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Abdominal muscles are selectively active in normal subjects during stress and may increase the potential energy for inspiration by reducing the end-expiratory lung volume (EELV). We hypothesized that a similar process would occur in subjects with myotonic muscular dystrophy (MMD), but would be less effective, because of to their weakness and altered chest wall mechanics. Fine-wire electromyography (EMG) of the transversus abdominis (TA), internal oblique (IO), external oblique, and rectus abdominis was recorded in 10 MMD and 10 control subjects. EMG activity, respiratory inductive plethysmography, and gastric pressure were recorded during static pressure measurement and at increasing levels of inspiratory resistance breathing. EELV was reduced and chest wall motion was synchronous only in controls. Although the TA and IO were selectively recruited in both groups, EMG activity of the MMD group was twice that of controls at the same inspiratory pressure. In MMD subjects with mildly reduced forced vital capacity, significant differences can be seen in abdominal muscle recruitment, wall motion, work of breathing, and ventilatory parameters.

Respiratory muscle (RM) dysfunction is a progressive process, including both RM weakness and fatigue, that may advance to the point of respiratory failure. It occurs as a result of increased RM workloads, altered length-tension relationship of respiratory muscles, malnourished states, and altered cellular environment in chronic obstructive pulmonary disease (COPD). Consideration of multiple patient factors is necessary when identifying patient risk for RM dysfunction and designing plans of care. This article discusses the RM pump, including its measurement, in patients with COPD.

Data from the present study indicate a change in the pattern of chest wall muscle recruitment and improved ventilation with pursed-lip breathing (PLB) in COPD. Pursed lip breathing led to increased rib cage and accessory muscle recruitment during inspiration and expiration, increased abdominal muscle recruitment during expiration, decreased duty cycle of the inspiratory muscles and respiratory rate, and improved SaO2. In addition, PLB resulted in no change in pressure across the diaphragm and a less fatiguing breathing pattern of the diaphragm. Changes in chest wall muscle recruitment and respiratory temporal parameters concomitant with the increased SaO2 indicate a mechanism of improving ventilation with PLB while protecting the diaphragm from fatigue in COPD. Alterations in the pattern of respiratory muscle recruitment with PLB may be associated also with the amelioration of dyspnea. Further investigation is necessary to explore the relationship between the pattern of respiratory muscle recruitment during PLB and dyspnea.

The purpose of this study was to determine the relationship between recruitment of the DI and SM muscles measured as EMG signal amplitudes, the pattern of respiratory muscle recruitment measured with inductive plethysmography, and the intensity of the sensation of dyspnea, measured with 100 mm VAS. Eighteen normal subjects between the ages of 33 and 47 breathed under two conditions: normal controlled breathing and breathing against an inspiratory resistance at 60 percent of their maximal inspiratory pressure (MIP). The PM, RR, duty cycle (TI/TTOT, and VT were held constant. During resistance breathing, VAS dyspnea was increased when EMG-DI decreased; EMG-SM increased in association with the sensation of dyspnea. During inspiratory resistance breathing, dyspnea markedly increased and rib cage and accessory muscle recruitment was the predominant pattern of breathing. These data suggest that dyspnea may be associated with the recruitment of the accessory respiratory muscles rather than the recruitment of the diaphragm.