Inspiratory muscle training in patients with cystic fibrosis

Little information is available about the effects of inspiratory muscle training in patients with cystic fibrosis (CF). In this study the effects of inspiratory-threshold loading in patients with CF on strength and endurance of the inspiratory muscles, pulmonary function, exercise capacity, dyspnoea and fatigue were evaluated. Sixteen patients were assigned to one of two groups using the minimization method: eight patients in the training group and eight patients in the control group. The training was performed using an inspiratory-threshold loading device. Patients were instructed to use the threshold trainer 20 min a day, 5 days a week for 6 weeks. Patients in the training group trained at inspiratory threshold loads up to 40% of maximal static inspiratory pressure (Pimax) and patients in the control group got 'sham' training at a load of 10% of Pimax. No significant differences were found among the two groups in gender, age, weight, height, pulmonary function, exercise capacity, inspiratory-muscle strength and inspiratory-muscle endurance before starting the training programme. Mean (SD) age in the control group was 19 (5.5) years, mean (SD) age in the training group was 17 (5.2) years. Mean FEV1 in both groups was 70% predicted, mean inspiratory-muscle strength in both groups was above 100% predicted. All patients except one, assigned to the training group, completed the programme. After 6 weeks of training, mean inspiratory-muscle endurance (% Pimax) in the control group increased from 50% to 54% (P = 0.197); in the training group mean inspiratory muscle endurance (% Pimax) increased from 49% to 66% (P = 0.003). Statistical analysis showed that the change in inspiratory-muscle endurance (% Pimax) in the training group was significantly higher than in the control group (P = 0.012). After training, in the training group there was a tendency of improvement in Pimax with an increase from 105 to 123% predicted, which just fell short of statistical significance (P = 0.064). After training no significant differences were found in changes from baseline in pulmonary function, exercise capacity, dyspnoea and fatigue. It is concluded that low-intensity inspiratory-threshold loading at 40% of Pimax was sufficient to elicit an increased inspiratory-muscle endurance in patients with CF.     

Inspiratory muscle training in patients with heart failure and inspiratory muscle weakness: a randomized trial.

OBJECTIVES: This study sought to evaluate the effects of inspiratory muscle training in inspiratory muscle strength, as well as in functional capacity, ventilatory responses to exercise, recovery oxygen uptake kinetics, and quality of life in patients with chronic heart failure (CHF) and inspiratory muscle weakness. BACKGROUND: Patients with CHF may have reduced strength and endurance in inspiratory muscles, which may contribute to exercise intolerance and is associated with a poor prognosis. METHODS: Thirty-two patients with CHF and weakness of inspiratory muscles (maximal inspiratory pressure [Pi(max)] <70% of predicted) were randomly assigned to a 12-week program of inspiratory muscle training (IMT, 16 patients) or to a placebo-inspiratory muscle training (P-IMT, 16 patients). The following measures were obtained before and after the program: Pi(max) at rest and 10 min after maximal exercise; peak oxygen uptake, circulatory power, ventilatory oscillations, and oxygen kinetics during early recovery (VO2/t-slope); 6-min walk test; and quality of life scores. RESULTS: The IMT resulted in a 115% increment Pi(max), 17% increase in peak oxygen uptake, and 19% increase in the 6-min walk distance. Likewise, circulatory power increased and ventilatory oscillations were reduced. The VO2/t-slope was improved during the recovery period, and quality of life scores improved. CONCLUSIONS: In patients with CHF and inspiratory muscle weakness, IMT results in marked improvement in inspiratory muscle strength, as well as improvement in functional capacity, ventilatory response to exercise, recovery oxygen uptake kinetics, and quality of life.     

Clinical study on respiratory muscle training for chronic respiratory failure]

The purpose of respiratory muscle training for patients with chronic respiratory failure is to improve exercise performance during daily life. Firstly, to confirm the clinical effect on respiratory muscle training, the abdominal pad method for inspiratory muscle training and abdominal pad method with expiratory resistor for both inspiratory and expiratory muscle training were simultaneously performed. Both methods were clinically useful to increase respiratory muscle power and to subjectively decrease dyspnea. Ventilatory pattern analyzed by the Konno-Mead (K-M) diagram during exercise also showed their effectiveness. Secondly, the influence of hypoxemia and hypophosphatemia, which are important factors producing respiratory muscle fatigue, was investigated in a patient with respiratory failure. (1) O2 inhalation in patients receiving home oxygen therapy was effective in terms of the endurance time and ventilatory pattern analyzed by the K-M diagram during exercise. (2) A case of hypercapnea due to hypoventilation caused by respiratory muscle fatigue developed reduced PaCO2 following correction of serum phosphate level, suggesting that hypophosphatemia is an important clinical factor producing respiratory muscle fatigue.     

Inspiratory muscle training in patients with bronchial asthma.

In patients with asthma, the respiratory muscles have to overcome the increased resistance while they become progressively disadvantaged by hyperinflation. We hypothesized that increasing respiratory muscle strength and endurance with specific inspiratory muscle training (SIMT) would result in improvement in asthma symptoms in patients with asthma. Thirty patients with moderate to severe asthma were recruited into 2 groups; 15 patients received SIMT (group A) and 15 patients were assigned to the control group (group B) and got sham training in a double-blind group-comparative trial. The training was performed using a threshold inspiratory muscle trainer. Subjects of both groups trained five times a week, each session consisted of 1/2-h training, for six months. Inspiratory muscle strength, as expressed by the PImax at RV, increased significantly, from 84.0 +/- 4.3 to 107.0 +/- 4.8 cm H2O (p < 0.0001) and the respiratory muscle endurance, as expressed by the relationship between Pmpeak and PImax from 67.5 +/- 3.1 percent to 93.1 +/- 1.2 percent (p < 0.0001), in patients of group A, but not in patients of group B. This improvement was associated with significant improvements compared with baseline for asthma symptoms (nighttime asthma, p < 0.05; morning tightness, p < 0.05; daytime asthma, p < 0.01; cough, p < 0.005), inhaled B2 usage (p < 0.05), and the number of hospital (p < 0.05) and sick-leave (p < 0.05) days due to asthma. Five patients were able to stop taking oral/IM corticosteroids while on training and one in the placebo group. We conclude that SIMT, for six months, improves the inspiratory muscle strength and endurance, and results in improvement in asthma symptoms, hospitalizations for asthma, emergency department contact, absence from school or work, and medication consumption in patients with asthma.     

Inspiratory muscle training in pulmonary rehabilitation program in COPD patients

Most pulmonary rehabilitation (PR) programs do not currently incorporate IMT in their PR programs for COPD patients. The aim of the present study was to assess the influence of adding IMT to the patients already involved in a rehabilitation program. Thirty-four patients with significant COPD were recruited for the study. All patients participated in a general exercise reconditioning (GER) program for 12 weeks. The patients were then randomized to receive IMT or sham IMT, in addition to GER for the next 6 months. Following three months of GER training there was a significant increase in the 6-min walk test (6MWT) (from mean+/-SEM 254+/-38 to 322+/-42 m, p<0.01), and small but non-significant decreases in the perception of dyspnea (POD), and in the St. George Respiratory Questionnaire score (SGRQ). Following the addition of IMT to the GER program there was a significant increase in the PI(max) in the GER+IMT group (from 66+/-4.7 to 78+/-4.5 cm H(2)O, p<0.01). This was accompanied by a significant improvement in the POD and a further significant improvement in the SGRQ score. IMT provides additional benefits to patients undergoing PR program and is worthwhile even in patients who have already undergone a GER program.     

Inspiratory muscle training in patients with chronic obstructive pulmonary disease

To investigate the effects of inspiratory muscle resistive loading training (IMT) on exercise performance in chronic obstructive pulmonary disease (COPD), 13 patients undergoing standard pulmonary rehabilitation were divided into control (n = 6) and experimental (n = 7) groups. Prior to training, we measured inspiratory muscle strength and endurance, resting pulmonary function, and exercise performance on a bicycle ergometer (a progressive test and an endurance test at two thirds of maximal work load). We then determined their resistive loads for training by measuring their 10-min maximal sustainable resistance. Training by patients in the experimental group involved inspiring against a predetermined resistive load. The control subjects breathed through a sham training tube, so that studies were performed in double-blind fashion. The training consisted of 15-min sessions twice daily for 4 wk. The IMT dramatically improved inspiratory muscle endurance--represented as either sustainable inspiratory pressure (SIP) or endurance time at 60% of maximal inspiratory mouth pressure (Pimmax) at functional residual capacity. The SIP of the trained group increased from 29 +/- 11 to 46 +/- 11% of Pimmax (p less than 0.005). Training slightly increased inspiratory muscle strength (p less than 0.05), as determined by Pimmax. In contrast, resting pulmonary function and performance of both progressive and constant-load exercise remained unchanged. We conclude that 4-wk IMT in a pulmonary rehabilitation setting improves inspiratory muscle endurance in patients with COPD without changing pulmonary function or exercise performance.     

Inspiratory muscle training in Morquio's syndrome: a case study

We reported a case of MPS IV A presented with dyspnea on exertion and respiratory muscle weakness. The patient underwent inspiratory muscle training (IMT) using threshold loading for 18 weeks. After 6 weeks of initial IMT, aerobic exercise training consisting of walking was added to the treatment program. Inspiratory muscle strength increased 70%, and 6-minute walk test (6MWT) distance increased to 47 m. With the inclusion of aerobic exercise training, additional increases in inspiratory muscle strength (7%) and 6MWT distance (26.5 m) were obtained. Exertional dyspnea improved from severe to slight after 6 weeks of IMT, and to very slight after additional 12 weeks of combined aerobic training and IMT. Health-related quality of life improved especially in social function, emotional function, vitality, and physical role. In conclusion, inspiratory muscles can be trained with the improvement of muscle strength in a patient with Morquio's syndrome.     

Inspiratory muscle weakness and dyspnea in chronic heart failure.

Dyspnea is a common, disabling symptom in chronic heart failure, yet the underlying mechanisms remain unknown. The respiratory muscle pump is composed of skeletal muscles whose strength directly influences the pump's performance. Respiratory muscle weakness is important in the dyspnea experienced by some patients with pulmonary disease; however, the role of the respiratory muscle pump in the dyspnea of chronic heart failure has not previously been examined. To assess respiratory muscle strength and its relation to dyspnea during daily activity, we measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength and the baseline dyspnea index in nine stable, chronic cardiac pump failure patients who had no evidence of primary lung disease, and in nine age- and sex-matched healthy control subjects. The chronic heart failure patients, when compared with their matched control subjects, had reduced inspiratory and expiratory muscle strength, and both inspiratory and expiratory muscle strength were significantly correlated with dyspnea during daily activity (r2 = 0.80, p = 0.001 and r2 = 0.45, p = 0.05, respectively). Inspiratory muscle strength accounted for all of the variance in dyspnea that was correlated with respiratory muscle strength when the relative contributions of inspiratory and expiratory muscle strength were examined. There was no correlation between lung volumes or spirometry and dyspnea in the heart failure patients. These findings indicate that patients with stable chronic heart failure have inspiratory and expiratory muscle weakness and further suggest that the respiratory muscle pump significantly contributes to the dyspnea during the activities of daily living.     

Inspiratory muscle endurance in patients with chronic heart failure.

OBJECTIVE: To assess the significance of changes in respiratory muscle endurance in relation to respiratory and limb muscle strength in patients with mild to moderate chronic heart failure using a threshold loading technique. SUBJECTS: 20 patients with chronic heart failure (17 male) aged 63.8 (SD 7.4) years and 10 healthy men aged 63.1 (5.6) years. Heart failure severity was New York Heart Association (NYHA) grade II (n = 11) and NYHA grade III/IV (n = 9). METHODS: Respiratory muscle strength was measured from mouth pressures during maximum inspiratory effort (MIP) at functional residual capacity (FRC) and limb muscle strength was measured using a hand grip dynamometer. Inspiratory muscle endurance was measured using a threshold loading technique. The total endurance duration, the maximum threshold pressure achieved (P-Max), and the inspiratory load (% ratio of P-Max/MIP) were recorded in all subjects. RESULTS: Inspiratory muscles were weaker in patients with heart failure than in the controls [MIP 53.6 (16.5) v 70.9 (20.2) cm H2O, P < 0.05]. Hand grip strength was similar in both subject groups [31.6 (SD) v 36.1 (15.9) dynes]. Total endurance duration was significantly reduced in the patient group [494 (223) v 996 (267) s, P < 0.01], as was the maximal threshold pressure achieved [P-Max 18.5 (6.4) v 30.7 (6.6) cm H2O, P < 0.01]. When expressed as a percentage of MIP, P-Max was also lower in the patients [35.2 (11.8) v 44.8 (11.4)%, P < 0.05]. There was no significant correlation between any measure of endurance and limb muscle strength. CONCLUSIONS: Respiratory muscle endurance is reduced in patients with chronic heart failure. These changes probably reflect a generalised skeletal myopathy and provide further evidence of respiratory muscle dysfunction in patients with this disease. Respiratory muscle endurance needs now to be related to symptoms and the effects of treatment and respiratory muscle training should also be explored.     

Inspiratory muscle strength and respiratory drive in patients with rheumatoid arthritis

In 15 patients with rheumatoid arthritis (RA) and in 12 age- and sex-matched normal subjects, we evaluated inspiratory muscle strength and respiratory control system. Inspiratory muscle strength was assessed by measuring maximal inspiratory pressure (MIP). Respiratory drive was assessed by evaluating surface electromyographic activity of the diaphragm (EMGd) during both room-air breathing and hypercapnic rebreathing. Compared to the predicted value (mean +/- 1.65 SD), MIP was significantly reduced in nine patients (60%). All told, we noticed a significant inverse relationship in the patients between MIP and duration of steroid therapy (p less than 0.01). During room-air breathing, both EMGd and mouth occlusion pressure (P0.1), expressed both in actual values and as percentage of MIP, were significantly greater in patients than in the normal control group (p less than 0.001 for both). Both EMGd and P0.1 (%MIP) response slopes to CO2 were significantly greater in patients than in the normal control group (p less than 0.01 and p less than 0.001, respectively) and significantly related to the functional stage of disease. During quiet breathing and for a PETCO2 of 60 mm Hg, both EMGd (p less than 0.01 and p less than 0.05, respectively) and P0.1 (%MIP) (p less than 0.01 and p = 0.001, respectively) were inversely related to MIP. These results indicate that RA patients may exhibit inspiratory muscle weakness and increased respiratory drive. Steroid myopathy and rheumatoid myositis could explain the reduction in MIP, whereas neural afferents arising from respiratory muscle, lung, or joint receptors could be involved in the observed increase in neural drive.     

Inspiratory resistive load detection in children with life-threatening asthma.

The detection of inspiratory resistive (R) loads was studied in nonasthmatic children (NA), asthmatic children (A), and children with a history of life-threatening asthma (LTA). It was hypothesized that the LTA children would have a reduced ability to detect added mechanical loads as measured by the Weber fraction, which assesses the resistive load detection threshold (DeltaR(50)/R(0)). Subjects were separated from the investigator, were seated in a soundproofed room, and breathed through a nonrebreathing valve with the inspiratory port connected to the loading manifold. The subject's inspiratory baseline resistance (R(aw)) was measured by the interrupter method. Ten magnitudes of R loads and no-load were presented randomly 10 times each for a single inspiration. The loads were presented in three trials. Subjects pressed a button if they detected the presence of a load. The DeltaR(50) was determined from the % detection-DeltaR curve. R(0) was the sum of the subject's R(aw) and the minimal resistance of the apparatus. The DeltaR(50)/R(0) for children with life- threatening asthma was significantly greater than for asthmatic and nonasthmatic children. The increased DeltaR(50)/R(0) suggests that children with LTA are at risk of life-threatening asthma attacks, in part because it requires a greater change in resistance above their baseline resistance before they sense an increased mechanical load such as presented to them by bronchoconstriction during an asthmatic attack.