle, the firing rates elicited by a maximal voluntary effort are sufficient to generate a fully fused tetanus in each motor unit. For the biceps brachii and adductor pollicis muscles, the mean firing rates (+/- SD) were 31.1 +/- 10.1 and 29.9 +/- 8.6 Hz, respectively, while for soleus they were only 10.7 +/- 2.9 HZ. For each muscle the firing rates distribution covered approximately a four-fold range about the mean value. The mean firing rates for each muscle varied roughly in proportion to their respective twitch contraction and half relaxation times. These contractile time measurements for both biceps brachii and adductor pollicis agreed well with the mean values reported for human fast-twitch motor units, while those for soleus fell in the range observed for human slow-twitch units. An argument is presented that suggests that, in response to voluntary effort, the range of discharge rates of each motor-unit pool is limited to those only just sufficient to produce maximum force in each motor unit. This suggestion is based on the relationship between the range of motor-unit firing frequencies observed during maximum voluntary contractions, their range of contraction times, and the stimulation frequencies required for maximum force generation. The implications of this hypothesis for motor control are discussed.

Adult↗
PubMed1983

Linear and non-linear surface EMG/force relationships in human muscles. An anatomical/functional argument for the existence of both.

The EMG/force relations of various human muscles were examined over the full isometric force range using uniform experimental methods. The muscles chosen reflected varying fiber composition, fiber distribution and force generating patterns (recruitment/frequency coding). Our results generally suggest linear relations for muscles of near uniform fiber composition. Non-linear relations were obtained from muscles of mixed fiber composition. The non-linearity persisted despite variations in recording configuration, electrode placement and limb position. These were suggested by others to account for the lack of linearity in the basic EMG/force relation. The roles of uneven fiber distribution, motor unit potential amplitudes and possible supratetanic motor unit driving are discussed within the context of muscle force generating mechanisms as possible explanations for non-linear EMG/force relations.

Adult↗
PubMed1982

The absence of neuromuscular transmission failure in sustained maximal voluntary contractions.

1. Muscle mass action potentials (M waves) were evoked by supramaximal single shocks to the ulnar nerve given at 5-10 s intervals throughout sustained isometric maximal voluntary contractions (m.v.c.) of the adductor pollicis and first dorsal interosseous muscles. Both muscles were fatigued simultaneously. Recordings were made from the muscle surface and also intramuscularly. 2. During a maximal contraction lasting for 60 s there was 30-50% loss of force. No decline was observed in intramuscularly recorded M wave amplitude, while the areas of the total and half M wave forms increased due to a slowing in conduction velocity. The area measured over a fixed time period declined. No evidence was obtained that these M wave potentials were contaminated by electrical activity arising in adjacent muscles. The size of the single unit potentials appeared to remain unaltered during maximal voluntary activity. 3. We conclude that neuromuscular block is not a cause of force loss during this type of fatiguing voluntary contraction.

Action Potentials↗
PubMed1981

EMG and fatigue of human voluntary and stimulated contractions.

During a 60s maximal voluntary isometric contraction (MVC) of the adductor pollicis muscle the loss of force is accompanied by a parallel decline in both the integrated surface electromyogram (EMG) and the single muscle fibre spike counts recorded intramuscularly. This decline is not due to neuromuscular block since the muscle mass action potential (M wave) evoked by single maximal shocks to the nerve is well maintained; nor does the size of the single fibre spike change. It must, therefore, reflect a decline in the firing pattern of the motor neuron pool. The force of a sustained MVC continues to match that from maximal tetanic nerve stimulation; thus, all motor units remain active. Continuous nerve stimulation at the frequency required to match the voluntary force of unfatigued muscle leads to a progressive failure of the M wave, and a more rapid force loss than in an MVC. Both are largely restored by reducing the stimulus frequency. The decline in neural firing rate correlates well with the rate of muscle contractile slowing. It thus optimizes force by maintaining a relatively constant degree of tetanic fusion, while avoiding peripheral failure of electrical propagation.

Action Potentials↗
PubMed1981

Conduction velocity and EMG power spectrum changes in fatigue of sustained maximal efforts.

The relationship between the electromyographic (EMG) power spectrum and muscle conduction velocity was investigated during both fatiguing and nonfatiguing contractions of the adductor pollicis muscle. Changes in the EMG power spectrum were measured by Fourier transform analysis and by comparing the power in the high (130-238 Hz) and low (20--40 Hz) frequency bands. Changes in conduction velocity were measured during voluntary activity from changes in the muscle mass action potential evoked by periodic maximal shocks to the nerve. This was varied independently either by maintaining a 60-s fatiguing maximal voluntary contraction involving 30--50% loss of force or by changing muscle temperature in the absence of fatigue. Both procedures resulted in similar changes in the power spectrum. However, the change in conduction velocity required to generate equal changes in the EMG was about 10 times greater in the absence of fatigue than those observed during a 60-s maximum contraction initiated at any initial muscle temperature. This suggests that during fatigue of maximal voluntary contractions, factors other than changes in the wave form of individual muscle fiber action potentials must contribute to the observed shift in the total surface EMG frequency components.

Electromyography↗