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Malnutrition reduces respiratory muscle mass and contractile force through atrophy of Type II fibers and impaired energy metabolism. Nutritional repletion restores respiratory muscle function, but may add to ventilatory work. Nutritional repletion also enhances weaning from mechanical ventilation.
We studied 53 patients with proximal myopathy to determine at what level of muscle weakness hypercapnic respiratory failure is likely, and which tests of pulmonary function or respiratory muscle strength would best suggest this development. Respiratory muscle strength was determined from maximal static efforts and in half the patients, both inspiratory and expiratory muscle strengths were less than 50% of normal. In the 37 patients without lung disease respiratory muscle weakness was accompanied by significant decreases in vital capacity, total lung capacity, and maximum voluntary ventilation; by significant increases in residual volume and arterial carbon dioxide tension (PaCO2); and greater likelihood of dependence on ventilators, atelectasis, and pneumonia. Hypercapnia was particularly likely when respiratory muscle strength was less than 30% of normal in uncomplicated myopathy, and when vital capacity was less than 55% of the predicted value in any patient.
1. Eight subjects maintained maximal inspiratory pressure as long as possible. The subjects accurately judged the pressure developed, but considered that the sense of effort or motor command increased progressively during the contraction as fatigue developed. 2. A reference inspiratory load was overestimated after maximal inspiratory contractions. 3. These findings are consistent with the hypothesis that awareness of the motor command or effort contributes to the estimation of respiratory loads.
UNLABELLED: Respiratory muscle fatigue after prolonged mechanical ventilation of the lungs is a common occurrence. This is probably due to disuse atrophy. The standard technique used to overcome this problem is to gradually wean the patient from the respirator over the course of several days or weeks. HYPOTHESIS: based on experience with the rehabilitation of skeletal muscles during long-term immobilisation of the extremities following trauma or surgery and on experience with diaphragm pacing in quadriplegics, intermittent electrical or magenetic stimulation of the diaphragm while the lungs are still being mechanically ventilated may be beneficial. The result of such stimulation would be to preserve the dysfunctioning diaphragm from atrophy. CONSEQUENCES: dependence on the respirator, length of intubation time, risk of complications and length of stay in the ICU would be considerably reduced.
Patients with respiratory muscle weakness show nocturnal hypoventilation, with oxygen desaturation particularly during rapid eye movement (REM) sleep, but evidence in individuals with isolated bilateral diaphragmatic paresis (BDP) is conflicting. The effect of sleep on relative activity of the different respiratory muscles of such patients and, consequently, the precise mechanisms causing desaturation have not been clarified. We have studied eight patients, four with generalized muscle weakness and four with isolated BDP during nocturnal sleep with measurements including oxygen saturation and surface electromyographic (EMG) activity of various respiratory muscle groups. Nocturnal oxygenation correlated inversely with postural fall in vital capacity, an index of diaphragmatic strength. During REM sleep, hypopnoea and desaturation occurred particularly during periods of rapid eye movements (phasic REM sleep). In most subjects, such events were "central" in type and associated with marked suppression of intercostal muscle activity, but two subjects had recurrent desaturation due to "obstructive" hypopnoea and/or apnoea. Expiratory activity of the external oblique muscle was present whilst awake and during non-rapid eye movement (NREM) sleep in seven of the eight subjects in the semirecumbent posture. This probably represents an "accessory inspiratory" effect, which aids passive caudal diaphragmatic motion as the abdominal muscles relax at the onset of inspiration. Expiratory abdominal muscle activity was suppressed in phasic REM sleep, suggesting that loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea. We conclude that, in patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Specific respiratory muscle training can improve respiratory muscle function in patients with COPD, but the magnitude of improvement appears dependent on the magnitude of the training load. High training loads are difficult to achieve using conventional, constant loading techniques, but may be possible using interval-based training techniques. METHODS: To assess the feasibility of high-intensity respiratory muscle training, nine subjects with moderate-to-severe COPD (FEV(1) 34 +/- 12% predicted [mean +/- SD]) completed 8 weeks of interval-based respiratory muscle training combined with a general exercise program. This involved three 20-min sessions per week, each session comprising seven 2-min bouts of breathing against a constant inspiratory threshold load, each bout separated by 1 min of unloaded recovery. Inspiratory load was progressively incremented. Respiratory muscle strength (maximum inspiratory pressure generated against an occluded airway [PImax]) and endurance (maximum pressure generated against a progressively increasing inspiratory threshold load [Pthmax]) were measured before and immediately after the 8-week training period. RESULTS: By the third training session (week 1), subjects breathed against a threshold that required generation of pressures equivalent to 68 +/- 5% of the pretraining PImax. By week 8, this had increased to 95 +/- 12% of the pretraining PImax. On completion of training, PImax had increased by 32 +/- 27% (p < 0.05), Pthmax had increased by 56 +/- 33% (p < 0.05), and Pthmax/PImax had increased by 20 +/- 20% (p < 0.05). CONCLUSIONS: This study has demonstrated that high-intensity, interval-based respiratory muscle training is feasible in patients with moderate-to-severe COPD, resulting in significant improvements in respiratory muscle strength and endurance when performed three times a week for 8 weeks.
The alveolar pressure was measured in 15 healthy men at different flow rates breathing without and with additional resistance from a stenosis (diameter 7 mm). Ventilation, breathing frequency, pulse rate, O2-uptake, and CO2-elimination were also measured during rest and during bicycle exercise. At rest, FRC and gas exchange were unaltered, while ventilation and breathing frequency little with the additional resistance. During work, however, the stenosis, caused increased O2-uptake and CO2-elimination and decreased ventilation and breathing frequency. The mean O2-consumption by the respiratory musculature necessary to overcome the airway resistance is 0.00042 ml/gcm.
1. Normal respiratory muscles have a large functional reserve. 2. Muscles have a tremendous capacity for adaptation. Adaptation is task-specific (eg, muscles use similar motor units for the same tasks). 3. Muscular fatigue results when motor units are required to perform an unaccustomed task. Continued effort in the face of fatigue, especially high-tension low-repetition effort, may produce a reversible "use atrophy" (eg, fiber damage, splitting, and regeneration). 4. Exercising damaged or regenerating muscle may produce irreversible damage. 5. Exercising the respiratory muscles of some patients may make them more susceptible to fatigue or, at least, produce no further improvement in function. Alternating rest and exercise improves pulmonary function tests in some patients. 6. Retraining a weak or damaged muscle requires that it first be "shut down" and rested before attempting retraining. 7. Training a rested muscle to different tasks--before these tasks are needed--may be the critical step in successful rehabilitation. 8. Resistance breathing probably improves both respiratory muscle strength and respiratory muscle endurance. 9. There are at least three immediate tasks for clinicians to define: Where in the present natural history of COPD should respiratory muscles be rested? How long should they be rested? How best can they be retrained?
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.
How the respiratory muscles, the so-called "vital pump", works is relevant to medicine and nevertheless, poorly understood. The present studies attempt to obtain a better insight in the action and interaction of respiratory muscles by measuring the mechanical outcome of individual respiratory muscle contraction with two different techniques in anesthetized dogs. First, we measured the changes in length undergone by respiratory muscles using sonomicrometry. We observed that the costal and crural parts of the diaphragm frequently behaved differently, supporting the concept that these two parts behave as two different muscles. Moreover, crural diaphragmatic length appeared to be linked to abdominal dimensions, the classical used estimate of diaphragmatic length, whereas costal diaphragmatic length was not. The parasternal or the interchondral parts of the internal intercostals invariably shortened with inspiration supporting their role as inspiratory agonists. By way of contrast, the respiratory length changes in the external and interosseus internal intercostal were variable and not consistently in different directions for the two layers. The changes in length, during rotation of the trunk were consistent, larger and systematically in opposite directions for these two layers, suggesting that these muscles predominantly function as rotators of the trunk or at least that a role in rotation of the trunk explains better the need for two layers of intercostal muscles with different fiber orientation than a respiratory role. Second, we measured changes in intramuscular pressure in the costal and crural parts of the diaphragm, and in the parasternal intercostals, using mini-transducers. In the diaphragm intramuscular pressure appeared to be a complex variable determined by the tension developed by the muscle as well as the pleural and abdominal pressures applied to the muscle. As a consequence, intramuscular pressure often decreased during contraction, suggesting that in contrast to other muscles, diaphragmatic contraction may enhance diaphragmatic blood flow. Conversely, in the parasternal intercostals, intramuscular pressure invariably increased during contraction, and a linear relationship between intramuscular pressure and contractile force was present. The forces developed by these muscles during quiet breathing and other respiratory maneuvers were found to be significant, supporting the important inspiratory role of the parasternal intercostals. Intramuscular pressure thus appeared to be a perfect estimate of the force developed by these muscles. Finally, we examined the changes in respiratory muscle interaction with hyperinflation.(ABSTRACT TRUNCATED AT 400 WORDS)
Respiratory muscle fatigue has been demonstrated in the laboratory as well as in pathological states, but whether it occurs in healthy individuals under physiological conditions is unknown. To determine whether fatigue of the respiratory muscles may develop with endurance exercise, we measured spirometry and respiratory muscle strength and endurance in four runners before and after completion of a marathon race (42.2 km). Strength was assessed by measuring maximal inspiratory (PImax) and expiratory (PEmax) pressures and transdiaphragmatic pressure during inspiratory capacity (PdiIC); endurance was determined by measuring maximal voluntary ventilation (MVV). After marathon running (mean time, 3 h 24 min) there was no change in forced vital capacity, inspiratory capacity, or flow rates from prerace values. Decreases were observed between pre- and postrace PImax (165.8 +/- 11.0 vs. 138.5 +/- 7.6 cmH2O; P less than 0.01) PEmax (240.0 +/- 20.4 vs. 173.0 +/- 22.6 cmH2O; P less than 0.05), PdiIC (78.8 +/- 11.6 vs. 63.3 +/- 7.0 cmH2O; P less than 0.10), and MVV (178 +/- 24.2 vs. 161.2 +/- 23.2 l/min; P less than 0.005). The decrements in respiratory muscle strength and endurance suggest the development of respiratory muscle fatigue after marathon running.
1. Changes in posture can affect the resting length of the diaphragm, which is corrected through increases in both diaphragm and abdominal muscle activity. Furthermore, postural alterations can diminish airway patency, which must be compensated for through increases in firing of particular upper airway muscles. 2. Recent evidence has shown that the vestibular system participates in adjusting the activity of both upper airway muscles and respiratory pump muscles during movement and changes in body position. 3. Vestibulo-respiratory responses do not appear to be mediated through the brainstem respiratory groups; labyrinthine influences on respiratory pump muscles may be relayed through neurons in the medial medullary reticular formation, which have recently been demonstrated to provide inputs to both abdominal and diaphragm motoneurons. 4. Three regions of the cerebellum that receive vestibular inputs, the fastigial nucleus, the nodulus/uvula and the anterior lobe, also influence respiratory muscle activity, although the physiological role of cerebellar regulation of respiratory activity is yet to be determined. 5. It is practical for the vestibular system to participate in the control of respiration, to provide for rapid adjustments in ventilation such that the oxygen demands of the body are continually matched during movement and exercise.
The respiratory muscles constitute a pump as vital to life as the heart. In patients with severe lung disease, the work of breathing is increased greatly, whereas the capacity of the respiratory muscles to generate tension and ventilation is impaired. In these circumstances, respiratory muscle fatigue may occur. When the cardiac pump fails, it often is possible to improve its performance by drug therapy with inotropic agents. In recent years, attention has been focused on the possibility of enhancing respiratory muscle function with drugs. The agents most studied have been the methylxanthines, theophylline and aminophylline. In vitro studies have demonstrated an inotropic effect of theophyllines on all skeletal muscles tested, including the diaphragm. The effect of theophyllines on skeletal muscle is dose related and animal studies show that any effect in humans, where dosage is limited by toxicity, is likely to be small. Early studies in humans showed a substantial positive inotropic effect on the diaphragm, but subsequently, a large number of studies have yielded mixed results. Up to the present time, most studies have failed to demonstrate a positive action of theophyllines. Although is it possible that these drugs may have a very small beneficial effect on contractility, not easily detected by the methods of some investigators, such as small effect of potentially toxic drugs is likely to be of limited clinical value.
The functional anatomy of the respiratory muscles and their actions and interactions are presented, particularly of the diaphragm. The large amount of blood flow to respiratory muscles and the determination of blood flow are reviewed, while the role these muscles play in the overall economy of the body in health and disease are discussed. Finally the failure of the respiratory muscles in the context of the development of hypercapnic respiratory failure is examined. It is argued that as the respiratory muscles become fatigued, afferent information from the respiratory muscles modifies the breathing pattern, which might be beneficial to respiratory muscle function, but it might compromise alveolar ventilation.
The aim of this study was to evaluate the effects of low intensity, home inspiratory muscle training on respiratory muscle endurance in children with Duchenne muscular dystrophy, using a double-blind protocol. The originality aspect of this study is the use of a reproducible method of endurance and of the same method for evaluation and training. We studied eight trained children (mean age 14.7+/-4.5 years) and eight control children (mean age, 12.6+/-1.8 years). For 6 weeks, children breathed twice a day for 10 min through a valve with either 30% (training group) or less than 5% (control group) of their maximum inspiratory pressure (P(imax)). The results showed (1) a 46% improvement in the time limit after training in the training group and no change in the control group and (2) a significant correlation between the total time of respiratory muscle training and the percentage of endurance improvement in the training group. We conclude that specific training improves respiratory muscle endurance in Duchenne muscular dystrophy and the effectiveness of training appears to be dependent on the quantity of training.
Respiratory muscles can fatigue during prolonged and maximal exercise, thus reducing performance. The respiratory system is challenged during underwater exercise due to increased hydrostatic pressure and breathing resistance. The purpose of this study was to determine if two different respiratory muscle training protocols enhance respiratory function and swimming performance in divers. Thirty male subjects (23.4 +/- 4.3 years) participated. They were randomized to a placebo (PRMT), endurance (ERMT), or resistance respiratory muscle training (RRMT) protocol. Training sessions were 30 min/day, 5 days/week, for 4 weeks. PRMT consisted of 10-s breath-holds once/minute, ERMT consisted of isocapnic hyperpnea, and RRMT consisted of a vital capacity maneuver against 50 cm H(2)O resistance every 30 s. The PRMT group had no significant changes in any measured variable. Underwater and surface endurance swim time to exhaustion significantly increased after RRMT (66%, P < 0.001; 33%, P = 0.003) and ERMT (26%, P = 0.038; 38%, P < 0.001). Breathing frequency (f (b)) during the underwater endurance swim decreased in RRMT (23%, P = 0.034) and tidal volume (V (T)) increased in both the RRMT (12%, P = 0.004) and ERMT (7%, P = 0.027) groups. Respiratory endurance increased in ERMT (216.7%) and RRMT (30.7%). Maximal inspiratory and expiratory pressures increased following RRMT (12%, P = 0.015, and 15%, P = 0.011, respectively). Results from this study indicate that respiratory muscle fatigue is a limiting factor for underwater swimming performance, and that targeted respiratory muscle training (RRMT > ERMT) improves respiratory muscle and underwater swimming performance.
Respiratory muscle dysfunction associated with ventilatory loading may be partially attributed to respiratory muscle injury. Exertion-induced muscle injury can be defined as structural alterations of the muscle, however, a better understanding of the biochemical, morphologic, and functional correlates of injured respiratory muscles will facilitate discrimination of how injury, fatigue, and weakness contribute to respiratory muscle dysfunction. In addition to the increased loads associated with lung disease, many factors such as poor arterial blood gases, immobilization, sepsis, decreased nutrition, and corticosteroids may increase susceptibility to exertion-induced respiratory muscle injury. Respiratory muscle injury in humans is not well-described, however, more extensive evidence has been shown in animal models of increased ventilatory loading. Potential mechanisms of respiratory muscle injury are mechanical stress, metabolic stress, and inflammation. In order to optimize therapeutic interventions, a better understanding of these mechanisms and the patients that are most susceptible to respiratory muscle injury needs to be determined.
Respiratory muscle injury may result from excessive loading due to a decrease in respiratory muscle strength, an increase in the work of breathing, or an increase in the rate of ventilation. Other conditions such as hypoxemia, hypercapnia, aging, decreased nutrition, and immobilization may potentiate respiratory muscle injury. Respiratory muscle injury has been shown in animal models using direct muscle or phrenic nerve stimulation, acute inspiratory resistive loading, tracheal banding, corticosteroids, phrenic nerve section, and the mdx mouse. Although numerous examples of diaphragm injury have been shown in animal models, evidence in humans is sparse. Potential mechanisms which may contribute to respiratory muscle injury include high levels of intracellular calcium-activated degradative enzymes, non-uniformity of stresses and strains, plasma membrane disruptions, and activation of the inflammatory process.