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Respiratory muscle performance as a possible determinant of exercise capacity in patients with ankylosing spondylitis.

Reduction of exercise capacity in patients with ankylosing spondylitis is associated with skeletal muscle performance. The contribution of respiratory muscle performance is questionable. This pilot study was designed to investigate the relationship between respiratory muscle performance and exercise capacity in ankylosing spondylitis. Subjects were 12 patients with ankylosing spondylitis. Measurements of maximal respiratory pressures and inspiratory muscle endurance were performed and correlated with maximal exercise capacity. Lung function and chest wall expansion were reduced on average. Maximal inspiratory and expiratory pressures were reduced to 82 +/- 20% of predicted values and 75 +/- 22% of predicted values respectively. On average there was no reduction in inspiratory muscle endurance which remained at 103 +/- 36% of predicted values. No overall reduction was found in maximal exercise capacity, either expressed as maximal workload or as peak oxygen uptake; however, a wide range was found. Maximal workload and peak oxygen uptake correlated significantly with maximal respiratory pressures and respiratory muscle endurance. The best regression model for explaining the total variation of maximal workload and peak oxygen uptake selected maximal inspiratory pressures as the independent variable (r(2) = 59.6%, p = 0.003 and r(2) = 62.5%, p = 0.05 respectively.) These data suggest respiratory pressure and respiratory muscle endurance, in particular maximal inspiratory pressure, may be determinants of exercise capacity in patients with ankylosing spondylitis.

Exercise↗

Exercise training for heart failure patients improves respiratory muscle endurance, exercise tolerance, breathlessness, and quality of life.

PURPOSE: Increased respiratory muscle endurance and peak oxygen consumption (VO(2peak)) induced by respiratory muscle training support the relationship between respiratory muscle function and exercise capacity in patients with heart failure. This raises the question whether exercise-training results in increased respiratory muscle function contributing to an increased exercise tolerance, a decreased perception of breathlessness, and an improved quality of life. METHODS: Prospective cohort analysis was completed on 24 patients with New York Heart Association (NYHA) Class III heart failure [18 men, 6 women; aged = 64 (SD 7.9) years; percent ejection fraction (%EF) = 24.0 (SD 7.8)]. Maximal sustainable ventilatory capacity (MSVC), submaximal and peak exercise responses, perception of breathlessness, and quality of life were measured before (baseline) and after (end of study) 12 weeks of exercise training. RESULTS: As a result of exercise training, VO(2peak) (P=.01) and MSVC (P<.001) increased, with MSVC contributing to a larger proportion of the variability for VO(2peak) at study completion (r=0.57 vs 0.42). Although stroke volume did not increase beyond exercise at 25 W and did not change with exercise training, ventilation decreased during exercise (P<.05), perception of breathing difficulty (P<.05) was reduced, and quality of life was enhanced (P=.008). CONCLUSIONS: Despite no increase in cardiac output and stroke volume, respiratory muscle endurance improved with exercise training, contributing to increased exercise capacity, decreased breathlessness, and decreased perception of breathlessness. Practical implications can include less frequent rest periods and fatigue, greater confidence, maintenance of independence, and enhanced quality of life.

Aged↗

[Preliminary study on determination methods of respiratory muscle functions].

Attention has been paid to the research of respiratory muscle functions recently. In this paper some lung function indices concerning respiratory muscle functions, such as maximal inspiratory and expiratory pressure at mouth, inspiratory and expiratory tolerance time, transdiaphragmatic pressure and maximal transdiaphragmatic pressure and diaphragmatic electromyogram etc, were determined in 24 healthy young men and the normal values were obtained. They were important in the study of respiratory muscle functions in hard physical labours, especially in divers, pilots and sportsmen etc. These indices were also useful for evaluating convalescent therapy chronic lung diseases, respiratory muscles training programs or the drug effects on respiratory muscle fatigue etc.

Adult↗

Disorders of the respiratory muscles.

The act of breathing depends on coordinated activity of the respiratory muscles to generate subatmospheric pressure. This action is compromised by disease states affecting anatomical sites ranging from the cerebral cortex to the alveolar sac. Weakness of the respiratory muscles can dominate the clinical manifestations in the later stages of several primary neurologic and neuromuscular disorders in a manner unique to each disease state. Structural abnormalities of the thoracic cage, such as scoliosis or flail chest, interfere with the action of the respiratory muscles-again in a manner unique to each disease state. The hyperinflation that accompanies diseases of the airways interferes with the ability of the respiratory muscles to generate subatmospheric pressure and it increases the load on the respiratory muscles. Impaired respiratory muscle function is the most severe consequence of several newly described syndromes affecting critically ill patients. Research on the respiratory muscles embraces techniques of molecular biology, integrative physiology, and controlled clinical trials. A detailed understanding of disease states affecting the respiratory muscles is necessary for every physician who practices pulmonary medicine or critical care medicine.

Collagen Diseases↗

Non-invasive assessment of respiratory muscle strength in patients with previous poliomyelitis.

UNLABELLED: In patients with poliomyelitis, respiratory failure requiring ventilatory support may occur during the acute illness. Some patients continue to require long-term nocturnal ventilatory support; others are weaned but subsequently require support because of a late deterioration in ventilatory function. OBJECTIVES: To assess the sensitivity of sniff nasal inspiratory pressure (SNIP) to post-poliomyelitis respiratory muscle weakness and to assess the relationship between the respiratory muscle strength and the need for ventilatory support in patients with previous poliomyelitis (post-polio patients). METHODS: Respiratory muscle strength was measured in 50 post-polio patients. Tests included forced vital capacity (FVC), maximum inspiratory and expiratory pressures (MIP and MEP), and SNIP. RESULTS: Twenty-one patients used non-invasive nocturnal ventilatory support (NIV group) compared to 29 on no support (non-NIV group). The percentage predicted FVC was significantly lower in the NIV group compared to the non-NIV group (P=0.01). Similarly, the percentage predicted MIP was significantly lower in NIV group (P=0.007). Low SNIP values (both absolute value and percentage predicted) were associated with the need for ventilatory support (P<0.001). Of the patients requiring no support, those who had been ventilated during the acute episode of poliomyelitis had a significantly lower SNIP than those who had never been ventilated (P=0.04). CONCLUSIONS: Post-polio patients who are currently on nocturnal ventilation have significantly lower FVC, MIP and SNIP compared to currently non-ventilated patients. Non-ventilated patients who were ventilated during the acute episode of poliomyelitis have significantly weaker respiratory muscle strength than patients who were never ventilated. This study indicates that SNIP is more sensitive to post-polio respiratory muscle weakness than other non-invasive tests. Thus measurement of SNIP is a valuable tool for monitoring the progression of respiratory muscle weakness due to previous poliomyelitis and this can be applied to other neuromuscular disorders.

Acute Disease↗

Pulmonary mechanics in patients with respiratory muscle weakness.

Pulmonary mechanics and respiratory muscle pressures were studied in 7 patients with severe respiratory muscle weakness. Minimal pleural pressures were grossly abnormal and showed little variation with lung volume. Both the maximal transpulmonary pressure and static expiratory compliance were low; therefore, the pressure-volume curves of the lungs resembled those obtained after strapping the chest in normal subjects. The low compliance may result from either microatelectasis or a generalized alteration in alveolar elastic properties and is probably a major determinant of both the total lung capacity and the breathing pattern of patients with neuromuscular disease. Airway and gas exchange function were less abnormal than the elastic properties of the lungs.

Adult↗

Effects of laparoscopic cholecystectomy on global respiratory muscle strength.

Laparoscopic cholecystectomy has a better postoperative outcome than the traditional open technique, which has been shown to significantly affect respiratory muscle function. The aim of this study was to investigate the effects of laparoscopic surgery on respiratory function, and particularly that of the respiratory muscles. Respiratory muscle strength was assessed in 26 patients who underwent laparoscopic cholecystectomy and in 25 who underwent open cholecystectomy by measuring mouth pressure during maximum static inspiratory (PImax) and expiratory (PEmax) efforts. PImax, PEmax, and blood gases were measured 24 h preoperatively (-24 h) as well as 24 h (+24 h) and 48 h (+48 h) postoperatively. FEV1 and FVC were measured at -24 h and +48 hr, and the ratio of FEV1 to FVC (FEV1/FVC) was calculated. PImax decreased at +24 h and +48 h in both groups, but this decrease was significantly greater in the patients who had open surgery, (p < 0.01, and p < 0.005, respectively). Similarly, PEmax was significantly smaller in the open- than in the laparoscopic-surgery group (p < 0.0001) at +48 h. Spirometric indices showed a more severe restrictive defect at +48 h after open surgery than after laparoscopy (p = 0.01). The arterial oxygen tension (PaO2) was significantly greater in the laparoscopic- than in the open-surgery group at +24 h (p < 0.007). Laparoscopic cholecystectomy caused smaller decreases in respiratory muscle strength than did open surgery. This accords with the hypothesis of phrenic nerve inhibition during open surgery. The results are of clinical importance, since they may explain the different outcomes with the two techniques.

Adult↗

Respiratory muscle testing in children.

The range of techniques available to assess respiratory muscles weakness has greatly expanded over recent years. Respiratory muscle tests can be divided into non-invasive tests, such as lung function parameters, maximal static pressures and sniff nasal pressure and invasive tests, such as transdiaphragmatic pressures during crying, maximal static pressures and magnetic stimulation of the phrenic nerves. Sniff nasal pressure and magnetic stimulation should have increasing relevance in children in the coming years. However, probably the most important message is to arrange for the evaluation of respiratory muscles in children with unexplained or disproportionate breathlessness such as in patients with neuromuscular diseases. Improvements are needed to evaluate respiratory muscle endurance in children, which is more difficult but complementary to the assessment of respiratory muscle strength.

Adolescent↗

[Control mechanism of the respiratory muscle during forced expiration].

Control mechanism of the respiratory muscle during forced expiration was analyzed. Respiratory flow. EMG of the intercostal muscle (IC), external oblique (EO) and internal oblique (IO) abdominal muscle were analyzed in eleven healthy volunteers. The pattern of EMG activity during forced expiration could be classified according to its shape i.e., taper- or hill-shaped. The taper shape was found in 7 of 9 subjects for IC and in 8 of 11 subjects for EO. The hill shape was found in 4 of 6 subjects for 10. Twelve consecutive trials without intervals did not alter the pattern of flow-volume curve, activity of respiratory muscle and frequency component (i.e., H/L ratio). When the expiratory circuit was obstructed for a short interval during forced expiration, the rise in pleural pressure was slight but that in oral pressure was large, and the activity of respiratory muscle decreased for a short period. The latencies from the onset of expiratory circuit obstruction to the reduction in EMG activity were 61.5-100 msec. In IC, 61.5-106.5 msec in EO. and 58.0-92.3 msec in 10. These values did not differ significantly any given subject. Airway anesthesia with xylocaine did not alter latency. In conclusion, the pattern of respiratory muscle activity for forced expiration is predetermined and is specific for each muscle. Negative feedback from receptors in airway or in respiratory muscle was strongly suggested. Repetitive trials up to twenty times did not cause respiratory muscle fatigue.

Adult↗

[The effect of aging on respiratory muscle function].

To elucidate the effect of aging on respiratory muscle function, the authors performed respiratory muscle function tests in 116 normal subjects. Respiratory muscle function was evaluated with maximal expiratory mouth pressure at the TLC level (PEmax) and maximal inspiratory mouth pressure at the RV level (PImax). PEmax and PImax in both sexes showed significant correlations with age. PEmax in males was significantly higher than that in females (123.6 +/- 29.7 cmH2O and 79.0 +/- 21.1 cmH2O, p less than 0.01, respectively). PImax in males was also significantly higher than that in females (98.4 +/- 26.0 cmH2O and 71.9 +/- 26.4 cmH2O, p less than 0.01, respectively). PEmax correlated significantly with TLC, and PImax showed a significant inverse correlation with RV/TLC. Furthermore, there was a significant inverse correlation between RV/TLC and age. Our data suggest that inspiratory muscle weakness in aging may be responsible for the increase in RV/TLC.

Adult↗

Effects of intermittent negative pressure ventilation on respiratory muscle function in patients with severe chronic obstructive pulmonary disease.

The reduced respiratory muscle strength and increased work of breathing in patients with severe chronic obstructive pulmonary disease (COPD) may predispose these patients to the development of respiratory muscle fatigue and consequent respiratory failure. To test the hypothesis that these patients may be experiencing chronic respiratory muscle fatigue, we studied the effects of resting the respiratory muscles in a group of patients with severe COPD. Fifteen stable patients with severe COPD were randomized into study and control groups. In 8 study group patients (Group B), breathing was assisted with a negative pressure ventilator 3 to 6 h daily for 3 consecutive days. The remaining 7 patients served as controls (Group A) and did not receive any intervention. Baseline lung function was evaluated by spirometry and arterial blood gas determinations. Respiratory muscle strength and endurance were evaluated by maximal inspiratory and expiratory pressures (MIP and MEP, respectively) and the maximal duration that isocapnic hyperventilation equal to 50 and 70% of the 12-s maximal voluntary ventilation could be sustained (DSV). Baseline DSV was determined as the best effort of several practice trials. All measurements were repeated on the final day of assisted ventilation approximately 2 to 3 h after its discontinuation. After assisted ventilation, the DSV at 50 and 70% of the maximal voluntary ventilation improved significantly (p less than 0.05). Maximal inspiratory pressure and MEP increased to 114% (p less than 0.05) and 112% (p = 0.05) of baseline values, respectively. Mean arterial PCO2 in the hypercapnic subgroup of Group B patients decreased from 60 mm Hg before to 52 mm Hg after assisted ventilation (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon Dioxide↗

Benefit of selective respiratory muscle training on exercise capacity in patients with chronic congestive heart failure.

BACKGROUND: Diminished respiratory muscle strength and endurance have been demonstrated in patients with heart failure. This may contribute to exertional dyspnea and reduced exercise capacity in these patients. The purpose of this study was to investigate whether selective respiratory muscle training could alleviate dyspnea and improve exercise performance in patients with chronic congestive heart failure. METHODS AND RESULTS: Fourteen patients with chronic heart failure (left ventricular ejection fraction, 22 +/- 9%) were enrolled in a supervised respiratory muscle training program. This consisted of three weekly sessions of isocapnic hyperpnea at maximal sustainable ventilatory capacity, resistive breathing, and strength training. Maximum sustainable ventilatory capacity, maximum voluntary ventilation, maximal inspiratory and expiratory pressures, peak VO2, and the 6-minute walk test were measured before (pre) and after (post) 3 months of training. Eight patients completed the training program. Respiratory muscle endurance was improved with training, as evidenced by increases in maximal sustainable ventilatory capacity (pre, 48.6 +/- 10.7 versus post, 76.9 +/- 14.5 L/min; P < .05) and in maximal voluntary ventilation (pre, 100 +/- 36 versus post, 115 +/- 39 L/min; P < .05). Respiratory muscle strength was also increased with training as maximal inspiratory (pre, 64 +/- 31 versus post, 78 +/- 33 cm, H2O; P < .01) and expiratory (pre, 94 +/- 30 versus post, 133 +/- 53 cm H2O; P < .001) pressures rose. Submaximal and maximal exercise capacity were significantly improved with selective respiratory muscle training as the 6-minute walk (pre, 1101 +/- 351 versus post, 1421 +/- 328 ft; P < .001) and peak exercise VO2 (pre, 11.4 +/- 3.3 versus post, 13.3 +/- 2.7 mL.kg-1.min-1; P < .05) both significantly increased. Dyspnea during activities of daily living was subjectively improved in the majority of trained patients. Dyspnea quantified by the Borg scale was significantly reduced during progressive isocapnic hypernea but not during bicycle exercise. No statistically significant improvement in maximal sustainable ventilatory capacity, maximum voluntary ventilation, maximal inspiratory or expiratory mouth pressures, 6-minute walk, or peak VO2 was observed in the 6 patients who did not complete the training program. CONCLUSIONS: Selective respiratory muscle training improves respiratory muscle endurance and strength, with an enhancement of submaximal and maximal exercise capacity in patients with heart failure. Dyspnea during activities of daily living was subjectively improved in the majority of trained patients.

Adult↗

[Skeletal and respiratory muscle strength in chronic heart failure].

BACKGROUND: The aim of this study was to investigate limb and respiratory muscle strength in chronic heart failure (CHF). METHODS: Our study population consisted of 45 male CHF patients, 25 in NYHA Class II and 20 in NYHA Class III, and 22 male post-MI patients without left ventricular dysfunction (LVEF > 50%). All patients underwent assessment of respiratory muscle strength by maximal inspiratory (MIP) and expiratory (MEP) pressures, of handgrip force and peak torque developed during isokinetic Knee extension (EX) (quadriceps) and flexion (hamstring) at 120 degrees/sec. RESULTS: CHF patients showed a significant decrease in all limb and respiratory muscle strength compared to control patients. Moreover, NYHA Class III patients showed significantly reduced values of MIP, handgrip, and EX forces, as well as significantly reduced exercise tolerance in terms of METS (2.8 +/- 0.9 vs 4.4 +/- 1.2, p < .05) and anaerobic threshold level (9.4 +/- 3 vs 12.8 +/- 1.7 mlO2/Kg, p < .05), as compared to those patients in NYHA Class II, while no significant differences were observed in LVEF, cardiac index and pulmonary capillary wedge pressures. Weak, but significant (p < .05) were the correlations between limb muscle and respiratory muscle strength. No correlations were found between muscle force and hemodynamic parameters. Significant correlations (from p < .05 to p < .0001) were found among exercise tolerance and limb muscle strength, but not between exercise tolerance and respiratory muscle strength. In summary: 1) respiratory and skeletal muscle strength is impaired in CHF; 2) respiratory and limb muscle strength reductions are partially related to each other; 3) the degree of central hemodynamic impairment is not correlated with muscle force. Deconditioning could be a major determinant of skeletal but not respiratory muscle weakness. Other factors link limb and respiratory weakness in CHF.

Adult↗

Respiratory muscle dysfunction associated with human immunodeficiency virus infection.

Although skeletal muscle abnormalities have been described in association with human immunodeficiency virus (HIV), the effects of HIV infection on respiratory muscle function have not been well characterized. We hypothesized that HIV+ individuals may develop respiratory muscle weakness and that respiratory muscle dysfunction may contribute to the unexplained dyspnea that occurs in the setting of HIV. To test this hypothesis we studied maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), inspiratory muscle endurance, and respiratory symptoms in 23 HIV+ male outpatients who had no history of acquired immune deficiency syndrome (AIDS)-related pulmonary complications, with a CD4+ T-lymphocyte count of 331.6 +/- 62.1 (mean +/- SEM). Respiratory muscle endurance was measured with an incremental threshold loading (ITL) protocol. We compared these results to those for 14 HIV- males matched for age and weight. Compared with the controls, HIV+ subjects had a significantly lower mean MIP (98.7 +/- 7.4 versus 121.4 +/- 9.3 cm H2O, p < 0.05) and MEP (115.0 +/- 9.3 versus 152.1 +/- 14.8 cm H2O, p < 0.05). Furthermore, during ITL, the mean load at task failure in the HIV+ group was 295.7 +/- 36.2 g, versus 405.8 +/- 52.2 g in the control group (p < 0.05). In the HIV+ subjects there was no relationship between muscle performance and CD4+ count or azidothymidine (AZT) use. There was, however, a highly significant relationship between respiratory muscle dysfunction and symptoms of dyspnea. We conclude that HIV seropositivity is associated with a decline in respiratory muscle performance. This impairment in respiratory muscle function may contribute to the feeling of breathlessness that has been well described in this patient population.

Adult↗

Human respiratory muscles: fibre morphology and capillary supply.

In man the diaphragm (DIA) and abdominal muscles comprise approximately 50% slow-twitch (ST) fibres, whereas a higher proportion (60%) is found in intercostal muscles and the scalenes. All respiratory muscles show an equal distribution of fast-twitch (FTa and b) fibres with the exception of the expiratory intercostal muscles which have few FTb fibres. The inspiratory muscles have a uniformly small fibre size, in contrast to the expiratory intercostal muscle fibres which are large. The fibre size of the inspiratory muscles is maintained with ageing, whereas that of the expiratory intercostal muscles appears to be reduced after the age of 50 yrs. Capillary supply is most abundant in the expiratory muscles followed by DIA and the inspiratory intercostal muscles. In patients with chronic obstructive pulmonary disease (COPD) it is unknown whether a reduction in fibre size of the thoracic respiratory muscles is caused by extreme use due to increased ventilatory work, or by disuse due to an increased involvement of the extrathoracic respiratory muscles. Histochemical characteristics suggest that, in normal humans, the load on the inspiratory muscles is relatively small during contractions, whereas the expiratory intercostal muscles are exposed to severe continuous activity with a heavy load.

Adolescent↗

Respiratory muscle pressure analysis in pressure-support ventilation.

The extent to which respiratory muscles are exerted during partially supported ventilation is difficult to differentiate, because these muscles and the ventilator work simultaneously to produce ventilation. We have developed a new method for determining the pressure developed by the respiratory muscles in partially supported ventilation. In seven patients on pressure-support ventilation (PSV), pressure, flow, and lung volume change were measured at the airway opening. Various PSV levels (0-15 cmH2O) were applied to each patient in random order. By utilizing a model of respiratory mechanics, we calculated the pressure developed by the respiratory muscles and the inspiratory work performed by the muscles from the measured parameters by use of the resistance and elastance of the respiratory system obtained during controlled ventilation. Increasing PSV from 0 to 15 cmH2O modulated the resultant breathing pattern, i.e., increasing tidal volume and decreasing respiratory rate. The respiratory muscle pressure, although less negative, had a shape that corresponded to the shape of airway occlusion pressure at each PSV level, and both pressures decreased concomitantly with increasing PSV. The respiratory muscle work progressively decreased with increasing PSV. This analysis enabled clear and continuous quantifications of the respiratory muscle force generation and inspiratory work during partially supported ventilation.

Adult↗

Respiratory muscle function.

The functional anatomy of the respiratory muscles has been reviewed. The diaphragm has been emphasized, since this is the most important inspiratory muscle, but the view has been presented that the intercostal, scaleni, and other accessory inspiratory muscles become increasingly important as airflow obstruction leads to hyperinflation. As work increases, the demand for energy and hence blood flow to those muscles has to increase. In spite of a large reserve there are situations in which demands may outstrip supply. This leads to local metabolic changes that result in muscle fatigue. We are now capable of detecting this change as alterations in EMG or in the ability to generate pressures. The latter leads to a decrease in the capacity of the respiratory pump to exchange gas, ultimately resulting in hypercapnia and hypoxemia. The true importance of respiratory muscle fatigue and its differentiation from weakness in patients with severe CAO requires more analysis. It is intuitively appropriate to address the overall decrement in the ability to maintain adequate ventilatory work at low energy cost with the different therapeutic modalities thought to be beneficial. A combination of a decrease in the load imposed on the respiratory muscles, an improvement in the contractility of those muscles, and, when there is absolute need, the resting of the fatigued muscles should result in a better chance to lead a meaningful life and perhaps to improve survival in these patients.

Diaphragm↗