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BACKGROUND: Functional adaptations of patients with posterior cruciate ligament deficiency (grade II) are largely unknown despite increased recognition of this injury. HYPOTHESIS: Posterior cruciate ligament-deficient subjects (grade II, 6- to 10-mm bilateral difference in posterior translation) will present with neuromuscular and biomechanical adaptations to overcome significant mechanical instability during gait and drop-landing tasks. STUDY DESIGN: Controlled laboratory study. METHODS: Bilateral comparisons were made among 10 posterior cruciate ligament-deficient subjects using radiographic, instrumented laxity, and range of motion examinations. Biomechanical and neuromuscular characteristics of the involved limb of the posterior cruciate ligament-deficient subjects were compared to their uninvolved limb and to 10 matched control subjects performing gait and drop-landing tasks. RESULTS: Radiographic (15.3 +/- 2.9 to 5.6 +/- 3.7 mm; P = .008) and instrumented laxity (6.3 +/- 2.0 to 1.4 +/- 0.5 mm; P < .001) examinations demonstrated significantly greater posterior displacement of the involved knee within the posterior cruciate ligament-deficient group. The posterior cruciate ligament-deficient group had a significantly decreased maximum knee valgus moment and greater vertical ground reaction force at midstance during gait compared to the control group. During vertical landings, the posterior cruciate ligament-deficient group demonstrated a significantly decreased vertical ground reaction force loading rate. All other analyses reported no significant differences within or between groups. CONCLUSION: Posterior cruciate ligament-deficient subjects demonstrate minimal biomechanical and neuromuscular differences despite significant clinical laxity. CLINICAL RELEVANCE: The findings of this study indicate that individuals with grade II posterior cruciate ligament injuries are able to perform gait and drop-landing activities similar to a control group without surgical intervention.
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We investigated the role of central and peripheral factors in repeated cold exposure of the hand and their effects on temperature response, neuromuscular function, and subjective thermal sensation. Eleven subjects immersed their left hand repeatedly in 8 degrees C cold water for 30 min, 5 d/week, for 2 weeks. Before and following the 2 weeks of exposure, neuromuscular function, blood markers, thermal sensation, and temperature responses of both acclimated (left) and control (right) hands were tested. Minimum index finger temperature pre-acclimation was 10.9 +/- 3.4 degrees C and 10.0 +/- 2.0 degrees C in the left and right hand, respectively, and did not change significantly post-acclimation (left, 12.8 +/- 4.2 degrees C; right, 10.2 +/- 1.1 degrees C). Neuromuscular function was impaired with cooling, but this was significantly different neither between the hands nor over time. Central factors, measured by catecholamines and changes in temperature and cardiovascular response over time, did not change and there were no differences in responses between the exposed and non-exposed hand over time (peripheral adaptation) nor were there any differences in local factors endothelial-1 and nitric oxide. Subjective thermal comfort was improved and the discrepancy that was found between the change in actual and perceived temperature may increase the risk of cold injury in partially acclimatized individuals, owing to an adjustment in behavioural thermoregulation.
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1. Previous studies have demonstrated that initial transmitter release, fatigability, and the morphology of identified crayfish neuromuscular synapses adapt to long-term changes in motoneuron impulse activity. 2. Experiments were performed to determine whether these long-term, adaptive alterations in neuromuscular synaptic physiology are triggered by changes in neuromuscular synaptic activity, muscle activity, or neuronal impulse activity. The fast closer excitor of the crayfish claw, a phasic motoneuron, was studied. Either the central or the peripheral region of the motoneuron was selectively stimulated in vivo by blocking impulse activity midway along the motor axon with localized application of tetrodotoxin and stimulating either central or distal to the blocked region. 3. Neither muscle activity nor transmitter release from the neuromuscular synapses was required to trigger the changes in synaptic physiology. Stimulation central to the block induced changes in neuromuscular transmission that included a long-lasting decrease in initial transmitter release and increased fatique resistance. 4. Because peripheral stimulation also produced decreased initial transmitter release, it appears that increased impulse activity in either region of the motoneuron can produce the synaptic changes. These results along with earlier findings suggest that neuronal depolarization induces adaptive, long-term changes in synapses. 5. These results are discussed in relation to findings at vertebrate and invertebrate synapses.
Strength loss following disuse may result from alterations in muscle and/or neurological properties. In this paper, we report our findings on human plantar flexor muscle properties following 4 wk of limb suspension (unilateral lower limb suspension), along with the effect of applied ischemia (Isc) on these properties. In the companion paper (Part II), we report our findings on the changes in neurological properties. Measurements of voluntary and evoked forces, the compound muscle fiber action potential (CMAP), and muscle cross-sectional area (CSA) were collected before and after 4 wk of unilateral lower limb suspension in adults (n = 18; 19-28 yr). A subset of subjects (n = 6) received applications of Isc 3 days/wk (3 sets; 5-min duration). In the subjects not receiving Isc, the loss in CSA and strength was as expected ( approximately 9 and 14%). We observed a 30% slowing in the duration of the CMAP, a 10% decrease in evoked doublet force, a 12% increase in the twitch-to-doublet force ratio, and an altered postactivation potentiation response (11% increase in the postactivation potentiation-to-doublet ratio). We also detected a 10% slowing in the ability of the plantar flexor to develop force during the initial phase of an evoked contraction, along with a 6% reduction in in vivo specific doublet force. In the Isc subjects, no preservation was observed in strength or the evoked muscle properties. However, the Isc group did maintain CSA of the lateral gastrocnemius, as the control subjects' lateral gastrocnemius atrophied 10.2%, whereas the subjects receiving Isc atrophied 4.7%. Additionally, Isc abolished the unweighting-induced slowing in the CMAP. These findings suggest that unweighting alters the contractile properties involved in the excitation-contraction coupling processes and that Isc impacts the sarcolemma.
The neuromuscular junction (NMJ) allows communication between motor neurons and muscle fibers. During development, marked morphological changes occur as the functional NMJ is formed. During the postnatal period of rapid growth and muscle enlargement, endplate size concurrently increases. Even beyond this period of pronounced plasticity, the NMJ undergoes subtle morphological remodeling--expansion and retraction--although its overall dimensions remain stable. This natural, continual NMJ remodeling is amplified with alterations in neuromuscular activity. Increased activity, presented by exercise training, typically results in expansion of NMJ size. Disuse, brought about by neurotoxins, denervation, or spaceflight, also elicits substantial reconfiguring of the endplate.
Strength loss following disuse may result from alterations in muscle and/or neurological properties. In this paper, we report our findings on human plantar flexor neurological properties following 4 wk of limb suspension [unilateral lower limb suspension (ULLS)], along with the effect of motor imagery (MI) training on these properties. In the companion paper (Part I), we report our findings on the changes in skeletal muscle properties. Additionally, in the present paper, we analyze our findings to determine the relative contribution of neural and muscular factors in strength loss. Measurements of central activation, the H-reflex, and nerve conduction were made before and after 4 wk of ULLS (n = 18; 19-28 yr). A subset of the subjects (n = 6) performed PF MI training 4 days/wk. Following ULLS, we observed a significant increase in the soleus H-reflex (45.4 +/- 4.0 to 51.9 +/- 3.7% expressed relative to the maximal muscle action potential). Additionally, there were longer intervals between the delivery of an electrical stimulus to the tibial nerve and the corresponding muscle action potential (M-wave latency; mean prolongation 0.49 ms) and H-reflex wave (H-wave latency; mean prolongation 0.46 ms). The efficacy of MI on strength was ambiguous, with no significant effect detected (although a modest effect size was observed; eta2 = 0.18). These findings suggest that unweighting induces plastic changes in neural function that appear to be spatially distributed throughout the nervous system. In terms of the relative contribution of neural and muscular factors regulating strength loss, we observed that neural factors (primarily deficits in central activation) explained 48% of the variability in strength loss, whereas muscular factors (primarily sarcolemma function) explained 39% of the variability.
The objective of this investigation was to compare the effects of decreased vs. increased activity on the neuromuscular system. Twenty-four young adult (7 weeks old) Sprague-Dawley rats were randomly assigned to three treatment groups (N=8/group). Increased activity was achieved by treadmill running for up to 1 h/day. Decreased activity was induced by muscle unloading via the hindlimb suspension model. Control animals engaged in normal weight bearing and ambulatory activity. At the end of the 10 week intervention period, animals were killed and soleus muscles were removed, quickly frozen, and examined using cytofluorescent (neuromuscular junctions) and histochemical (myofibers) procedures. Pre-synaptic morphology was quantified by measuring nerve terminal branching, and post-synaptic assessment was conducted by staining acetylcholine receptors at the endplate. Myofiber profiles of solei were compiled by determining fiber size (cross-sectional area) and fiber type composition. Results show that exercise training significantly (P<or=0.05) enhanced nerve terminal branching without modifying endplate size. In contrast, muscle unloading failed to influence nerve terminal branching, but significantly reduced endplate dimensions. Likely, the diminution of endplate size among unloaded myofibers was caused by the dramatic loss of size (approximately 60%) observed among those fibers. Both increased and decreased activity evoked reductions in the ratio of endplate area to length of nerve terminal branches, thus altering the pre- to post-synaptic relationship of neuromuscular junctions. In conclusion, the present data demonstrate that both increased and decreased activity significantly remodels the neuromuscular junction, but the locus (pre- vs. post-synaptic) and nature (expansion vs. reduction) of that remodeling are specific to the form of the alteration in activity.
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The disturbances of neuromuscular transmission due to chronic (1 to 30 days) administration of phospholine to rats were investigated upon the isolated diaphragm preparation. Phospholine treatment impaired the ability of the muscle to maintain tetanic contraction in response to indirect stimulation and caused post-tetanic depression of twitch responses. In the later stage marked recovery of neuromuscular function occurred in spite of further phospholine administration. This recovery was not accompanied by any increase in the already lowered acetylcholinesterase activity. The concentration of d-tubocurarine needed to block twitch response increased during the first days of phospholine treatment and then, during the following period gradually returned to the normal level. The concentration of carbachol needed to block twitch response during 2 to 30 days of continued treatment was higher than that in control animals. The possible explanations for the spontaneous recovery of neuromuscular function are discussed.
An adaptive closed-loop control of neuromuscular block by pharmacokinetic dynamic model-based feedback is described. Mean (+/- SD) offsets from setpoints at 70, 80 and 90% neuromuscular blockade were 2.2 +/- 1.1, 1.8 +/- 0.6 and 0.4 +/- 0.4%, respectively. Correspondingly, the mean standard deviations from mean neuro-muscular blockade were 3.9 +/- 2.3, 2.7 +/- 0.6 and 1.3 +/- 0.2% and the mean average vecuronium requirements 0.5 +/- 0.2, 0.7 +/- 0.2 and 1.0 +/- 0.5 micrograms kg-1 min-1. The described closed-loop vecuronium administration system gives a solution to the problem of adapting pharmacokinetic and pharmacodynamic data to individuals when using mean data as starting values for drug therapy.
An adaptive feedforward control system has been evaluated for use in functional neuromuscular stimulation (FNS) systems. The control system, which utilizes neural network techniques, was used to generate isometric muscle contractions to track a periodic torque trajectory signal. The evaluation of the control system was performed using percutaneous intramuscular electrodes to stimulate the quadriceps muscles of spinal cord injured adolescents. Results of the evaluation indicate that the control system automatically customized its parameters for controlling isometric muscle torque in a particular muscle and that the parameters were adapted on-line to account for changes in muscle properties due to fatigue. This study demonstrates that this control system may play an important role in the development of practical FNS systems that are capable of automatically adjusting stimulation parameters to fit the needs of a particular individual at a given time.
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Prolonged changes in crayfish motoneuron electrical activity result in adaptations in neuromuscular synapses which are consistent with findings at other synapses. In this study we establish that this long-term adaptation (LTA) of crayfish neuromuscular synapses to increased activation of the motoneuron does not require the activation of any other neurons. Selectively increasing the impulse activity of the relatively inactive fast closer excitor motoneuron (FCE) over a period of 7 days results in a 41% reduction in initial amplitude of the excitatory postsynaptic potential (EPSP), and a 42% decrease in synaptic fatigue. These changes in EPSP properties have been previously shown to be due to decreased initial transmitter release and greater sustained release of transmitter during prolonged stimulation. Chronic stimulation of sensory receptors known to produce subthreshold synaptic potentials in the central processes of the FCE elicits LTA of its neuromuscular synapses. The initial EPSP is decreased by 21%, and the synaptic fatigue is reduced by 17%. These results lead to the hypothesis that the primary event leading to LTA of neuromuscular synapses is depolarization of the motoneuron.
PURPOSE: The purpose of this study was to clarify the reason for the difference in the preferred cadence between cyclists and noncyclists. METHODS: Male cyclists and noncyclists were evaluated in terms of pedal force, neuromuscular activity for lower extremities, and oxygen consumption among the cadence manipulation (45, 60, 75, 90, and 105 rpm) during pedaling at 150 and 200 W. Noncyclists having the same levels of aerobic and anaerobic capacity as cyclists were chosen from athletes of different sports to avoid any confounding effect from similar kinetic properties of cyclists for lower extremities (i.e., high speed contraction and high repetitions in prolonged exercise) on both pedaling performance and preferred cadence. RESULTS: The peak pedal force significantly decreased with increasing of cadence in both groups, and the value for noncyclists was significantly higher than that for cyclists at each cadence despite the same power output. The normalized iEMG for vastus lateralis and vastus medialis muscles increased in noncyclists with rising cadence; however, cyclists did not show such a significant increase of the normalized iEMG for the muscles. On the other hand, the normalized iEMG for biceps femoris muscle showed a significant increase in cyclists while there was no increase for noncyclists. Oxygen consumption for cyclists was significantly lower than that for noncyclists at 105 rpm for 150 W work and at 75, 90, and 105 rpm for 200 W work. CONCLUSIONS: We conclude that cyclists have a certain pedaling skill regarding the positive utilization for knee flexors up to the higher cadences, which would contribute to a decrease in peak pedal force and which would alleviate muscle activity for the knee extensors. We speculated that pedaling skills that decrease muscle stress influence the preferred cadence selection, contributing to recruitment of ST muscle fibers with fatigue resistance and high mechanical efficiency despite increased oxygen consumption caused by increased repetitions of leg movements.