SEARCH · PubMed Health

Results for “Respiratory Muscles”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources

PubMed1994

Evidence of reduced respiratory muscle endurance in patients with heart failure.

OBJECTIVES: We sought to investigate whether reduced respiratory muscle endurance contributes to increased dyspnea and decreased exercise capacity in patients with chronic heart failure. BACKGROUND: In patients with heart failure, the sensation of dyspnea may be related to abnormalities of respiratory muscle function, such as diminished strength or endurance, or both. METHODS: Respiratory muscle endurance was assessed by measuring maximal sustainable ventilatory capacity in 15 patients with congestive heart failure and 8 normal subjects using progressive isocapnic hyperpnea. Near-infrared spectroscopy of an accessory respiratory muscle, Borg scale recordings of perceived dyspnea, time in inspiration, time per breath and minute ventilation were measured. Exercise testing with measurement of oxygen consumption was also performed. RESULTS: Maximal voluntary ventilation (normal subjects 167 +/- 40, heart failure group 89 +/- 31 liters/min) and maximal sustainable ventilatory capacity (normal subjects 90 +/- 23, heart failure group 53 +/- 22 liters/min) were significantly reduced in patients with heart failure (both p < 0.05). No significant accessory respiratory muscle deoxygenation was observed in either group. Borg scale recordings at maximal sustainable ventilatory capacity were comparable in both groups. At rest, the inspiratory duty cycle (i.e., time in inspiration divided by the time per breath) was comparable in the two groups (normal subjects 0.34 +/- 0.09, heart failure group 0.37 +/- 0.12, p = NS). However at maximal sustainable ventilatory capacity, only normal subjects had a significant increase in the inspiratory duty cycle (normal subjects 0.49 +/- 0.04, heart failure group 0.36 +/- 0.10, p < 0.05). This finding suggests obstruction to airflow in patients with congestive heart failure. Values for peak exercise minute ventilation did not differ significantly from values in maximal sustainable ventilatory capacity in either group and were significantly correlated (r = 0.84, p < 0.0001). CONCLUSION: Respiratory muscle endurance as assessed by maximal sustainable ventilatory capacity is reduced in patients with heart failure.

Adult↗

PubMed1995

Respiratory muscle strength in chronic heart failure.

BACKGROUND: Several studies have suggested that the respiratory muscles are weak in patients with heart failure, but the aetiology and clinical relevance of this weakness are unclear. In order to see if respiratory muscle weakness in this context is part of a more generalised myopathic process, respiratory and limb muscle strength were compared in patients with heart failure. The relation between respiratory muscle strength, breathlessness on exercise, and exercise capacity was also examined. METHODS: Twenty patients (three women) with New York Heart Association (NYHA) class II-IV heart failure of mean age 63 years were studied. Respiratory muscle strength was assessed using maximum inspiratory and expiratory mouth pressures (MIP and MEP) and transdiaphragmatic pressure during sniffs (sniff PDI). These parameters were compared with cardiac output (indirect Fick) and with limb muscle strength as assessed by grip strength. The patients also performed two exercise tests during which they rated their breathlessness on a Borg scale. RESULTS: Mean (SD) cardiac index was 2.2 (0.4) l/min/m2. MIP and MEP were 66 (27) and 99 (29) cm H2O respectively. Sniff PDI was 103 (21) cm H2O and was positively correlated with grip strength and cardiac output (Spearman rank correlation coefficients 0.527 and 0.451, respectively). None of the indices of respiratory muscle strength were related to exercise time or breathlessness during exercise. CONCLUSIONS: The respiratory muscles are weak in patients with heart failure. This weakness reflects a more generalised myopathic process, possibly related to reduced cardiac output. However, respiratory muscle weakness does not appear to be an important factor in the aetiology of breathlessness on exercise.

Aged↗

PubMed1995

Respiratory muscle function in infants.

In newborns and infants a variety of respiratory disorders lead to ventilatory failure. In early life the ventilatory response to loaded breathing is limited. The risk factors of ventilatory failure are related to the developing respiratory pump because of the immaturity of the chest wall, respiratory muscles and coupling between thoracic and abdominal movements. Assessment of respiratory muscle function in infants is limited, due to the objections to using invasive techniques. However, measurement of airway pressures during crying may provide an index of respiratory muscle strength in infants. Real-time ultrasonography allows investigation of diaphragmatic movements. Pattern of thoracoabdominal motion can be assessed using uncalibrated respiratory inductive plethysmography. Finally, electromyographic recording of respiratory muscles by surface electrodes is of clinical usefulness during sleep studies.

Humans↗

PubMed1992

Respiratory muscle fatigue does not limit exercise performance during moderate endurance run.

The role of respiratory muscle fatigue in limiting exercise performance in well-trained subjects is still controversial, especially as far as relatively short runs are concerned. To determine the occurrence of respiratory muscle impairment, we studied six well-trained athletes before, during (middle of the run) and after a 17 km run. They were all asked to produce the maximum effort they could during the race. Strength was assessed by measuring maximal inspiratory mouth pressure against close airways (MIP), dynamic lung volumes were monitored using a spirometer. No changes in forced vital capacity (FVC), maximal expiratory flow (PEF) and forced expiratory volume in 1 sec (FEV1) were observed throughout the experiment. This suggested that functional residual capacity and subsequently the initial length of respiratory muscle were unchanged. Respiratory muscle strength did not significantly vary at the different time of measurements (154.8 +/- 20.9 cm H2O at the beginning, 157.5 +/- 23.7 cm H2O after 7.5 km, 155.8 +/- 22.5 cm H2O at the end and 152.3 +/- 17.6 cm H2O after 30 min of recovery). We therefore conclude that respiratory muscle fatigue does not impair the exercise performance of well-trained athletes in a relatively short race. The difference between these results and others reported in literature, could be explained by the different degree of training of the subjects performing the race.

Adult↗

PubMed2001

Respiratory muscles in chronic obstructive pulmonary disease and asthma.

Chronic obstructive pulmonary disease (COPD) and asthma are characterized by airflow obstruction and significant increase of respiratory muscle workload, with concrete risk of ventilatory pump failure. Respiratory muscles, the main component of this pump, undergo structural and functional changes during the course of these diseases. Aim of the present paper is to analyze modifications of respiratory muscles in COPD and asthma. An analysis of the most important controlled clinical studies released during the past years was carried out. The patients suffered from chronic obstructive pulmonary disease and asthma. In COPD, respiratory muscles have to cope with an increased load, an intrinsic weakness and a mechanical disadvantage, especially in the diaphragmatic length-force relationship; in patients with acute asthma, the main features are a massive hyperinflation and a persistent inspiratory muscle activity during expiration. Modifications of respiratory muscles deserve great consideration not only for the complete comprehension of the underlying physiopathologic aspects of these diseases, but also for the optimal clinical management: a reduced pulmonary hyperinflation in COPD place the respiratory muscles in a better position of the force-length curve while great care must be payed to the metabolic and nutritional aspects. During asthmatic crisis respiratory muscles are subjected to a sort of intense training but anyway persistence of bronchospasm in most severe attacks can lead to exhaustion of the ventilatory pump and need of mechanical ventilatory support.

Asthma↗

PubMed1990

Respiratory muscle performance in patients with type 1 diabetes.

Respiratory muscle strength and endurance were examined in 31 Type 1 diabetic patients and in age, sex, and weight matched control subjects. No significant difference in respiratory muscle strength was noted between the two groups. Maximal static inspiratory pressure was 92.3 +/- 33.9 (+/- SD) and 99.5 +/- 23.0% of the predicted values in the patient and control groups, respectively. Maximal static expiratory pressures were 75.1 +/- 14.3 and 77.4 +/- 14.0% of the predicted values in the patient and control groups, respectively. Respiratory muscle endurance was significantly lower in the diabetic patients 88.9 +/- 20.7 vs 103.9 +/- 15.8% predicted in the control group (p less than 0.01). Total lung capacity, vital capacity, and maximal voluntary ventilation were also significantly lower in the diabetic group and correlated with the duration of diabetes.

Adult↗

PubMed2006

Optimal intensity for respiratory muscle endurance training in patients with spinal cord injury.

OBJECTIVE: Respiratory muscle endurance of able-bodied persons, assessed by normocapnic hyperpnoea at 70% of their maximal voluntary ventilation, usually ranges from 10 to 20 minutes. The aim of this study was to determine the level of ventilation that patients with paraplegia and tetraplegia can sustain for 10-20 minutes to later be used as the guideline for respiratory muscle endurance training. DESIGN: Pilot study; cross-over setting. SUBJECTS: Two groups, 8 patients with paraplegia and 6 with tetraplegia. METHODS: Respiratory muscle endurance tests were performed at 3 different intensities of normocapnic hyperpnoea, i.e. 20%, 40% and 60% maximal voluntary ventilation. Subjects performed partial re-breathing from a bag to assure normocapnia. Respiratory endurance was separately analysed for patients with paraplegia and tetraplegia. RESULTS: Mean respiratory endurance times were 46.0, 18.9 and 4.2 minutes at 20%, 40% and 60% maximal voluntary ventilation in patients with tetraplegia and 51.8, 38.8 and 12.2 minutes in patients with paraplegia. The duration differed significantly at 60% maximal voluntary ventilation between the groups. CONCLUSION: Minute ventilation to perform respiratory muscle endurance training can be set at around 40% of maximal voluntary ventilation for patients with tetraplegia and around 60% of maximal voluntary ventilation for patients with paraplegia, as these levels can be sustained for 10-20 minutes.

Adolescent↗

PubMed1989

[Volume, flow and respiratory muscle strength in mitral stenosis].

Pulmonary function and respiratory muscle strength was assessed in 20 patients with mitral stenosis uncomplicated by other illness. Pulmonary function was evaluated by spirometry, flow-volume curves, functional residual capacity (FRC) and total lung capacity (TLC). Respiratory muscle strength was evaluated by measurement of maximal static inspiratory and expiratory mouth pressure (PIM, PEM cmH2O) at FRC and TLC respectively. Spirometric, FRC and TLC average values were normal. The maximal expiratory flow rate at 50 and 25% of vital capacity were decreased to 49.5 and 38.3% from predicted values. The values of PIM and PEM in patients (-93 +/- 17; 128 +/- 32 cmH2O, respectively) were similar to those of 12 normal subjects studied at comparable lung volume. Our results were similar to previous reports. There was no evidence of decreased respiratory muscle force, probably because the patients nutritional status and cardiac output were normal.

Adolescent↗

PubMed1983

Respiratory muscle failure.

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.

Airway Obstruction↗

PubMed1992

Controlled trial of respiratory muscle training in chronic airflow limitation.

BACKGROUND: Whether respiratory muscle training is of benefit to patients with chronic airflow limitation is controversial. The objective of the study was to determine the effect of resistance breathing training on physiological and functional measures in patients with chronic airflow obstruction. METHODS: The design was a randomised, double blind, controlled trial with a six month follow up. Eighty two patients with a forced expiratory volume in one second (FEV1) of less than 70% predicted, and an FEV1/vital capacity ratio of less than 0.7, were randomised to receive training for 10 minutes five times daily with progressively larger resistances through a resistive breathing device (PFLEX) as tolerated or to a sham device which gave minimal resistance. The main outcome measures, respiratory muscle strength and endurance, a progressive exercise test, a six minute walk test and physical and emotional function (chronic respiratory questionnaire) were assessed at monthly intervals. Patients in both groups were also randomised to wear or not wear nose clips during their training. RESULTS: No significant differences were observed between treatment and control groups, with or without nose clips, for any of the outcomes. Confidence intervals on the difference between treatments were narrow, excluding clinically important difference in any major outcome. CONCLUSION: This training regimen fails to strengthen respiratory muscles or improve exercise or functional capacity in patients with chronic airflow limitation.

Aged↗

PubMedDate not supplied

Music therapy as a treatment method for improving respiratory muscle strength in patients with advanced multiple sclerosis: a pilot study.

Respiratory muscle weakness, predominantly of the expiratory muscles, is characteristic of individuals with advanced multiple sclerosis and can result in difficulty in clearing secretions and repeated episodes of pneumonia. This pilot study evaluated the effectiveness of music therapy in strengthening respiratory muscles through an emphasis on diaphragmatic breathing and coordination of breath and speech. Twenty patients were randomly assigned to one of two groups: one that received music therapy or one that attended music appreciation sessions. Participants' inspiratory and expiratory muscle strength was measured by testing mouth pressure before and after the intervention. The experimental group showed some improvement in terms of expiratory muscle strength, in contrast to the control group, which showed deterioration. The results were not statistically significant, however. Patients in both groups exhibited considerable weakness in their expiratory muscles, and results for 79% of the participants were below 30% of the predicted values. Variability, a major confounding factor that resulted in reduced statistical power, led the investigators to suggest an intercenter collaboration to amass sufficient numbers of patients for a future study. Early manifestation of respiratory muscle weakness warrants inclusion of respiratory muscle testing in examination protocols and early intervention efforts.

Adult↗

PubMed1987

Determinants of respiratory muscle weakness in stable chronic neuromuscular disorders.

In neuromuscular disease, the precise relationship between general and respiratory muscle weakness is at present unclear. That relationship and the influence on respiratory muscle strength of such factors as type and duration of neuromuscular disease, distribution of general muscle weakness, and nutritional status were studied in 30 patients with stable chronic neuromuscular disease not presenting with respiratory symptoms. The degree of general muscle weakness was assessed by clinical examination of the strength of 17 muscle groups, yielding a general muscle strength index. The degree of respiratory muscle weakness was assessed by measuring maximal static inspiratory and expiratory mouth pressures. Maximal inspiratory (mean +/- SD: 68 +/- 28 percent predicted) and expiratory (66 +/- 29 percent predicted) mouth pressures were frequently reduced, but did not correlate with general muscle strength. The ability to estimate the degree of respiratory muscle weakness improved to some extent when the type of neuromuscular disease and the distribution of general muscle weakness were taken into account: thus, maximal expiratory mouth pressure was significantly lower (p less than 0.05) in myopathy than in polyneuropathy, and in proximal than in distal muscle weakness. Duration of neuromuscular disease and nutritional status did not influence respiratory muscle strength. It is concluded that in stable chronic neuromuscular disease, respiratory muscle involvement depends on a complexity of factors, in particular the type of neuromuscular disease and the distribution, rather than the degree, of general muscle weakness. In the individual patient, however, only direct measurement of maximal inspiratory and expiratory mouth pressures allows accurate assessment of respiratory muscle strength. These tests ought to complement neurologic examination.

Adult↗

PubMed2005

Effect of respiratory muscle endurance training in patients with COPD undergoing pulmonary rehabilitation.

BACKGROUND: Respiratory muscle endurance training (hyperpnea training) has been shown to have beneficial effects in patients with COPD. STUDY OBJECTIVES: The purpose of this study was to determine whether hyperpnea training, when added to an endurance exercise training program, would lead to additional benefits compared with endurance training alone in patients with COPD. SETTING AND PARTICIPANTS: Patients with COPD entering an 8-week outpatient pulmonary rehabilitation program. Fifteen patients (mean [+/- SE] FEV1, 45 +/- 6% predicted) were randomized to combined therapy, and 14 patients (mean FEV1, 44 +/- 4% predicted) were randomized to endurance training. METHODS: Peak exercise capacity, exercise endurance time during constant workload cycle exercise, 6-min walk distance, quality of life as measured by the chronic respiratory questionnaire, respiratory muscle strength and endurance, and quadriceps fatigability were measured before and after endurance or combined training. RESULTS: After rehabilitation, peak exercise capacity, exercise endurance time, 6-min walk distance, and quality of life all increased in both groups, but there was no significant difference in the extent of improvement between groups. Mean respiratory muscle endurance increased to a significantly greater extent in the combined therapy group (17.5 +/- 2.7 vs 8.5 +/- 2.5 min, respectively; p = 0.02). Respiratory muscle strength was significantly increased, and quadriceps fatigability was significantly reduced after rehabilitation in the combined therapy group but not in the endurance training group, but the difference between groups did not reach statistical significance. CONCLUSION: The endurance of the respiratory muscles can be improved by specific training beyond that achieved by endurance training alone in patients with COPD. However, this improvement did not translate into additional improvement in quality of life or exercise performance.

Aged↗

PubMed1995

[Measurement of respiratory muscle performance in patients with chronic obstructive pulmonary disease].

Respiratory muscle performance is measured in terms of strength and endurance. A RMSE-1 type measuring system for evaluation of respiratory muscle strength (RMS) and endurance (RME) has been developed and tested in normal subjects and patients with stable chronic obstructive pulmonary disease (COPD). The results showed that there was no significant difference between normal subjects and stable COPD patients in RMS measured as maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP). The maximum load (Load(m)), mean mouth pressure at maximum load (Pmean), and the maximum sustainable inspiratory pressure (SIP(m)) as % MIP (SIP(m)/MIP) were taken as measure of RME. All measures of RME in COPD group were much lower than those in the normal. The measurement of RME can be used to evaluate the effect of respiratory muscle training and direct the respiratory rehabilitation in COPD patients.

Adult↗

PubMed2006

Respiratory muscle energetics during exercise in healthy subjects and patients with COPD.

The energy expenditure required by the respiratory muscles during exercise is a function of their work rate, cost of breathing, and efficiency. During exercise, ventilatory requirements increase further exacerbating the potential imbalance between inspiratory muscle load and capacity. High level of exercise intensity in conjunction with contracting respiratory muscles is the reason for respiratory muscle fatigue in healthy subjects. Available evidence would suggest that fatigue of the diaphragm and other respiratory muscles is an important mechanism involved in redistribution of blood flow. Reflex mechanisms of sympathoexcitation are triggered in fatigued diaphragm during heavy exercise when cardiac output is not sufficient to adequately meet the high metabolic requirements of both respiratory and limb musculature. It is very likely that local changes in locomotor muscle blood flow may occur during exhaustive endurance exercise and that changes may have important effect on O2 transport to the working locomotor muscles and, therefore, on their fatigability. In a condition when the respiratory muscles receive their share of blood flow at the expense of limb locomotor muscles, minimizing mechanical work of breathing and therefore its metabolic cost allows a greater amount of cardiac output to be available to be delivered to working limb muscles. Malfunction in any of the multiple components responsible for circulatory flow and O2 delivery will limit the blood supply therefore inhibiting the supply of O2 and the energy substrate to the contracting muscles. Studies are needed to overcome these limitations.

Energy Metabolism↗

PubMed1985

The effects of inspiratory resistive training on respiratory muscle function in patients with muscular dystrophy.

The effects of inspiratory resistive training on respiratory muscle function was evaluated in 11 patients with Duchenne, limb-girdle, and facio-scapulo-humeral (FSH) type muscular dystrophy. Muscle training consisted of breathing against an inspiratory resistance for two 15-minute sessions each day while at home. Following 6 weeks of training, there were significant increases in the maximum resistance that could be tolerated for at least 5 minutes (P < 0.01) and also in the maximum duration that ventilations equal to 30%, 50%, 70%, and 90% of the maximum voluntary ventilation could be sustained (P < 0.05). In six patients who trained for an additional 6-week period, respiratory muscle endurance increased even further. The degree of improvement in respiratory muscle endurance was positively correlated with baseline vital capacity (r = 0.84, P < 0.05) and maximal inspiratory pressure (r = 0.76, P < 0.05). Spirometry, functional residual capacity, and maximal inspiratory and expiratory pressures were not affected by training. We conclude that inspiratory resistive training improves respiratory muscle endurance in muscular dystrophy patients. Improvement in respiratory muscle function may serve to delay the onset of respiratory complications in patients with muscular dystrophy.

Adolescent↗

PubMed1994

An overview of respiratory muscle function.

This article reviews the important features of respiratory muscle structure and function, including fiber types, fatigue, work and efficiency of breathing, neural connections, circulation, and mechanical properties. Emphasis is placed on the functional anatomy and the coordination and interaction of respiratory muscle action. Normal function is contrasted with the respiratory muscle dysfunction seen in patients with neuromuscular disease.

Humans↗

PubMed1985

[Function of the respiratory muscles in acute cardiac decompensation].

In anesthetized dogs the performance of the respiratory muscles during cardiogenic shock and their influence on its outcome was studied. Shock was induced by cardiac tamponade. Cardiac output during shock amounted to 25-35% of control and was kept constant. Minute ventilation (VE) initially increased and then progressively decreased until respiratory arrest. The latter was due to impairment of respiratory muscle contractility, the pressure generated by the diaphragm (Pdi) decreasing despite a marked increase in the diaphragmatic electromyogram and of the phrenogram. Mechanical ventilation during shock prolonged survival for the same decrease in cardiac output, and also decreased substantially the severity of lactic acidosis. Furthermore, blood flow to the respiratory muscles during shock was different in the animals breathing spontaneously (SB) from that in mechanically ventilated animals (MV). The fraction of cardiac output distributed to the respiratory muscles during control amounted to 1.85% in MV and 2.79% in SB. With shock this decreased to 1.55% in MV while in SB it decreased by 21%, which suggests that mechanical ventilation during shock preserves a large portion of cardiac output used by the respiratory muscles during spontaneous breathing, thus making it available to other organs.

Animals↗