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We report the case of a uremic dialysis patient with severe secondary hyperparathyroidism, proximal muscle weakness and impaired respiratory muscle strength, the latter being assessed by maximal inspiratory pressure. After subtotal parathyroidectomy, we observed a marked improvement in respiratory muscle strength (27 vs. 87 cm H2O) and disappearance of proximal muscle weakness.
In this study, we searched for signs of thixotropic behavior in human rib cage respiratory muscles. If rib cage respiratory muscles possess thixotropic properties similar to those seen in other skeletal muscles in animals and humans, we expect resting rib cage circumference would be temporarily changed after deep rib cage inflations or deflations and that these aftereffects would be particularly pronounced in trials that combine conditioning deep inflations or deflations with forceful isometric contractions of the respiratory muscles. We used induction plethysmography to obtain a continuous relative measure of rib cage circumference changes during quiet breathing in 12 healthy subjects. Rib cage position at the end of the expiratory phase (EEP) was used as an index of resting rib cage circumference. Comparisons were made between EEP values of five spontaneous breaths immediately before and after six types of conditioning maneuvers: deep inspiration (DI); deep expiration (DE); DI combined with forceful effort to inspire (FII) or expire (FEI); and DE combined with forceful effort to inspire (FIE) or expire (FEE), both with temporary airway occlusion. The aftereffects of the conditioning maneuvers on EEP values were consistent with the supposition that human respiratory muscles possess thixotropic properties. EEP values were significantly enhanced after all conditioning maneuvers involving DI, and the aftereffects were particularly pronounced in the FII and FEI trials. In contrast, EEP values were reduced after DE maneuvers. The aftereffects were statistically significant for the FEE and FIE, but not DE, trials. It is suggested that respiratory muscle thixotropy may contribute to the pulmonary hyperinflation seen in patients with chronic obstructive pulmonary disease.
RATIONALE: Data on respiratory muscle performance in children with neuromuscular disorders are limited. OBJECTIVES: The aim of this study was to assess respiratory muscle strength by volitional and nonvolitional tests and to compare these tests with forced vital capacity. METHODS: Inspiratory muscle strength was assessed by measuring transdiaphragmatic and esophageal pressures generated during volitional and nonvolitional maneuvers, whereas expiratory muscle strength was assessed by measuring the gastric pressure generated during a cough maneuver. Lung volumes were assessed by measuring forced vital capacity. MEASUREMENTS AND MAIN RESULTS: Forty-one patients with Duchenne muscular dystrophy (n = 20), spinal amyotrophy (n = 8), and congenital myopathy (n = 13) were included, aged 2 to 18 yr. All the patients were able to perform the sniff and the cough maneuver. Sniff transdiaphragmatic pressure decreased with age in Duchenne patients, whereas it increased with age in patients with spinal amyotrophy and congenital myopathy. Magnetic stimulation of the phrenic nerves was obtained in all patients. Twenty-five (61%) patients were able to perform forced vital capacity. In the three groups of patients, a positive correlation was observed between volitional, assessed by the sniff maneuver, and nonvolitional respiratory muscle tests, assessed by the magnetic stimulation of the phrenic nerves. Also, forced vital capacity correlated with sniff transdiaphragmatic pressure and cough gastric pressure. CONCLUSIONS: Volitional respiratory muscle tests correlated with nonvolitional tests and with forced vital capacity. Simple volitional respiratory muscle tests constitute a valuable tool for the assessment of respiratory muscle strength in young patients with neuromuscular disorders.
In this review emphasis is placed on some major mechanisms involved in inspiratory muscle fatigue. It is certain that respiratory muscle fatigue is a clinical entity, with broad implication in internal medicine. As yet its prevalence is largely unknown. There is reasonable certainty of some of the mechanisms leading to fatigue, for example the effect of loads and circulation. However, the cellular mechanisms, both chemical and electrophysiological, remain obscure. In detecting respiratory muscle fatigue various tests already represent windows from which we can see the malfunction of some mechanisms, unfortunately often not understood. The ideal test to evaluate respiratory muscle fatigue (easy to perform, sensitive, specific, and reliable) has not been developed yet. The clinical identification of respiratory muscle fatigue is still developing, and only tentative guidelines for its treatment can be proposed at this stage. Clearly, much research is required to determine prevalence, establish the diagnosis, and evaluate therapy.
In planning a training programme for respiratory muscles several factors should be considered: establish the objective according to the patient's pathology, provide an adequate stimulus (both in intensity and quality), define if the goal is to increase coordination, strength, endurance, or all three. Several respiratory muscle conditioning plans have been used, mostly derived from three major protocols: sustained hyperventilation, resistive breathing, and manipulations of the breathing pattern. They have proved to be effective in quadriplegia, cystic fibrosis and to some extent in COPD patients. Respiratory muscle recovery and training in patients with respiratory failure is discussed.
To examine the relationship between nutrition, pulmonary function, respiratory muscle strength, and respiratory muscle morphometry, we compared physiologic data and muscle morphometry obtained from internal intercostal, external intercostal, and latissimus dorsi muscle biopsies in 68 patients who were having a thoracotomy. We stained the biopsies for myosin ATPase and measured the proportions and diameters of the type 1 and type 2 fibers. There were more qualitative changes in the external intercostal muscles than in the other two, and some of these changes related to the incidence of malignancy. There were more type 1 fibers in the external intercostal (64 +/- 10 percent) and internal intercostal muscles (59 +/- 12 percent) than in the latissimus dorsi (44 +/- 13 percent) (p less than 0.005). The mean diameter of the type 2 fibers in the external intercostal muscles was less (44 mu +/- 7 mu) than the diameter in the latissimus dorsi (51 mu +/- 9 mu) and the internal intercostal muscles (52 mu +/- 8 mu) (p less than 0.01). The diameters of both fiber types were greater in men than in women. There was no significant relationship between measures of pulmonary function or respiratory muscle strength and muscle fiber proportions and diameters. There were significant correlations between the percentage of ideal body weight and type 1 and type 2 fiber diameters. We conclude that sex and nutrition influence respiratory muscle morphometry.
To investigate the effect of hyperthyroidism on respiratory muscle function and its possible mechanism, the thyroid function, serum enzymology, serum potassium, pulmonary function and respiratory muscle function were examined in 60 patients with Grave's disease before treatment and 26 patients among them after treatment, and 20 normal subjects as control. T3, T4, and FT4 increased while FVC and PImax, which reflect the respiratory muscle strength, and Pi/PImax, which reflects the reserve capacity of inspiratory muscle, decreased significantly in the 60 patients with Grave's disease, compared with the ones of normal subjects. The comparison of above measurements in the 26 patients between before- and after-treatment showed that respiratory muscle strength increased obviously along with the improvement of throid function. The serum enzymology, potassium and TSH, however, were not abnormal and not changed after treatment. The thyroid functions in 10 patients with hyperthyroid heart disease were not different, compared with the ones of other 50 patients without hyperthyroid heart disease, but their respiratory muscle strength was significantly lower than the ones of latter. The above results suggested that hyperthyroidism could lead to significant decrease of respiratory muscle strength and its reserve capacity, whereas treatment for hyperthyroidism would improve respiratory muscle function, so the measurement of respiratory muscle function in hyperthyroidism cases might be useful in prediction of hyperthyroid heart disease.
To investigate the effects of chronic smoking on respiratory muscle function, 20 heavy smokers and 20 nonsmokers were studied. After familiarization, respiratory muscle strength, inspiratory muscle endurance and the spirometric function (including FVC, FEV 1, FEV1/FVC, tidal volume, breathing rate and duty cycle) were measured. The respiratory muscle strength was indicated by the maximal static inspiratory and expiratory pressures (PIMmax and PEMmax). Inspiratory muscle endurance was determined by a modified Nickerson-Keens method. The results showed that long-term smoking drastically enhanced expiratory muscle strength (p less than 0.01) and slightly increased inspiratory muscle strength (p less than 0.05). The inspiratory muscle endurance, in contrast, was reduced in the smokers (p less than 0.05). We also observed the tendency of decreases in the duty cycle and FEV1/FVC in the smokers. We, therefore, conclude that chronic smoking can raise respiratory muscle strength but impair the inspiratory muscle endurance.
To investigate the effects of gender and age on respiratory muscle function, 160 healthy volunteers (80 males, 80 females) were divided into four age groups. Twenty-eight of the male subjects were smokers. After the subjects were familiarized with the experimental procedure, respiratory muscle strength, inspiratory muscle endurance, and spirometric function, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, tidal volume, breathing rate, and duty cycle, were measured. The respiratory muscle strength was indicated by the maximal static inspiratory and expiratory pressures (PImmax and PEmmax). Inspiratory muscle endurance was determined by the time the subject was able to sustain breathing against an inspiratory pressure load on a modified Nickerson-Keens device. The results showed that 1) except for inspiratory muscle endurance and FEV1/FVC, men had greater respiratory muscle and pulmonary functions than women, 2) respiratory muscle function and pulmonary function decreased with age, 3) smoking tended to lower duty cycle and FEV1/FVC and to enhance PE,mmax, and 4) inspiratory muscle endurance was greater in men who were physically active than in those who were sedentary. Therefore we conclude that there are sexual and age differences in respiratory muscle strength and pulmonary function and that smoking or physical activity may affect respiratory muscle function.
In sarcoidosis, pulmonary and general symptoms often do not correlate with radiographic stage and routinely performed lung function tests. Asymptomatic muscle involvement in sarcoidosis is common, but little is known about respiratory muscle involvement. The aim of this study was to investigate any relationships between persistent complaints and/or quality of life and respiratory muscle strength and endurance, respectively. Measurements of maximal inspiratory and expiratory mouth pressures (PI,max and PE,max), respiratory muscle endurance and routine lung function were made in 18 patients with sarcoidosis. To assess health status and quality of life, patients completed the Sickness Impact Profile (SIP). Respiratory muscle strength and endurance time were lower in the patient group than in a group of healthy controls (p=0.05). Compared to a general population, the patients with sarcoidosis were found to be limited in physical and psychosocial functioning. The respiratory muscle endurance time correlated with the SIP subscales "mobility" (r=-0.56; p<0.01), and "body care and movement" (r=-0.79; p<0.001). The total lung capacity (TLC), inspiratory vital capacity (IVC) and forced expiratory volume in one second (FEV1) were normal in all subjects. In conclusion, patients with sarcoidosis and normal lung function showed reduced respiratory muscle strength and endurance time. Correlations were found between these indices and both symptoms and certain Sickness Impact Profile domains. Therefore, we suggest inclusion of measurements of respiratory muscle strength in the assessment and follow-up of patients with sarcoidosis.
BACKGROUND: Myasthenia gravis (MG) is a specific autoimmune disease characterized by weakness and fatigue. MG may affect also the respiratory muscles causing symptoms that may vary from dyspnea on severe exertion to dyspnea at rest. This study was undertaken in order to determine the effects of respiratory muscle training on respiratory muscle performance, spirometry data and the grade of dyspnea in patients with moderate to severe generalized MG. METHODS: Eighteen patients with MG were studied and divided into 2 groups: Group A included 10 patients (3 males and 7 females aged 29-68) with moderate MG, and Group B that included 8 patients (5 males and 3 females aged 21-74) with severe MG. Patients in Group A received both inspiratory and expiratory muscle training for 1/2 h/day, 6 times a week, for 3 months, while patients in Group B followed the same protocol but had inspiratory muscle training only. RESULTS: Mean PImax increased significantly from 56.6 +/- 3.9 to 87.0 +/- 5.8 cm H2O (p < 0.001) in Group A, and from 28.9 +/- 5.9 to 45.5 +/- 6.7 cm H2O (p < 0.005) in Group B. The mean PEmax also increased significantly in patients in Group A, but remained unchanged in the patients in Group B. The respiratory muscle endurance also increased significantly, from 47.9 +/- 4.0 to 72.0 +/- 4.2%, p < 0.001, in patients of Group A, and from 26.0 +/- 2.9 to 43.4 +/- 3.8, p < 0.001, in patients in Group B. The improved respiratory muscle performance was associated with a significant increase in the FEV1 values, and in the FVC values, in patients of both groups. Mean dyspnea index score also increased significantly from 2.6 +/- 0.8 to 3.6 +/- 0.4 (p < 0.005) in Group A, and from 0.7 +/- 0.2 to 2.0 +/- 0.2 (p < 0.001) in Group B. CONCLUSIONS: Specific inspiratory threshold loading training alone, or combined with specific expiratory training, markedly improved respiratory muscle strength and endurance in patients with MG. This improvement in respiratory muscle performance was associated with improved lung function and decreased dyspnea. Respiratory muscle training may prove useful as a complementary therapy with the aim of reducing dyspnea symptoms, delay the breathing crisis and the need for mechanical ventilation in patients with MG.
OBJECTIVE: To evaluate the efficiency of respiratory muscle training programs in pilots. METHODS: Twenty-four male pilots were divided into two groups. The training group (12 pilots) underwent respiratory strengthening training programs besides routine physical exercises. The other 12 pilots in the control group only did routine physical exercises, but the training time was the same in these two groups. Before and after training programs in the two groups, the respiratory muscle functions were examined. RESULTS: 24 pilots in these two groups completed training programs within four weeks. The pilots in the training group got improvement of respiratory muscle functions which was much better than those of the control group. CONCLUSION: It suggests that the strengthening training programs of respiratory muscles can improve and strengthen the respiratory muscle functions in pilots.
We assessed morphological, histochemical, and physiological characteristics of respiratory muscles of a non-human primate, Papio cynocephalus, from midgestation through adult life. Samples were taken of diaphragm muscles for histochemical analysis, electron microscopy, and assessment of contractile properties and fatigability. Histochemical analyses were also performed on samples of intercostal muscles. Initially, developing fibers are type IIc but differentiate into types I and IIa fibers by term. We observed no IIb fibers in respiratory muscles of premature baboons. Beginning late in gestation, muscle fibers grew rapidly. After term, IIb fibers were found, and fiber size ranked by increasing mean fiber area became types I, IIa, and IIb. After term, we rarely observed type IIc fibers. In electron micrographs we observed large numbers of interfibrillar mitochondria in all muscle fibers of premature baboons but not in all IIb fibers of adults. Histochemical observations were supported by contractile properties. Muscles of premature baboons had significantly longer contraction and relaxation times than adult muscles. Muscles from premature baboons were more resistant to fatigue than those of adult baboons. We conclude that the fibers of respiratory muscles are high in oxidative capacity and are resistant to fatigue during gestation. Fatigue of the respiratory muscle fibers secondary to low oxidative capacity is not a likely cause of respiratory distress in premature baboons.
Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.
BACKGROUND: Pulmonary and respiratory muscle function impairment are common in patients with Parkinson's disease (PD). However, dyspnea is not a frequent complaint among these patients, although it is well documented that the intensity of dyspnea is related to the activity and the strength of the respiratory muscles. PATIENTS AND METHODS: We studied pulmonary function, respiratory muscle strength and endurance and the perception of dyspnea (POD) in 20 patients with PD (stage II and III Hoehn and Yahr scale) before and after their first daily L-dopa dose. Respiratory muscle strength was assessed by measuring the maximal inspiratory and expiratory mouth pressures (PImax and PEmax), at residual volume (RV) and total lung capacity (TLC) respectively. The POD was measured while the subject breathed against progressive load and dyspnea was rated using a visual analog scale. RESULTS: Respiratory muscle strength and endurance were decreased and the POD was increased during the off medication period compared to normal subjects. There was a nonsignificant trend to an increase in Plmax, PEmax and endurance after L-dopa intake. The POD of PD patients decreased (p<0.05) following medication, although, it remained increased (p<0.01) as compared to the normal subjects. Even if patients had spirometry data showing a mild restrictive pattern, before medication, both forced vital capacity (FVC) and forced expiratory volume (FEV)1 remained almost identical after L-dopa intake. CONCLUSIONS: Patients with PD have higher POD, compared to normal subjects and this increased perception is attenuated when the patients are on dopaminergic medication. The change in the POD is not related to changes in respiratory muscle performance or pulmonary functions. A central effect or a correction of uncoordinated respiratory movements by L-dopa may contribute to the decrease in POD following L-dopa treatment.
When addressing the question of whether or not the respiratory muscles are weak, and quantifying exactly how severe any weakness might be, it is sensible to regard the tests available as complimentary, and to proceed by using simple tests first and invasive tests only when appropriate. This sequential and complimentary approach is illustrated in table 1. Thus, if the supine vital capacity is normal, it is very unlikely that there is clinically significant respiratory muscle weakness. However, if the vital capacity is low, it may then be appropriate to measure the maximal inspiratory and maximal expiratory pressures. If the mouth pressures are normal, weakness has been excluded, but if the pressures are low it will then be necessary to proceed to the next tests on the list. Thus, the process continues and, when all of the tests have been performed, a comprehensive description can be achieved of any respiratory muscle weakness that is present. We now have the capacity, if we so wish, to measure respiratory muscle weakness accurately. The challenge is to use these techniques to demonstrate the undoubted importance of respiratory muscle weakness in a wide variety of clinical circumstances.
This paper reviews respiratory muscle performance in patients suffering from congestive heart failure. Respiratory muscle dysfunction is well documented in these patients, and is thoroughly discussed. The mechanisms underlying its development and the potential consequences are also presented.
BACKGROUND: Pyridostigmine, an acetylcholinesterase antagonist, is useful in improving respiratory function in patients with myasthenia gravis. More recently, plasma exchange has been employed in myasthenia gravis because it acts presumably by removal of circulating antibodies against acetylcholine receptors. Surprisingly, comparative data on the effects of pyridostigmine and plasma exchange on lung volumes, respiratory muscle strength, and ventilatory control system in patients with myasthenia gravis are lacking. METHODS: Nine consecutive patients with grade IIb myasthenia gravis were studied under control conditions and after a therapeutic dose of pyridostigmine. In a second study the patients were re-evaluated a few days after a cycle of plasma exchange, before taking pyridostigmine. In each subject pulmonary volumes, inspiratory (MIP) and expiratory (MEP) muscle force, and respiratory muscle strength, calculated as average MIP and MEP as percentages of their predicted values, were measured. The ventilatory control system was evaluated in terms of volume (tidal volume, VT) and time (inspiratory time, TI, and total time, TTOT) components of the respiratory cycle. Mean inspiratory flow (VT/TI)--that is, the "driving"--and TI/TTOT: that is, the "timing"--components of ventilation were also measured. RESULTS: In each patient treatment relieved weakness and tiredness, and dyspnoea grade was reduced with plasma exchange. Following treatment, vital capacity (VC) increased on average by 9.7% with pyridostigmine and by 14% with plasma exchange, and MIP increased by 18% and 26%, respectively. In addition, with plasma exchange but not with pyridostigmine forced expiratory volume in one second (FEV1) increased by 16% and MEP increased by 24.5%, while functional residual capacity (FRC) decreased a little (6.8%). The change in respiratory muscle strength was related to change in VC (r2 = 0.48). With plasma exchange, VT increased by 18.6% and VT/TI increased by 13.5%, while neither TI nor TI/TTOT changed. CONCLUSIONS: Plasma exchange can be used in patients with myasthenia gravis when symptoms are not adequately controlled by anticholinesterase agents. Plasma exchange increases respiratory muscle force and tidal volume due to changes in "driving" but not "timing" of the respiratory cycle.