Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points

The aim of this present study is to test the hypothesis that nociceptive stimulation of latent myofascial trigger points (MTrPs) increases the occurrence of local muscle cramps. Nociceptive muscle stimulation was obtained by a bolus injection of glutamate (0.1 ml, 0.5 M) into a latent MTrP and a control point (a non-MTrP) located in the right or left gastrocnemius medialis muscles in 14 healthy subjects. A bolus of isotonic saline (0.9%, 0.1 ml) injection served as a control. The injections were guided by intramuscular electromyography (EMG) showing resting spontaneous electrical activity at a latent MTrP and no such activity at a non-MTrP. Intramuscular and surface EMG activities in the gastrocnemius medialis muscle were recorded pre-, during-, and post-injection for a period of 8 min to monitor the occurrence of muscle cramps, which are characterized by a brief episodic burst of high levels of EMG activity. The results showed that glutamate and isotonic saline injections into the latent MTrPs induced higher peak pain intensity than into the non-MTrPs (both P < 0.05). Glutamate injection induced higher peak pain intensity than isotonic saline injection into either latent MTrPs or non-MTrPs (both P < 0.05). Muscle camps were observed in 92.86% of the subjects following glutamate injection into the latent MTrPs, but not into the non-MTrPs (P < 0.001). No muscle cramps were recorded following isotonic saline injection into either the latent MTrPs or the non-MTrPs. These results suggest that latent MTrPs could be involved in the genesis of muscle cramps. Focal increase in nociceptive sensitivity at MTrPs constitutes one of the mechanisms underlying muscle cramps.     

Experimental muscle pain results in reorganization of coordination among trapezius muscle subdivisions during repetitive shoulder flexion

The aim of the study was to examine the effect of experimental unilateral upper trapezius muscle pain on the relative activation of trapezius muscle subdivisions bilaterally during repetitive movement of the upper limb. Surface EMG signals were detected from nine healthy subjects from the upper, middle and lower divisions of trapezius during a repetitive bilateral shoulder flexion task. Measurements were performed before and after injection of 0.5 ml hypertonic (pain condition) and isotonic (control) saline into the upper division of the right trapezius muscle in two experimental sessions. On the painful side, upper trapezius showed decreased EMG amplitude (average rectified value, ARV) and lower trapezius increased ARV throughout the entire task following the injection of hypertonic saline (40.0 ± 22.2 vs. 26.0 ± 17.4 μV, and 12.5 ± 7.6 vs. 25.6 ± 14.8 μV, respectively, at the beginning of the contraction). On the side contralateral to pain, greater estimates of ARV were identified for the upper division of trapezius as the task progressed (37.4 ± 20.2 vs. 52.7 ± 28.4 μV, at the end of the contraction). Muscle fiber conduction velocity did not change with pain in all three divisions of the right trapezius muscle. The results suggest that local elicitation of nociceptive afferents in the upper division of the trapezius induces reorganization in the coordinated activity of the three subdivisions of the trapezius in repetitive dynamic tasks.     

Localized muscle pain causes prolonged recovery after fatiguing isometric contractions

The purpose of this study was to investigate the force and electromyographic (EMG) signal recorded from the muscles immediately after a sustained fatiguing contraction with or without muscle pain. Ten subjects performed sustained dorsi- and plantarflexions at two contraction levels (50 and 80% of maximum voluntary contraction) until exhaustion with or without muscle pain induced by injection of 6% hypertonic saline in one of the torque producing muscles. The muscle pain intensity was scored on a visual analogue scale (VAS, 0–10 cm). The root mean square (RMS) of the surface EMG signal from plantarflexors and dorsiflexors were estimated during maximum voluntary contractions (MVC) and ramp contractions before and after the fatiguing task at 0, 5, 10 and 15 min during the recovery phase. VAS scores immediately after the contractions with hypertonic saline (on average 3.2 ± 1.1 cm) progressively decreased during recovery and no pain was experienced 15 min after the contraction. After the painful contraction the RMS-EMG during MVC was on average decreased (23.4 ± 7.4%) compared to the non-painful condition both in muscles where pain was previously induced and in non-painful synergists. During recovery, the slope of the torque–EMG curve during ramp contraction was significantly decreased (28.4 ± 8.1%) after the painful contraction compared to the control contraction both for the muscle previously exposed to pain and also the other active synergists. The decreased EMG during recovery after painful contractions compared with control was not accompanied by significant reductions in force during MVC indicating a change in the strategy for motor unit recruitment. This study shows that localized muscle pain inhibits muscle activation and increases the effects of fatigue on EMG recovery curves both for painful and non-painful synergists probably by a central effect. These effects can modify the normal patterns of synergistic activation and can also generate overload problems in muscle pain patients if compensatory motor control strategies are applied.     

Bilateral experimental muscle pain changes electromyographic activity of human jaw-closing muscles during mastication

 The effects of bilateral experimental muscle pain on human masticatory patterns were studied. Jaw movements and electromyographic (EMG) recordings of the jaw-closing muscles were divided into multiple single masticatory cycles and analyzed on a cycle-by-cycle basis. In ten men simultaneous bilateral injections of hypertonic saline (5%) into the masseter muscles caused strong pain (mean±SE: 7.5±0.4 on a 0–10 scale), significantly reduced EMG activity of jaw-closing muscles in the agonist phase, and significantly increased EMG activity in the antagonist phase. Nine of the subjects reported a sensation of less intense mastication during pain. Injections of isotonic saline (0.9%) did not cause pain or significant changes in masticatory patterns. The influence of higher brain centers on conscious human mastication can not be discarded but the observed phase-dependent modulation could be controlled by local neural circuits and/or a central pattern generator in the brain stem which are capable of integrating bilateral nociceptive afferent activity. Received: 19 February 1997 / Accepted: 14 April 1997     

Effects of experimental pain on jaw muscle activity during goal-directed jaw movements in humans

To study the effects of masseter muscle pain on jaw muscle electromyographic (EMG) activity during goal-directed tasks. Mandibular movement was tracked and EMG activity was recorded from bilateral masseter, and right posterior temporalis, anterior digastric, and inferior head of lateral pterygoid muscles in 22 asymptomatic subjects at postural jaw position, and during three tasks: (a) protrusion, (b) contralateral (left), (c) open jaw movement. Tasks were performed during three conditions: control (no infusion), test 1 [continuous infusion into right masseter of 4.5% hypertonic saline to achieve 30–60 mm pain intensity on 100-mm visual analog scale (VAS)], and test 2 (isotonic saline infusion; in 16 subjects only); the sequence of hypertonic and isotonic saline was randomized. The average EMG root-mean-square values at 0.5 mm increments of mid-incisor-point displacement were analysed using linear mixed effects model statistics (significance: P < 0.05). Right masseter hypertonic saline infusion resulted in significantly (P < 0.0005) more pain (mean ± SD VAS 47.3 ± 14.3 mm) than isotonic infusion (12.2 ± 17.3 mm). Although there was evidence of inter-subject variation, the principal EMG findings were that the significant effects of hypertonic saline-induced pain on EMG activity varied with the task in which the muscle participated irrespective of whether the muscle was an agonist or an antagonist in the tasks. The direction of the hypertonic saline-induced pain effect on EMG activity (i.e., whether the hypertonic saline-induced EMG activity was less than or greater than control EMG activity) could change with the magnitude of jaw displacement. Hypertonic saline infusion had no significant effect on postural EMG activity in any of the recorded jaw muscles. The data suggest that under constrained goal-directed tasks, the pattern of pain-induced changes in jaw muscle EMG activity is not clear cut, but can vary with the task performed, jaw displacement magnitude, and the subject being studied.     

Differential cerebral responses to aversive auditory arousal versus muscle pain: specific EEG patterns are associated with human pain processing

The specificity of electroencephalogram (EEG) activity in relation to processing of human pain needs further elucidation. This study was designed to determine if nociceptive input and general arousal responses to external stimulation exert different effects on EEG activity. Continuous aversive auditory stimuli (90 dB for 2 min) and painful injection of hypertonic saline (5.8%, 0.2 ml) into the left brachioradialis muscle were administered to 12 male subjects during separate sessions in a counterbalanced design. Intensity, arousal and unpleasantness were assessed during the muscle pain and auditory stimulation using a visual analogue scale and arousal-affective scales. The EEG data (32 channels) was acquired before, during and after application of painful and aversive auditory stimuli. Aversive auditory stimulation and intramuscular injection of hypertonic saline induced similar degrees of arousal and unpleasantness associated with a similarity of intensity of sensation of pain and auditory sensation. However, muscle pain induced a significant decrease of alpha-1 activity (8–14 Hz) at T6, PC2, PC6, Pz, P4, O2 and POz sites compared to the baseline, but aversive auditory stimulation did not produce any significant changes in alpah-1 activity compared to baseline. The alpha-1 EEG powers at P3, Pz, P4, PC1, PC2 and POz, and alpha-2 at Pz and POz sites were significantly decreased during muscle pain when compared with aversive noise stimulation. These results indicate that specific EEG patterns are associated with human pain processing. Electronic Publication     

Low-frequency oscillations of the neural drive to the muscle are increased with experimental muscle pain

We investigated the influence of nociceptive stimulation on the accuracy of task execution and motor unit spike trains during low-force isometric contractions. Muscle pain was induced by infusion of hypertonic saline into the abductor digiti minimi muscle of 11 healthy men. Intramuscular EMG signals were recorded from the same muscle during four isometric contractions of 60-s duration at 10% of the maximal force [maximal voluntary contraction (MVC)] performed before injection (baseline), after injection of isotonic (control) or hypertonic saline (pain), and 15 min after pain was no longer reported. Each contraction was preceded by three 3-s ramp contractions from 0% to 10% MVC. The low-frequency oscillations of motor unit spike trains were analyzed by the first principal component of the low-pass filtered spike trains [first common component (FCC)], which represents the effective neural drive to the muscle. Pain decreased the accuracy of task performance [coefficient of variation (CoV) for force: baseline, 2.8 ± 1.8%, pain, 3.9 ± 1.8%; P < 0.05] and reduced motor unit discharge rates [11.6 ± 2.3 pulses per second (pps) vs. 10.7 ± 1.7 pps; P < 0.05]. Motor unit recruitment thresholds (2.2 ± 1.2% MVC vs. 2.4 ± 1.6% MVC), interspike interval variability (18.4 ± 4.9% vs. 19.1 ± 5.4%), strength of motor unit short-term synchronization [common input strength (CIS) 1.02 ± 0.44 vs. 0.83 ± 0.22], and strength of common drive (0.47 ± 0.08 vs. 0.47 ± 0.06) did not change across conditions. The FCC signal was correlated with force (R = 0.45 ± 0.06), and the CoV for FCC increased in the painful condition (5.69 ± 1.29% vs. 7.83 ± 2.61%; P < 0.05). These results indicate that nociceptive stimulation increased the low-frequency variability in synaptic input to motoneurons.     

Effect of experimental muscle pain on motor unit firing rate and conduction velocity

The aim of this human study was to investigate the relationship between experimentally induced muscle pain intensity (i.e., amount of nociceptive activity) and motor unit (MU) firing decrease and MU conduction velocity (CV). In 12 healthy subjects, nociceptive afferents were stimulated in the right tibialis anterior muscle by three intramuscular injections of hypertonic saline (0.2, 0.5, and 0.9 ml) separated by 140 s. The subjects performed six isometric contractions (20 s long) at 10% of the maximal voluntary contraction during the experimental muscle pain. The same set of six contractions was performed without any infusion before the painful condition on the right leg. The procedure was repeated for the left leg with infusion of isotonic (nonpainful) saline. Intramuscular and surface electromyographic (EMG) signals were collected to assess MU firing rate and CV. The firing rate of the active MUs [range: 7.4-14.8 pulses/s (pps)] did not change significantly in the three control conditions (without infusion for the right and left leg and with infusion of isotonic saline in the left leg). There was, on the contrary, a significant decrease (on average, mean +/- SE, 1.03 +/- 0.21 pps) of the firing rates during the painful condition. Moreover, MU firing rates were inversely significantly correlated with the subjective scores of pain intensity. Single MU CV was 3.88 +/- 0.03 m/s (mean +/- SE, over all the MUs) with no statistical difference among any condition, i.e., the injection of hypertonic saline did not alter the muscle fiber membrane properties of the observed MUs. Progressively increased muscle pain intensity causes a gradual decrease of MU firing rates. This decrease is not associated with a change in MU membrane properties, indirectly assessed by CV. This study demonstrates a central inhibitory motor control mechanism with an efficacy correlated to the nociceptive activity.     

Experimental muscle pain changes motor control strategies in dynamic contractions

This study investigated the effect of muscle pain on muscle activation strategies during dynamic exercises. Ten healthy volunteers performed cyclic elbow flexion/extension movements at maximum speed for 2 min after injection of (1) hypertonic (painful) saline in the biceps brachii, (2) hypertonic saline in both biceps brachii and triceps brachii, and (3) isotonic (nonpainful) saline in the biceps brachii muscle. Surface electromyographic (EMG) signals were collected from the upper trapezius, biceps brachii, triceps brachii, and brachioradialis muscles (to estimate EMG amplitude) and with an electrode arrays from biceps brachii (to estimate muscle fiber conduction velocity [CV]). In all conditions, the acceleration of the movement decreased throughout the exercise, and kinematic parameters were not altered by pain. With respect to the control condition, pain induced a decrease of the biceps brachii (mean ± SE, –23±4%) and brachioradialis (–10±0.4%) integrated EMG (IEMG) in the beginning of the exercise, and an increase (45±3.5%) of the upper trapezius IEMG at all time points during the exercise. The biceps brachii IEMG decreased over time during the nonpainful exercises (–11±0.6%) while it remained constant in the painful condition. Biceps brachii CV decreased during painful conditions (–12.8±2.2%) while it remained constant during the nonpainful condition. In conclusion, muscle pain changes the motor control strategy to sustain the required dynamic task both in the relative contribution between synergistic muscles and in the motor unit activation within the painful muscle. Such a changed motor strategy may be highly relevant in models of occupational musculoskeletal pain conditions.     

Experimental muscle pain modulates muscle activity and work performance differently during high and low precision use of a computer mouse

The aim was to investigate the influence of experimental muscle pain on performance and upper extremity muscle activity during occupational work requiring different levels of precision. Experimental muscle pain was induced by infusing hypertonic saline (0.3 ml, 5% NaCl) into the extensor carpi ulnaris (ECU) muscle. The same amount of isotonic saline was infused on a separate day to act as a control. Tasks requiring use of a computer mouse with high and low levels of precision were performed during the two sessions. Electromyographic (EMG) activity was measured from the ECU, the flexor carpi radialis (FCR) and the trapezius muscles. A group of 13 men participated in the study. Performance measured as work cycle time, cursor movements on the screen, and velocity of cursor movement were unaffected by muscle pain. The ECU muscle pain did not modulate EMG profiles of either the trapezius or FCR muscles – either during high or during low precision work. During the low precision work the painful ECU muscle showed lower EMG activity in specific phases of the work cycle (highest activity phases) compared to the control session (P < 0.05), whereas during the high precision work, experimental pain had no effect on the activity of the ECU muscle. In conclusion experimental muscle pain seems to modulate motor control differently depending on the precision level of the task. This may be of importance for our understanding of why some tasks lead to chronic musculoskeletal disorders. Accepted: 29 August 2000     

The influence of muscle pain and fatigue on the activity of synergistic muscles of the leg

The purpose of this study was to investigate the effect of experimentally induced muscle pain on the motor-control strategies of synergistic muscles during submaximal fatiguing isometric contractions. The root mean square (RMS) and median frequency (MF) of the surface electromyographic (EMG) signal from synergistic plantarflexors and dorsiflexors were assessed to exhaustion. Ten subjects performed sustained dorsiflexions and plantarflexions at two contraction levels, 50% and 80% of maximum voluntary contraction, with or without muscle pain, induced by injection of 6% hypertonic saline in one synergist. In the painful contractions, the RMS of the EMG signal was decreased compared to the control condition in the initial phase of the contraction, in the muscles where pain was induced as well as in the nonpainful synergists. Moreover, the EMG signal MF decreased faster during muscle pain than in the control condition. The endurance time was shorter during muscle pain, and some of the nonpainful synergists showed increased compensatory activity at the end of the contractions to maintain the target force. The decreased EMG activation during pain was coupled with significantly decreased torque levels during the painful condition that would partly explain the results. However, the ratio between force and EMG amplitude was decreased for both the painful and nonpainful synergists, so other mechanisms might explain the present findings. This study shows that localized muscle pain can reorganize the EMG activity of synergists where no pain is present. These findings may have implications for the understanding of manifestations seen in relation to painful musculoskeletal disorders.     

The influence of experimentally induced pain on shoulder muscle activity

Muscle function is altered in painful shoulder conditions. However, the influence of shoulder pain on muscle coordination of the shoulder has not been fully clarified. The aim of the present study was to examine the effect of experimentally induced shoulder pain on shoulder muscle function. Eleven healthy men (range 22–27 years), with no history of shoulder or cervical problems, were included in the study. Pain was induced by 5% hypertonic saline injections into the supraspinatus muscle or subacromially. Seated in a shoulder machine, subjects performed standardized concentric abduction (0°–105°) at a speed of approximately 120°/s, controlled by a metronome. During abduction, electromyographic (EMG) activity was recorded by intramuscular wire electrodes inserted in two deeply located shoulder muscles and by surface-electrodes over six superficially located shoulder muscles. EMG was recorded before pain, during pain and after pain had subsided and pain intensity was continuously scored on a visual analog scale (VAS). During abduction, experimentally induced pain in the supraspinatus muscle caused a significant decrease in activity of the anterior deltoid, upper trapezius and the infraspinatus and an increase in activity of lower trapezius and latissimus dorsi muscles. Following subacromial injection a significantly increased muscle activity was seen in the lower trapezius, the serratus anterior and the latissimus dorsi muscles. In conclusion, this study shows that acute pain both subacromially and in the supraspinatus muscle modulates coordination of the shoulder muscles during voluntary movements. During painful conditions, an increased activity was detected in the antagonist (latissimus), which support the idea that localized pain affects muscle activation in a way that protects the painful structure. Further, the changes in muscle activity following subacromial pain induction tend to expand the subacromial space and thereby decrease the load on the painful structures.     

The influence of experimental muscle pain on motor unit activity during low-level contraction

In the present study we compared motor unit (MU) activity in a painful extensor carpi ulnaris (ECU) muscle to that of a pain-free control. According to the pain adaptation model the activity of the painful ECU muscle may be inhibited and its antagonist activity increased during wrist extension performed as a pre-defined low-force ramp. The pre-defined low force may then be maintained by increased activity in the pain-free synergist muscles such as the extensor carpi radialis (ECR) muscle. Nine females (31–47 years old) participated in the study. Maximal voluntary contraction (MVC) of the wrist extensors was performed. A catheter was inserted into the ECU muscle to allow the injection of hypertonic saline to evoke muscle pain, and a concentric needle was inserted for the recording of MU activity. Surface electromyograms were recorded from a synergist and an antagonist (ECR and flexor carpi radialis) to the painful ECU muscle. A force ramp of isometric wrist extensions up to 10% MVC, with a force increase of 1% MVC · s⁻¹, were performed followed by 60 s of sustained contraction at 10% MVC. The number of MUs recruited was almost identical for baseline and with pain, and no effect of experimental muscle pain was found on the properties of the MUs (amplitude, area) or their firing characteristics (mean firing rate, firing variability) during low-force ramp contraction. During the sustained 10% MVC, no effect of pain was found for concentric or surface EMG of the forearm muscles. At low force levels no pain-induced modulations were found in MU activity, when the mechanical condition was similar to that of a control situation. Accepted: 30 May 2000     

Nociceptive craniofacial muscle primary afferent neurons synapse in both the rostral and caudal brain stem

Limited information is available on muscle afferent neurons with fine fibers despite their presumed participation in musculoskeletal disorders, including temporomandibular disorders. To study these neurons, intracellular recordings were made from the central axons of slowly conducting muscle afferent neurons in anesthetized rats. After intraaxonal impalement, axons were characterized by masseter nerve stimulation, receptive field testing, muscle stretching and intramuscular injection of hypertonic saline. Intracellular recordings were made from 310 axons (conduction velocity: 6.5-60(M)/s, mean = 27.3(M)/s; following frequency: 27-250 Hz, mean = 110Hz). No neurons responded to cutaneous palpation or muscle stretching. Some axons (n = 34) were intracellularly stained with biotinamide. These neurons were classified as group II/III noxious mechanoreceptors because their mechanical threshold exceeded 15 mN, and conduction velocities ranged from 12 to 40.2(M)/s (mean = 25.3(M)/s). Two morphological types were recognized by using an object-based, three-dimensional colocalization methodology to locate synapses. One type (IIIHTM(Vp-Vc)) possessed axon collaterals that emerged along the entire main axon and synapsed in the trigeminal principal sensory nucleus and spinal trigeminal subnuclei oralis (Vo), interpolaris (Vi), and caudalis (Vc). A second type (IIIHTM(Vo-Vc)) possessed axon collaterals that synapsed only in caudal Vo, Vi, and Vc. Our previous studies show that muscle spindle afferent neurons are activated by innocuous stimuli and synapse in the rostral and caudal brain stem; here we demonstrate that nociceptive muscle mechanoreceptor afferent axons also synapse in rostral and caudal brain stem regions. Traditional dogma asserts that the most rostral trigeminal sensory complex exclusively processes innocuous somatosensory information, whereas caudal portions receive nociceptive sensory input; the data reported here do not support this paradigm.     

Isotonic and hypertonic sodium loading in supine humans

The hypothesis that hypertonic saline infusion induces a greater natriuresis than infusion of the same amount of sodium as isotonic saline was tested in 8 supine subjects on fixed sodium intake of 150 mmol NaCl day^–1. Sodium loads equivalent to the amount of sodium contained in 10% of measured extracellular volume were administered intravenously over 90 min either as isotonic saline or as hypertonic saline (850 mmol L^–1). A third series without saline infusion served as time control. Experiments lasted 8 h. Water balance and sodium loads were maintained by replacing the excreted amounts every hour. Plasma sodium concentrations only increased following hypertonic saline infusion (by 2.7 ± 0.3 mmol L^–1). Oncotic pressure decreased significantly more with isotonic saline (4.1 ± 0.3 mmHg) than with hypertonic saline (3.2 ± 0.2 mmHg), indicating that isotonic saline induced a stronger volumetric stimulus. Renal sodium excretion increased more than a factor of four with isotonic and hypertonic saline but also increased during time control (factor of three). Cumulated sodium excretions following isotonic (131 ± 13 mmol) and hypertonic saline (123 ± 10 mmol) were statistically identical exceeding that of time control (81 ± 9 mmol). Plasma angiotensin II decreased in all series but plasma ANP concentrations and urinary excretion rates of endothelin-1 remained unchanged. In conclusion, hypertonic saline did not produce excess natriuresis. However, as the two loading procedures induced similar natriureses during different volumetric stimuli, part of the natriuresis elicited by hypertonic saline could be mediated by stimulation of osmoreceptors involved in renal sodium excretion. The supine position does not provide stable time control conditions with regard to renal excretory function.     

Effects of experimental muscle pain on shoulder-abduction force steadiness and muscle activity in healthy subjects

We previously demonstrated that the steadiness of shoulder abduction is reduced in patients with subacromial impingement syndrome (SIS), which might be related to shoulder pain associated with the SIS. The aim of the present study was to examine the acute effects of experimental shoulder muscle pain on shoulder motor function in healthy subjects. The fluctuations in exerted force (force steadiness) and electromyographic (EMG) activity from eight shoulder muscles were determined during sub-maximal isometric and dynamic contractions with the shoulder abductors in nine healthy subjects (27.7 ± 4.2 years, mean ± 1 SD) before, during and after experimental pain induction. Experimental pain was induced by bolus injections of 6% hypertonic saline into the supraspinatus muscle. Experimental muscle pain reduced shoulder-abduction force steadiness on average by 21% during isometric contractions (P = 0.012) and tended to do so during concentric contractions (P = 0.083). Middle deltoid, and infraspinatus and lower trapezius muscle activity increased (3–5% EMG_max) during isometric and concentric contractions, respectively (P < 0.05). Thus, experimental shoulder muscle pain reduced the steadiness of isometric shoulder abduction and caused small changes in the abduction activation strategy. The observed effects of experimental pain on shoulder motor function differed from that observed previously in patients with SIS and chronic pain during the same types of contractions. A possible explanation may be that, even though the adopted experimental pain-paradigm may reflect the SIS in terms of the painful structures, it might not reflect the adaptations in the central nervous system seen with chronic pain.     

Study of the cremasteric muscle during erection

Background Mechanism of testicular elevation during erection is not known. We investigated the hypothesis that erection evokes reflex cremasteric muscle (CM) contraction which effects testicular elevation.Methods Electromyographic (EMG) response of CM to erection was recorded in 26 healthy volunteers (age 36.7 ± 6.8 SD years). Erection was induced by intracavernosal injection of alprostadil. CM response was tested before and after individual glans penis (GP) and CM anesthetization.Results The CM exhibited resting electric activity of mean amplitude of 74.8 ± 6.3 μV which, on erection, increased to 486.6 ± 36.8 μV (P < 0.001). Response was momentary. Anesthetization of erect GP did not effect increase of CM EMG activity, while bland gel did. Anesthetized CM did not respond to GC erection while saline infiltrated did.Conclusions The CM appears to contract during erection through a reflex which we call ‘peno-cremasteric reflex’. CM contraction assumingly elevates testicle and support cord veins; it may effect testicular compression, thus expressing its secretions into vas deferens.     

Blood flow in “red” and “white” calf muscles in cats during isometric and isotonic exercise

Muscle blood flow was measured with the radioactive microspheres technique in plantar flexors of seven cats. Right leg performed rhythmic isotonic and left leg sustained isometric contractions. Flows were determined at rest, during stimulation periods, and immediately after 90 sec of high frequency stimulation. During isotonic contraction, flow to m. soleus (a “red muscle”) increased progressively as stimulation increased: 0.06±0.02, 0.21±0.05, 0.41±0.12, and 0.26±0.06 ml/min/g during rest, 10 Hz, 50 Hz, and after 50 Hz stimulation frequencies, respectively. Corresponding values for gastrocnemius medialis were 0.06±0.01, 0.38±0.05, 0.27±0.03, and 0.28±0.06 (x± S.E.). These last values were characteristic also for the other “white” muscles investigated: gastrocnemius lateralis, and plantaris. During sustained isometric exercise at 5 and 25 Hz stimulation frequency the patterns were similar, except that higher flows were observed, and during recovery flows actually increased again in the “white” muscles. Blood pressure did not change. Resting flows were similar in innervated and denervated muscles. These data demonstrate that during isotonic as well as isometric exercise there is an increased resistance to flow with increasing muscle tension in “white” but not in “red” muscles. This supports the notion that a condition of relative ischaemia exists in “white” muscles during both isometric and isotonic contractions which is more pronounced during isometric exercise. The results corroborate previous studies on isometric exercise and suggest that the pattern during isotonic exercise is similar.     

Reflex inhibition of normal cramp following electrical stimulation of the muscle tendon

Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I(1), I(2)) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.     

The relative timing of trunk muscle activation is retained in response to unanticipated postural-perturbations during acute low back pain

The purpose of this study was to assess the activation of the erector spinae (ES) and external oblique (EO) in response to unanticipated, bi-directional postural perturbations before and after the induction of acute low back pain (LBP) in healthy individuals. An experimental session consisted of a baseline, control, and an acute LBP condition. For the control and acute LBP condition, isotonic or hypertonic saline (HS), respectively, was injected into the right ES muscle. In each condition, participants stood on a moveable platform during which 32 randomized postural perturbations (8 repetitions of 4 perturbation types: 8 cm anterior slides, 8 cm posterior slides, 10° anterior tilts, and 10° posterior tilts) with varying inter-perturbation time intervals were performed over a period of 4–5 min. Bilateral surface electromyography (EMG) was recorded from the ES and EO in addition to subjective pain records. During the acute LBP condition: (1) the onset time of the ES and EO was delayed for the forward and backward sliding perturbations (P < 0.05); (2) EMG amplitude was reduced bilaterally for all perturbations (P < 0.05); (3) the order of activation and interval between the onset times of the ES and EO were unaltered and (4) ES, but not EO, activity was adjusted to account for the directional differences between the perturbations. This study revealed that re-establishment of posture and balance was a result of the individuals’ ability to rapidly modulate ES with respect to EO activity and that the bi-directional postural responses, although shifted in time and amplitude, retained temporal features in the presence of acute LBP.