Specific inspiratory muscle training in well-trained endurance athletes.

PURPOSE: It has been reported that arterial O2 desaturation occurs during maximal aerobic exercise in elite endurance athletes and that it might be associated with respiratory muscle fatigue and relative hypoventilation. We hypothesized that specific inspiratory muscle training (SIMT) will result in improvement in respiratory muscle function and thereupon in aerobic capacity in well-trained endurance athletes. METHODS: Twenty well-trained endurance athletes volunteered to the study and were randomized into two groups: 10 athletes comprised the training group and received SIMT, and 10 athletes were assigned to a control group and received sham training. Inspiratory training was performed using a threshold inspiratory muscle trainer, for 0.5 h x d(-1) six times a week for 10 wk. Subjects in the control group received sham training with the same device, but with no resistance. RESULTS: Inspiratory muscle strength (PImax) increased significantly from 142.2 +/- 24.8 to 177.2 +/- 32.9 cm H2O (P < 0.005) in the training but remained unchanged in the control group. Inspiratory muscle endurance (PmPeak) also increased significantly, from 121.6 +/- 13.7 to 154.4 +/- 22.1 cm H2O (P < 0.005), in the training group, but not in the control group. The improvement in the inspiratory muscle performance in the training group was not associated with improvement in peak VEmax, VO2max breathing reserve (BR). or arterial O2 saturation (%SaO2), measured during or at the peak of the exercise test. CONCLUSIONS: It may be concluded that 10 wk of SIMT can increase the inspiratory muscle performance in well-trained athletes. However, this increase was not associated with improvement in aerobic capacity, as determined by VO2max, or in arterial O2 desaturation during maximal graded exercise challenge. The significance of such results is uncertain and further studies are needed to elucidate the role of respiratory muscle training in the improvement of aerobic-type exercise capacity.

Long term clinical comparison of single versus twice daily administration of inhaled budesonide in moderate asthma.

BACKGROUND: Inhaled steroids are widely used in the treatment of mild to moderate asthma. However, long term compliance with inhaled steroids is poor and administration of a single daily dose may improve compliance. METHODS: A double blind, randomised study was performed to determine whether inhaled steroids given once daily at bedtime are as efficacious as a twice daily regimen in the long term maintenance of moderate asthmatic patients. Forty adults of mean age 37 years with moderate asthma (mean (SE) forced expiratory volume in one second (FEV1) 73.6 (1.4)% predicted, mean morning peak expiratory flow (PEF) 328 l/min) were randomised to receive either a twice daily dose (400 micrograms morning and bedtime) of inhaled budesonide (group A) or a once daily dose of 800 micrograms (group B) and were followed for a period of 12 months. Asthma symptom scores (assessed according to a modified Borg scale), inhaled beta 2 agonist consumption, and peak expiratory flow rates were recorded daily. Spirometry and airways responsiveness to methacholine (PC20) were measured at the end of each period of three months of treatment. RESULTS: There was no difference between the two groups at baseline and during the follow up period in the PC20 for methacholine. However, a difference was seen between the two groups in the mean daily number of beta 2 agonist inhalations (1.4 (0.1) puffs/patient/day in group A v 2.3 (0.1) in group B), the PEF variability (episodes of decrease in PEF of > 20%) (0.22 (0.01) episodes/patient/day in group A v 0.40 (0.02) in group B), and for asthma symptom scores (0.30 (0.04) in group A v 0.42 (0.06) in group B) for the 12 month period of the study. CONCLUSIONS: Although both regimens provide good clinical control, twice daily doses of 400 micrograms inhaled budesonide are more effective than a single dose of 800 micrograms at bedtime in the long term control of stable moderate asthma.

Inhaled budesonide therapy for patients with stable COPD.

A significant minority of patients with COPD have favorable response to corticosteroid treatment. In addition, the benefit of corticosteroid treatment may be outweighed by the side effects. Long-term administration of inhaled steroids is a safe means of treatment. We hypothesized that treatment with high-dose inhaled budesonide would improve clinical symptoms and pulmonary function in subjects with COPD, and that the response to inhaled beta 2-agonist will serve to individualize steroid responders. We compared a 6-week course of 800 micrograms/d inhaled budesonide with placebo, separated by 4 weeks when no medication was taken, in a double-blind crossover trial, in 8 patients responding to inhaled beta 2-agonist, and in 22 nonresponders with stable COPD. In six of eight "responders to beta 2-agonist," there was a significant improvement in the FEV1 (defined as > or = 20%) following inhaled budesonide, as compared with placebo. In the 22 "nonresponders to beta 2-agonist," there was no significant improvement in the mean FEV1 (1.41 +/- 0.1 L before, and 1.61 +/- 0.1 L after treatment) with inhaled budesonide or placebo. Over the 6-week course of treatment by either budesonide or placebo, the nonresponders reported similar beta 2-agonist consumption (4.8 +/- 0.2 and 5.0 +/- 0.1 puffs per patient per day, respectively). However, there was a significant difference between the two periods of treatment in the responders as for the mean daily number of beta 2-agonist inhalations (2.4 +/- 0.1 in the budesonide period as compared with 5.3 +/- 0.1 in the placebo period; p < 0.005). We conclude that treatment with inhaled steroids improved spirometry data and inhaled beta 2-agonist consumption in about 25% of patients with stable COPD, and this rate is increased to about 75% in patients who respond to beta 2-agonist inhalation.

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

[Effect of corticosteroids on inspiratory muscle function].

Functional alteration in inspiratory muscles was evaluated in patients receiving corticosteroids for nonrespiratory diseases. Inspiratory muscle strength, as expressed by maximal inspiratory mouth pressure (PImax), and inspiratory muscle endurance (PmPeak/PImax), determined with a pressure threshold breathing device, were evaluated in 8 patients with normal pulmonary and inspiratory muscle function. There was a gradual decrease in both inspiratory muscle strength and endurance when corticosteroids were given. Tapered decrease in steroid dosage resulted in marked improvement in both strength and endurance, and the improvement was even more significant 6 months later. We also evaluated the ability of specific inspiratory muscle training to prevent the effects of therapeutic corticosteroids on inspiratory muscle function in 6 patients, as compared to 6 control patients who received sham training. Following corticosteroids there was a gradual decrease in both inspiratory muscle strength and endurance in those getting sham training. However, there was no significant change in inspiratory muscle function in those getting inspiratory muscle training. We conclude that corticosteroids result in significant deterioration in respiratory muscle function. This weakness is reversible by tapering steroid dosage, but can be prevented by specific inspiratory muscle training during corticosteroid treatment.

The effect of corticosteroids on inspiratory muscle performance in humans.

Functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. Inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax), and inspiratory muscle endurance (PmPeak/PImax), using a pressure threshold breathing device, were evaluated in eight patients with normal pulmonary and inspiratory muscle functions (two patients with rapidly progressive glomerulonephritis, two with glomerulonephritis with minimal changes, two with idiopathic thrombocytopenic purpura, and two with subacute thyroiditis). There was a gradual decrease in both inspiratory muscle strength and endurance following corticosteroid administration. After 8 weeks of treatment PmPeak/PImax decreased from 84.4 +/- 2.4 to 67.9 +/- 3.1 percent (p < 0.001), while inspiratory muscle strength dropped from 126.9 +/- 9.6 to 86.5 +/- 7.4 cm H2O (p < 0.005). Gradual steroid dosage tapering resulted in marked improvement in both strength and endurance; the inspiratory muscle strength rose significantly to 112.2 +/- 8.1 cm H2O (p < 0.0005) when steroid treatment was stopped, and even more significantly 6 months later (to 123.1 +/- 8.1 cm H2O [p < 0.0001]), and the PmPeak/PImax rose to 60.6 +/- 3.4 percent (p < 0.001) and to 74.7 +/- 3.2 percent (p < 0.0001), respectively. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is reversible while tapering steroid dosage. Steroid therapy should be reconsidered in patients with underlying lung disease.

[Inspiratory muscle training combined with general exercise reconditioning in chronic obstructive pulmonary disease].

In a controlled clinical trial, we compared the effect of 6 months of specific inspiratory muscle training combined with general exercise reconditioning, with that of general exercise reconditioning alone. We measured the effects of the 2 regimens on inspiratory muscle strength, endurance, and exercise performance in patients with chronic obstructive pulmonary disease (COPD), 2 groups of 10 patients each. Inspiratory muscle strength (expressed as the PImax at RV) increased significantly from 43.2 +/- 3.0 to 67.8 +/- 2.9 cm H2O (p < 0.0001) and respiratory muscle endurance (expressed as the relationship between PmPeak, the pressure achieved with the heaviest load tolerated for at least 60 sec, and PI max) increased significantly from 60.2 +/- 2.5 to 85.6 +/- 2.8% (p < 0.001) in the first group (combined treatment). After the 6-month training period, in both groups there were significant increases in 12-minute walk and endurance work time at 2/3 of Wmax (maximal work each subject achieved on a progressive bicycle exercise test of maximum work load). However, those in the first group showed significantly greater improvement in distance walked and endurance time than the others. We conclude that specific inspiratory muscle training for 6 months improves inspiratory muscle strength and endurance in patients with COPD. This training, combined with general exercise reconditioning, also results in improvement in exercise tolerance significantly greater than that of general exercise reconditioning alone.

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 combined with general exercise reconditioning in patients with COPD.

We compared, in a controlled clinical trial, the effect of specific inspiratory muscle training combined with general exercise reconditioning, for six months, with that of general exercise reconditioning alone on inspiratory muscle strength, endurance, and exercise performance in patients with COPD. Thirty-six patients were recruited into three groups; 12 patients received specific inspiratory muscle training combined with general exercise reconditioning, 12 patients underwent general exercise reconditioning alone, and the remaining 12 patients received no training. Specific inspiratory muscle training, for six months, improved the inspiratory muscle strength and endurance in patients with COPD. This training combined with general exercise reconditioning also provided improvement in exercise tolerance, and this improvement was significantly greater than that of general exercise reconditioning alone.

[Inspiratory muscle training for bronchial asthma].

In patients with asthma the respiratory muscles have to overcome increased resistance while they become progressively disadvantaged by hyperinflation. We hypothesized that increasing respiratory muscle strength and endurance with specific inspiratory muscle training would improve asthmatic symptoms. Of 8 women and 12 men, aged 17-55, with moderate to severe asthma, 10 received such training (group A) and 10 were controls who were given sham training (group B) in a double-blind, group comparative trial. Both groups trained 3 times a week in 1-hour sessions for 6 months. Inspiratory muscle strength, as expressed by the PImax at RV, increased from 72.6 +/- 3.9 to 97.0 +/- 4.6 cm H2O (p less than 0.001) and respiratory muscle endurance, as expressed by the relationship between PmPeak and PImax, increased from 70.6 +/- 3.8 to 94.6 +/- 4.6% (p less than 0.001), in group A patients, but not those of group B. This improvement was associated with significant improvement in asthmatic symptoms: night-time asthma (p less than 0.05), morning tightness (p less than 0.05), daytime asthma (p less than 0.01), cough (p less than 0.005), use of inhaled B2 (p +/- 0.05), and hospital days (p less than 0.05) and days of sick-leave due to asthma. 5 patients were able to stop oral or IM corticosteroids during training, but only 1 in the sham training group. We conclude that 6-months of specific inspiratory muscle training in asthmatic patients improves inspiratory muscle strength and endurance and results in improvement in asthmatic symptoms, hospitalizations for asthma, emergency room contacts, absence from school or work, and use of medication.