Effects of non-fatiguing respiratory muscle loading induced by expiratory flow limitation during strenuous incremental cycle exercise on metabolic stress and circulating natural killer cells.

Exercise induces release of cytokines and increase of circulating natural killers (NK) lymphocyte during strong activation of respiratory muscles. We hypothesised that non-fatiguing respiratory muscle loading during exercise causes an increase in NK cells and in metabolic stress indices. Heart rate (HR), ventilation (VE), oesophageal pressure (Pes), oxygen consumption (VO2), dyspnoea and leg effort were measured in eight healthy humans (five men and three women, average age of 31 ± 4 years and body weight of 68 ± 10 kg), performing an incremental exercise testing on a cycle ergometer under control condition and expiratory flow limitation (FL) achieved by putting a Starling resistor. Blood samples were obtained at baseline, at peak of exercise and at iso-workload corresponding to that reached at the peak of FL exercise during control exercise. Diaphragmatic fatigue was evaluated by measuring the tension time index of the diaphragm. Respiratory muscle overloading caused an earlier interruption of exercise. Diaphragmatic fatigue did not occur in the two conditions. At peak of flow-limited exercise compared to iso-workload, HR, peak inspiratory and expiratory Pes, NK cells and norepinephrine were significantly higher. The number of NK cells was significantly related to ΔPes (i.e. difference between the most and the less negative Pes) and plasmatic catecholamines. Loading of respiratory muscles is able to cause an increase of NK cells provided that activation of respiratory muscles is intense enough to induce a significant metabolic stress.

Tidal volume inflection and its sensory consequences during exercise in patients with stable asthma.

Sixteen patients with stable asthma performed a symptom-limited constant work-rate CWR cycle exercise during which breathing pattern, operating lung volumes, dyspnea intensity and its qualitative descriptors were measured. An inflection in the relation between tidal volume (V(T)) and ventilation (V˙(E)) was observed in each subject. The sense of "work/effort" was the dominant dyspnea descriptor selected up to the V(T)/V˙(E) inflection, whereas after it dyspnea intensity and the selection frequency of "unsatisfied inspiration" rose steeply in 37.5% of subjects in whom inspiratory reserve volume (IRV) had decreased to a critical level of 0.6L at the V(T) inflection point. In contrast, dyspnea increased linearly with exercise time and V˙(E), and "work/effort" was the dominant descriptor selected throughout exercise in 62.5% of subjects in whom the V(T)/V˙(E) inflection occurred at a preserved IRV. The V(T) inflection during exercise in patients with stable asthma marked a mechanical event with important sensory consequences only when it occurred at a critical reduced IRV.

Dyspnea, chest wall hyperinflation, and rib cage distortion in exercising patients with chronic obstructive pulmonary disease.

PURPOSE: Whether dyspnea, chest wall dynamic hyperinflation, and abnormalities of rib cage motion are interrelated phenomena has not been systematically evaluated in patients with chronic obstructive pulmonary disease (COPD). Our hypothesis that they are not interrelated was based on the following observations: (i) externally imposed expiratory flow limitation is associated with no rib cage distortion during strenuous incremental exercise, with indexes of hyperinflation not being correlated with dyspnea, and (ii) end-expiratory chest wall volume may either increase or decrease during exercise in patients with COPD, with those who hyperinflate being as breathless as those who do not. METHODS: Sixteen patients breathed either room air or 50% supplemental O2 at 75% of peak exercise in randomized order. We evaluated the volume of chest wall (V(cw)) and its compartments: the upper rib cage (V(rcp)), lower rib cage (V(rca)), and abdomen (V(ab)) using optoelectronic plethysmography; rib cage distortion was assessed by measuring the phase angle shift between V(rcp) and V(rca). RESULTS: Ten patients increased end-expiratory V(cw) (V(cw,ee)) on air. In seven hyperinflators and three non-hyperinflators, the lower rib cage paradoxed inward during inspiration with a phase angle of 63.4° ± 30.7° compared with a normal phase angle of 16.1° ± 2.3° recorded in patients without rib cage distortion. Dyspnea (by Borg scale) averaged 8.2 and 9 at the end of exercise on air in patients with and without rib cage distortion, respectively. At iso-time during exercise with oxygen, decreased dyspnea was associated with a decrease in ventilation regardless of whether patients distorted the rib cage, dynamically hyperinflated, or deflated the chest wall. CONCLUSIONS: Dyspnea, chest wall dynamic hyperinflation, and rib cage distortion are not interrelated phenomena.

Effect of limb muscle fatigue on perception of respiratory effort in healthy subjects.

The role of nonrespiratory peripheral afferents in dyspnea perception has not been fully elucidated yet. Our hypothesis is that fatigue-induced activation of limb muscle metaboreceptors served by group IV fine afferent fibers may impact on respiratory effort perception. We studied 12 healthy subjects breathing against progressive inspiratory resistive loads (10, 18, 30, 40, and 90 cmH(2)O x l(-1) x s) before and after inducing low-frequency fatigue of quadriceps muscle by repeating sustained contractions at > or = 80% of maximal voluntary contraction. Subjects also underwent a sham protocol while performing two loaded breathing runs without muscle fatigue in between. During the loaded breathing, while subjects mimicked the quiet breathing pattern using a visual feedback, ventilation, tidal volume, respiratory frequency, pleural pressure swings, arterial oxygen saturation, end-tidal partial pressure of CO(2), and dyspnea by a Borg scale were recorded. Compared with prefatigue, limb muscle fatigue resulted in a higher increase in respiratory effort perception for any given ventilation, tidal volume, respiratory frequency, pleural pressure swings, end-tidal partial pressure of CO(2), and arterial oxygen saturation. No difference between the two runs was observed with the sham protocol. The present data support the hypothesis that fatigue of limb muscles increases respiratory effort perception associated with loaded breathing, likely by the activation of limb muscle metaboreceptors.

Desensitization of the cough reflex by exercise and voluntary isocapnic hyperpnea.

Little is known about the effects of exercise on the sensory and cognitive aspects of coughing evoked by inhalation of tussigenic agents. The threshold for the cough reflex induced by inhalation of increasing nebulizer outputs of ultrasonically nebulized distilled water (fog), an index of cough reflex sensitivity, was assessed in twelve healthy humans in control conditions, during exercise and during voluntary isocapnic hyperpnea (VIH) at the same ventilatory level as the exercise. The intensity of the urge to cough (UTC), a cognitive component of coughing, was recorded throughout the trials on a linear scale. The relationships between inhaled fog nebulizer outputs and the correspondingly evoked UTC values, an index of the perceptual magnitude of the UTC sensitivity, were also calculated. Cough appearance was always assessed audiovisually. At an exercise level of 80% of anaerobic threshold, the median cough threshold was increased from a control value of 0.73 to 2.22 ml/min (P<0.01), i.e., cough sensitivity was downregulated. With VIH, the threshold increased from 0.73 to 2.22 ml/min (P<0.01), a similar downregulation. With exercise and VIH compared with control, mean UTC values at cough threshold were unchanged, i.e., control, 3.83 cm; exercise, 3.12 cm; VIH, 4.08 cm. The relationship of the fog nebulizer output/UTC value was linear in control conditions and logarithmic during both exercise and VIH. The perception of the magnitude of the UTC seems to be influenced by signals or sensations arising from exercising limb and thoracic muscles and/or by higher nervous (cortical) mechanisms. The results indicate that the adjustments brought into action by exercise-induced or voluntary hyperpnea exert inhibitory influences on the sensory and cognitive components of fog-induced cough.

Effect of biventricular pacing on ventilatory and perceptual responses to exercise in patients with stable chronic heart failure.

Despite the growing evidence supporting the use of biventricular cardiac resynchronization therapy (CRT) in patients with chronic heart failure (CHF), the mechanisms whereby acute hemodynamic improvements lead to improved exertional dyspnea are not precisely known. We hypothesized that improved cardiac function and ventilation-perfusion relations following CRT would reduce ventilatory demand, thereby improving dynamic operating lung volumes and enhancing tidal volume expansion during exercise. This, in turn, would be expected to reduce perceived exertional dyspnea and contribute to improved exercise performance. In a randomized, double-blind, crossover study, we compared cardiovascular, metabolic, ventilatory responses (breathing pattern, operating lung volumes, pulmonary gas exchange) and exertional symptoms in seven stable CHF patients who undertook incremental cardiopulmonary cycle exercise test with CRT switched to the "on" (CRT(on)) or "off" (CRT(off)) modality. Following CRT(on), peak oxygen uptake was significantly increased by 15%, and dyspnea ratings were lower for a given work rate (at work rate of 40 W, dyspnea = 1 +/- 0.4 vs. 2.5 +/- 0.9 Borg units, P < 0.05) and ventilation (at ventilation of 31 l/min, dyspnea = 2 +/- 0.7 vs. 3.3 +/- 1.1 Borg units, P < 0.05). CRT(on) was associated with improvements in ventilatory threshold, oxygen pulse, and oxygen uptake/work rate relationships (10.2 +/- 1 vs. 7.9 +/- 1.3 ml.min(-1).W(-1), P < 0.05). CRT(on) reduced the ventilatory requirement during exercise as well as the steepness of ventilation-CO(2) production slope (35 +/- 4 vs. 45 +/- 7, P < 0.05). Changes in end-expiratory lung volume during exercise were less with CRT(on) than with CRT(off) (0.12 vs. 0.37 liter, P < 0.05), and breathing pattern was correspondingly slower and deeper. Biventricular pacing improved all noninvasive indexes of cardiac function and oxygen delivery during exercise. The decreased ventilatory demand, improved dynamic operating lung volumes, and the increased ability to expand tidal volume during exercise are potential factors in the reduction of exertional dyspnea.

Inhaled furosemide does not alleviate respiratory effort during flow-limited exercise in healthy subjects.

Expiratory muscle loading results in increased perception of respiratory effort; this response is mediated by non-vagal reflexes originating in the chest wall. Furosemide, due to its vagal effect, might not affect the perception of respiratory effort during expiratory flow-limited incremental exercise. In this study, we compared in nine healthy subjects the following determinants of exercise performance such as respiratory effort (Borg), workload (W'), ventilation (V'E), tidal volume (VT), respiratory frequency (f), and mean inspiratory flow (VT/TI), an index of central respiratory drive, during either standard incremental cycling exercise, or expiratory flow-limited incremental exercise. In addition we examined the effect of inhaled placebo, furosemide (40 or 80 mg) on the perception of respiratory effort following standard incremental cycling exercise and expiratory flow-limited incremental exercise. Compared with standard incremental cycling exercise, expiratory flow-limited incremental exercise increased the Borg score and VT/Ti, and decreased W',V'E ,VT, and f in all subjects at iso-workload. Neither placebo nor furosemide modified peak ventilatory variables, slopes, or intercepts of the relationships of the Borg score with W', V'E, VT/TI and VT during expiratory flow-limited incremental exercise. We conclude that (a) compared with standard incremental exercise, expiratory flow limited exercise increases central respiratory drive and perception of respiratory effort, and (b) furosemide does not affect the sensation of respiratory effort under the present conditions of increased drive to the respiratory muscles.

Dyspnea during exercise in hyperbaric conditions.

INTRODUCTION: Length-tension and force-velocity characteristics of respiratory muscles and hyperinflation are the likely determinants of dyspnea in subjects exercising under hyperbaric conditions. We hypothesize that hyperinflation plays a minor role and that the reduced velocity of shortening of the respiratory muscles modulates dyspnea for any given pleural pressure. METHODS: We studied five normal subjects who performed an incremental exercise test on a cycloergometer in both normobaric (SL) and hyperbaric (4 ATA) conditions. We measured breathing pattern, inspiratory pleural pressure swing (Pessw), Delta Pes (i.e., the difference between the most and the less negative pleural pressures during tidal breathing), and dyspnea intensity (Borg score). End-expiratory lung volume (EELV) changes were evaluated by measuring changes in inspiratory capacity. Mean inspiratory flow (VT/TI) was used as an index of velocity of shortening of respiratory muscles. RESULTS: Compared with SL, at 4 ATA, peak exercise ventilation (VE) (84.5 vs 62.2 L x min(-1)) and VT/TI (2.99 vs 2.16 L x s)(-1) were lower, Pessw (30.9 vs 38.6 cm H2O) and Delta Pes (43.8 vs 62.2 cm H2O) were higher, and Borg score was not different (7.60 vs 8.20 au). EELV decreased progressively during exercise but remained higher than at SL. Borg score was greater for a same VE and lower for a same Delta Pes. VT/TI was lower for a same Pessw. The differences in EELV between SL and 4 ATA did not relate with the concurrent changes in Borg score. CONCLUSION: The results confirm our hypothesis that during exercise in hyperbaric conditions, decreased velocity of shortening of respiratory muscles modulates pressure-induced increases in dyspnea, with hyperinflation playing a minor role.

Is there a link between the qualitative descriptors and the quantitative perception of dyspnea in asthma?

BACKGROUND: There is no obvious link between qualitative descriptors and overall intensity of dyspnea during bronchoconstriction in patients with asthma. AIMS: To determine whether qualitative and quantitative perception of methacholine-induced bronchoconstriction independently contribute to characterizing clinically stable asthma. MATERIAL AND METHODS: We assessed changes in inspiratory capacity, and quantitative (by Borg scale) and qualitative (by a panel of eight dyspnea descriptors) sensations of dyspnea at 20 to 30% fall in FEV(1) during methacholine inhalation in 49 asthmatics. Furthermore, we calculated the level of perception of bronchoconstriction at 20% fall in FEV(1) (PB(20)). RESULTS: Descriptors selected by patients during methacholine inhalation allowed us to define three language subgroups: (1) chest tightness (subgroup A, n = 21); (2) work/effort (subgroup B, n = 7); and (3) both descriptors (subgroup C, n = 13). Eight of the 49 patients (subgroup D) were not able to make a clear-cut distinction among descriptors. The subgroups exhibited similar function at baseline and during methacholine inhalation. Most importantly, patients selected chest tightness to a greater extent (42.85%), and work/effort (14.3%) and both descriptors (26.5%) to a lesser extent at the lowest level of bronchoconstriction (FEV(1) fall < 10%) as at 20% fall in FEV(1). Thirty-two patients were normoperceivers (PB(20) > or = 1.4 to < 5 arbitrary units [au]), 7 patients were hyperperceivers (PB(20) > or = 5 au), and 10 patients were hypoperceivers (PB(20) < 1.4 au). Language subgroups were equally distributed across the perceiver subgroups. CONCLUSIONS: In patients with clinically stable asthma, PB(20) and language of dyspnea independently contribute to defining the condition of the disease. However, the possibility that this independence may be due to a beta-error should be taken into account.

Respiratory muscles and dyspnea in obese nonsmoking subjects.

To our knowledge no data have been reported on the contribution to acute increase in dyspnea by the respiratory muscles in obese nonsmoking subjects. To better focus on this topic, we studied seven obese subjects and an age-matched normal control group, assessing baseline pulmonary function, breathing pattern, esophageal pressure (Pes), and gastric (Pga) and transdiaphragmatic (Pdi) pressures. Pes was also recorded during a sniff maneuver (Pessn). During a hypercapnic rebreathing test we recorded inspiratory swing in Pes (Pessw), expiratory changes in Pga, and inspiratory swings in Pdi (Pdisw). Change in inspiratory capacity was considered the mirror image of end-expiratory lung volume (EELV). Dyspnea was assessed by a modified Borg scale. Under control conditions, patients exhibited a reduced expiratory reserve volume and intrinsic positive end-expiratory pressure (PEEPi). At the end of hypercapnic stimulation, compared with controls our obese subjects exhibited greater respiratory frequency (Rf), shorter expiratory time, greater Pessw, and lower Pdisw. Increases in EELV and PEEPi were found in the obese subjects but not in controls. Changes in Borg correlated with changes in PETCO2, VE, Pessw (%Pessn), and Pdisw to a greater extent in patients than in controls. Stepwise regression analysis indicated the amount of variability in Borg that was predicted by both Pdisw (r2 = 0.31, p < 0.0004), and Pessw (%Pessn) (r2 = 0.09, p < 0.005) in controls, and by Pessw (%Pessn) (r2 = 0.40, p < 0.00001) in obese subjects. We conclude that the rib cage muscles contributed to dyspnea to a greater extent in this subset of obese subjects.

Walking modality affects respiratory muscle action and contribution to respiratory effort.

We hypothesized that walking at increased speed or increasing gradient might have different effects on chest wall kinematics and respiratory muscle power components, and contribute differently to respiratory effort sensation. We measured the volumes of chest wall compartments by optoelectronic plethysmography, esophageal, gastric and transdiaphragmatic ( P(di)) pressures, and the sensation of the respiratory effort by a Borg scale in five normal subjects walking both at ascending gradient with constant speed (AG) and at ascending speed with constant gradient (AS). Chest wall kinematics, evaluated by displacement of chest wall compartments, did not show any significant difference between AS and AG. Muscle power, calculated as the product of mean flow and mean pressure, increased similarly, but its partitioning into pressure and velocity of shortening differed in the two modes. A greater increase in the pressure developed by the abdominal muscles ( P(abm)) (4.06-fold), and in the velocity of shortening of both rib cage inspiratory muscles ( v(rcm,i)) (2.01-fold) and the diaphragm ( v(di)) (1.90-fold) was associated with a lower increase in the pressure developed by the rib cage inspiratory muscles ( P(rcm,i)) (1.24-fold) and P(di) (0.99-fold) with AG. Instead, with AS, a lower increase in P(abm) (2.12-fold), v(rcm,i) (1.66-fold) and v(di) (1.54-fold) was associated with a greater increase in P(rcm,i) (1.56-fold) and P(di) (1.97-fold). A combination of P(abm) and v(di) during AG (Wald chi(2)=23.19, P<0.0000), with the addition of P(rcm,i) during AS (Wald chi(2)=29.46, P<0.0000), was the best predictor of Borg score. In conclusion, the general strategy adopted by respiratory centers during different walking modes does not differ in terms of ventilation, chest wall kinematics, and respiratory muscle power production, whereas it does in terms of partitioning of power into pressure and velocity of shortening, and respiratory muscle contribution to respiratory effort sensation. Combinations of different patterns of flow and pressure generation made the respiratory effort sensation similar during AS and AG modes.

Overall contribution of chest wall hyperinflation to breathlessness in asthma.

BACKGROUND: Studies suggest that the increased volume of both abdominal and rib cage compartments of the chest wall contribute to dyspnea during methacholine-induced airway narrowing. MATERIAL: Eight male patients with asthma aged 34 +/- 13 years (mean +/- SD) before and during methacholine challenge. METHODS: The volume of the chest wall (Vcw), volume of the abdomen (Vab), and volume of the rib cage (Vrc) were measured by using a three-dimensional optoelectronic plethysmography. RESULTS: During methacholine challenge, the increase in end-expiratory Vcw (Vcw,ee) [0.55 +/- 0.23 L, p < 0.001] was due to increased Vrc (0.37 +/- 0.20 L, p < 0.01) and, to a lesser extent, Vab (0.18 +/- 0.10 L, p < 0.005). Linear univariate regression analysis showed that changes in dyspnea (Borg scale) with the highest methacholine dose correlated with both DeltaFEV(1) and DeltaVcw,ee. Multiple regression analysis with the Borg score as dependent variable and all other ventilatory indexes as independent variables showed that DeltaVcw,ee and DeltaFEV(1) were the only significant contributors to the Borg score. Taken together Vcw,ee and FEV(1) explained 56% of variance in the Borg score (r(2) = 0.56), although Vcw,ee explained 48% of it. CONCLUSIONS: During methacholine challenge in patients with asthma, the overall increase in Vcw,ee is a better predictor of dyspnea that the reduction in FEV(1).

Inspiratory capacity and decrease in lung hyperinflation with albuterol in COPD.

STUDY OBJECTIVES: Inspiratory capacity (IC) has been proposed as a simple method to assess acute changes in functional residual capacity (FRC) with bronchodilation, assuming that total lung capacity (TLC) is unchanged. This assumption is based on studies using body plethysmography, which may not accurately measure TLC in severely obstructed subjects. The aim of this study is to validate the use of IC measured by optoelectronic plethysmography (OEP) [ICOEP], a noninvasive technique capable of computing changes in absolute lung volumes with great accuracy. MEWTHODS AND MEASUREMENTS: We studied 13 subjects with COPD in clinically stable condition at baseline and after 200 microg of inhaled albuterol. Changes in lung volumes were obtained from changes in chest wall volume (Vcw) measured by OEP and were compared with those measured by standard techniques. RESULTS: Albuterol treatment caused a small but significant increase in FEV(1) and FVC, a significant decrease of Vcw at FRC (VcwFRC), but no changes of Vcw at TLC (VcwTLC) and breathing pattern variables. The reduction of VcwFRC was not correlated with either spirometric or breathing-pattern variables. IC measured with a pneumotachograph was highly correlated with and not significantly different from ICOEP (p < 0.001). CONCLUSIONS: A single dose of inhaled albuterol does not significantly modify VcwTLC in subjects with COPD, thus validating the use of IC to measure changes of FRC in the assessment of reversibility of airway obstruction.

Determinants of exercise performance in normal men with externally imposed expiratory flow limitation.

To understand how externally applied expiratory flow limitation (EFL) leads to impaired exercise performance and dyspnea, we studied six healthy males during control incremental exercise to exhaustion (C) and with EFL at approximately 1. We measured volume at the mouth (Vm), esophageal, gastric and transdiaphragmatic (Pdi) pressures, maximal exercise power (W(max)) and the difference (Delta) in Borg scale ratings of breathlessness between C and EFL exercise. Optoelectronic plethysmography measured chest wall and lung volume (VL). From Campbell diagrams, we measured alveolar (PA) and expiratory muscle (Pmus) pressures, and from Pdi and abdominal motion, an index of diaphragmatic power (W(di)). Four subjects hyperinflated and two did not. EFL limited performance equally to 65% W(max) with Borg = 9-10 in both. At EFL W(max), inspiratory time (TI) was 0.66s +/- 0.08, expiratory time (TE) 2.12 +/- 0.26 s, Pmus approximately 40 cmH2O and DeltaVL-DeltaVm = 488.7 +/- 74.1 ml. From PA and VL, we calculated compressed gas volume (VC) = 163.0 +/- 4.6 ml. The difference, DeltaVL-DeltaVm-VC (estimated blood volume shift) was 326 ml +/- 66 or 7.2 ml/cmH2O PA. The high Pmus and long TE mimicked a Valsalva maneuver from which the short TI did not allow recovery. Multiple stepwise linear regression revealed that the difference between C and EFL Pmus accounted for 70.3% of the variance in DeltaBorg. DeltaW(di) added 12.5%. We conclude that high expiratory pressures cause severe dyspnea and the possibility of adverse circulatory events, both of which would impair exercise performance.

Respiratory muscle dynamics and control during exercise with externally imposed expiratory flow limitation.

To determine how decreasing velocity of shortening (U) of expiratory muscles affects breathing during exercise, six normal men performed incremental exercise with externally imposed expiratory flow limitation (EFLe) at approximately 1 l/s. We measured volumes of chest wall, lung- and diaphragm-apposed rib cage (Vrc,p and Vrc,a, respectively), and abdomen (Vab) by optoelectronic plethysmography; esophageal, gastric, and transdiaphragmatic pressures (Pdi); and end-tidal CO2 concentration. From these, we calculated velocity of shortening and power (W) of diaphragm, rib cage, and abdominal muscles (di, rcm, ab, respectively). EFLe forced a decrease in Uab, which increased Pab and which lasted well into inspiration. This imposed a load, overcome by preinspiratory diaphragm contraction. Udi and inspiratory Urcm increased, reducing their ability to generate pressure. Pdi, Prcm, and Wab increased, indicating an increased central drive to all muscle groups secondary to hypercapnia, which developed in all subjects. These results suggest a vicious cycle in which EFLe decreases Uab, increasing Pab and exacerbating the hypercapnia, which increases central drive increasing Pab even more, leading to further CO2 retention, and so forth.

Effects of vibratory stimulation on muscular pain threshold and blink response in human subjects.

The effects of vibratory stimulation on muscular pain threshold were investigated in 28 healthy subjects. Pain sensation was evaluated by the subjects' verbal reports in response to electrical stimulation of the vastus medialis muscle. Concomitant variations of blink response evoked as a component of the startle reaction were also studied. In all the subjects tested, high frequency vibration (110 Hz) induced a marked and long lasting elevation of the muscular pain threshold but only when vibration was applied to the skin overlying the ipsilateral quadriceps tendon or neighbouring areas and not when applied to remote ipsi- or contralateral regions. This effect was prevented either when tonic vibration reflex (TVR) of the quadriceps muscle was elicited or the skin underlying the vibrator was anaesthetized. Vibratory stimulation at low frequency (30 Hz) failed to produce any consistent effect on muscular pain threshold. Variations in threshold for blink response, as a rule, closely followed those of muscular pain threshold. However, a facilitation of the blink response, not accompanied by changes in pain sensation, was observed during the first period of both high and low frequency vibratory stimulation. The effectiveness of high frequency vibration in raising the muscular pain threshold is coherent with previous results showing that vibration is able to affect pain sensation. Present results suggest a role for rapidly adapting receptors (RA) and/or pacinian corpuscles (PC) in this effect and support the hypothesis of an inhibition of nociceptive messages, possibly at spinal segmental levels, by volleys in large myelinated afferent fibres.

Pain thresholds and electromyographic features of periarticular muscles in patients with osteoarthritis of the knee.

Electrical stimulation pain thresholds and EMG activity were studied, using the vastus medialis muscle of healthy control subjects and of patients with osteoarthritis of the knee. Various categories of sensation elicited by progressive increases of the level of electrical stimulation (including one defined as pain threshold) were defined for control subjects. For patients, muscular pain thresholds differed significantly for the two sides of the body; they were usually lower in the more affected side. Involuntary activity of certain motor units and delayed relaxation following voluntary contraction were consistently observed in patients. The involuntary activity was affected by limb position and by mechanical stimulation of tender areas of the muscle or joint. Differences in pain threshold between the two sides were significantly reduced and the EMG pattern became normal following treatment with injections of local anaesthetic into tender periarticular areas and systemic administration of lysine acetylsalicylate. In standing patients, abnormal EMG activity (which was characteristically sensitive to body load and its variations) was found. Injection of a local anaesthetic into the joint cavity was able to induce a rapid subjective improvement and a consistent reduction of EMG activity.