The influence of natural body sway on neuromuscular responses to an unpredictable surface translation

Previous research has shown that the postural configuration adopted by a subject, such as active leaning, influences the postural response to an unpredictable support surface translation. While those studies have examined large differences in postural conditions, it is of additional interest to examine the effects of naturally occurring changes in standing posture. Thus, it was hypothesized that the normal postural sway observed during quiet standing would affect the responses to an unpredictable support surface translation. Seventeen young adults stood quietly on a moveable platform and were perturbed in either the forward or backward direction when the location of the center of pressure (COP) was either 1.5 standard deviations anterior or posterior to the mean baseline COP signal. Postural responses, in the form of electromyographic (EMG) latencies and amplitudes, were recorded from lower limb and trunk muscles. When the location of the COP at the time of the translation was in the opposite, as compared to the same, direction as the upcoming translation, there was a significantly earlier onset of the antagonists (10-23%, i.e. 15-45 ms) and a greater EMG amplitude (14-39%) in four of the six recorded muscles. Stepping responses were most frequently observed during trials where the position of the COP was opposite to the direction of the translation. The results support the hypothesis that postural responses to unpredictable support surface translations are influenced by the normal movements of postural sway. The results may help to explain the large variability of postural responses found between past studies.

Proprioceptive neuromuscular facilitation stretching - Mechanisms and clinical implications

Proprioceptive neuromuscular facilitation (PNF) stretching techniques are commonly used in the athletic and clinical environments to enhance both active and passive range of motion (ROM) with a view to optimising motor performance and rehabilitation. PNF stretching is positioned in the literature as the most effective stretching technique when the aim is to increase ROM, particularly in respect to short-term changes in ROM. With due consideration of the heterogeneity across the applied PNF stretching research, a summary of the findings suggests that an 'active' PNF stretching technique achieves the greatest gains in ROM, e.g. utilising a shortening contraction of the opposing muscle to place the target muscle on stretch, followed by a static contraction of the target muscle. The inclusion of a shortening contraction of the opposing muscle appears to have the greatest impact on enhancing ROM. When including a static contraction of the target muscle, this needs to be held for approximately 3 seconds at no more than 20% of a maximum voluntary contraction. The greatest changes in ROM generally occur after the first repetition and in order to achieve more lasting changes in ROM, PNF stretching needs to be performed once or twice per week. The superior changes in ROM that PNF stretching often produces compared with other stretching techniques has traditionally been attributed to autogenic and/or reciprocal inhibition, although the literature does not support this hypothesis. Instead, and in the absence of a biomechanical explanation, the contemporary view proposes that PNF stretching influences the point at which stretch is perceived or tolerated. The mechanism(s) underpinning the change in stretch perception or tolerance are not known, although pain modulation has been suggested.

The motor neurite terminal determines where neuromuscular synapses form in the absence of agrin

Agrin is a proteoglycan secreted by motor neurite terminals that functions to initiate and maintain AChR clusters at the nerve terminal. This led to the theory that neurite terminals decide where neuromuscular synapses form by secreting agrin. However, initiation of AChR clustering occurs in the absence of the innervating motoneuron and in the absence of agrin. In this instance, the muscle, not the nerve, is deciding the location of neuromuscular synapses by drawing neurite terminals towards pre-existing AChR clusters. If this were true, one would expect the initial innervation patterns to be the same in agrin-deficient mice and wild-type mice. To test this we quantified the intramuscular axonal branching and synapse formation in the diaphragm at E14.5 in agrin-deficient mice and wild-type mice. Heterozygote mothers were anaesthetised with Nembutal (30 mg) and killed via cervical dislocation. In the diaphragm, the nerve trunk runs down the centre of the muscle and extends branches primarily toward the lateral side. In agrin-deficient mice however, we found significantly more branches exited the phrenic nerve trunk, branched in the periphery and extended further on the medial side. Moreover, we found that the percentage α-bungarotoxin/synaptophysin colocalisations, markers of pre- and postsynaptic differentiation, respectively, was the same in agrin-deficient mice and wild-type mice. These results show that initial innervation patterns are not the same in agrin-deficient mice and wild-type mice indicating neurite terminals, not muscle, decide the placement of neuromuscular synapses in the absence of agrin.

The effects of persistent articholinesterase action at the neuromuscular junction

The effects of organophosphorus compounds which form a rapidly-ageing complex with acetylcholinesterase (AChE) (e.g. pinacolyl S-(2- trimethylaminoethyl)methylphosphonothioate (BOS)) and hence exert a persistent anticholinesterase (anti-ChE) action have been compared with other compounds with a shorter time course of inhibition (e.g. ecothiopate iodide (ECO)). Although the inhibition of AChE produced by BOS lasted longer than that seen with ECO, the time course of the myopathy appeared very similar. BOS also possessed a number of properties which have been seen with other anti-ChEs. BOS and ECO produced significant increases in neuromuscular "jitter" 5 days after injection, not only in the diaphragm but also in the soleus and extensor digitorum longus muscles. Increases in "jitter" produced by ECO could be prevented by pyridostigmine prophylaxis or rapid treatment with pyridine-2- aldoxime methiodide. Some protection from the BOS-induced increases in "jitter" could be gained by repeated treatment with pyridine-2-aldoxime methiodide, an effect which could not be accounted for simply by enzyme reactivation. From experiments performed in Rej 129 mice it was determined that increases in "jitter", although demonstrated in some dystrophic muscles, could not be used as an early diagnostic tool. Because sequalae of inhibition were present some time after intoxication, by which time AChE appeared biochemically normal, experiments were performed to investigate inactivation of physiologically important AChE. The time course of extracellular MEPPs was utilised as an indicator of physiologically important AChE and compared with the AChE activity measured by the technique of Ellman et al. (1961). It was concluded that the degree of persistence of anti-ChE action was unimportant for the induction of myopathy with a time course of 3-24 hours, but had some importance in events of longer duration.

The neurotoxic effects of enzyme inhibitors at the neuromuscular junction

Current knowledge of the long-term, low dose effects of carbamate (CB) anti-cholinesterases on skeletal muscle or on the metabolism and regulation of the molecular forms of acetylcholinesterase (AChE) is limited. This is largely due to the reversible nature of these inhibitors and the subtle effects they induce which has generally made their study difficult and preliminary investigations were conducted to determine suitable study methods. A sequential extraction technique was used to rapidly analyse AChE molecular form activity at the mouse neuromuscular junction and also in peripheral parts of muscle fibres. AChE in the synaptic cleft involved in the termination of cholinergic transmission was successfully assessed by the assay method and by an alternative method using a correlation equation which represented the relationship between synaptic AChE and the prolongation of extra-cellular miniature endplate potentials. It was found that inhibition after in vivo Carbamate (CB) dosing could not be maintained during tissue analysis because CB-inhibited enzyme complexes decarbamoylated vary rapidly and could not be prevented even when maintained on ice. The methods employed did not therefore give a measure of inhibition but presented a profile of metabolic responses to continual, low dose CB treatment. Repetitive and continual infusion with low doses of the CBs: pyridostigmine and physostigmine induced a variety of effects on mouse skeletal muscle. Both compounds induced a mild myopathy in the mouse diaphragm during continual infusion which was characterised by endplate deformation without necrosis; such deformation persisted on termination of treatment but had recovered slightly 14 days later. Endplate and non-endplate AChE molecular forms displayed selective responses to CB treatment. During treatment endplate AChE was reduced whereas non-endplate AChE was largely unaffected, and after treatment, endplate AChE recovered, whereas non-endplate AChE was up-regulated. The mechanisms by which these responses become manifest are unclear but may be due to CB-induced effects on nerve-mediated muscle activity, neurotrophic factors or morphological and physiological changes which arise at the neuromuscular junction. It was concluded that, as well as inhibiting AChE, CBs also influence the metabolism and regulation of the enzyme and induce persistent endplate deformation; possible detrimental effects of long-term, low-dose determination requires further investigation.

Neuromuscular response to whole body vibration treatment during static and dynamic squat exercises

The impact of whole body vibrations (vibration stimulus mechanically transferred to the body) on muscular activity and neuromuscular response has been widely studied but without standard protocol and by using different kinds of exercises and parameters. In this study, we investigated how whole body vibration treatments affect electromyographic signal of rectus femoris during static and dynamic squat exercises. The aim was the identification of squat exercise characteristics useful to maximize neuromuscular activation and hence progress in training efficacy. Fourteen healthy volunteers performed both static and dynamic squat exercises without and with vibration treatments. Surface electromyographic signals of rectus femoris were recorded during the whole exercise and processed to reduce artifacts and to extract root mean square values. Paired t-test results demonstrated an increase of the root mean square values (p<0.05) in both static and dynamic squat exercises with vibrations respectively of 63% and 108%. For each exercise, subjects gave a rating of the perceived exertion according to the Borg's scale but there were no significant changes in the perceived exertion rate between exercises with and without vibration. Finally, results from analysis of electromyographic signals identified the static squat with WBV treatment as the exercise with higher neuromuscular system response. © 2012 IEEE.