The Impact of Respiratory Muscle Training on the Therapy of Obstructive Sleep Apnea Syndrome (OSAS) Patients
Overview
- Phase
- Not Applicable
- Intervention
- Not specified
- Conditions
- Obstructive Sleep Apnea Syndrome
- Sponsor
- Idiag AG
- Enrollment
- 10
- Locations
- 1
- Primary Endpoint
- Apnea-hypopnea index, Snoring
- Status
- Completed
- Last Updated
- 16 years ago
Overview
Brief Summary
The purpose of this study is to determine whether respiratory muscle training by means of normocapnic hyperpnea leads to clinical and polysomnographical improvements in patients with mild to intermediate sleep apnea syndrome.
Detailed Description
The obstructive sleep apnea syndrome (OSAS) is of great significance for affected individuals as well as for public health service. Patients suffer from reduced quality of life and show an increased accident risk in road traffic and on the job. Furthermore, OSAS represents an independent risk factor for cardiovascular diseases, in particular arterial hypertension. In sleep apnea patients, the relatively early stimulation of the upper respiratory tract muscles compared to the thoracic respiratory muscles is abrogated in many cases. Alternatively, nerve damage with impaired sensory function in the pharynx area and impaired motor function of the upper air tract musculature, in particular the musculus genioglossus can be observed. The disturbed sensory function impairs the reflex activation of the genioglossus. Moreover, the pattern of neurogenic muscle damage with a loss of the pattern of different types of fibers changed to the point of adjoining atrophic and hypertrophic sections and a more monotonous appearance of fiber types could be detected. During waking hours the activity of the musculus genioglossus is enhanced compared with control persons, which is interpreted as a compensatory mechanism. During sleep time, however, this compensation seems to disappear. In several studies either direct or indirect stimulation of the musculus genioglossus and its supplying nerves were deployed. Yet, the results were inconsistent. The direct muscle stimulation using intramuscular electrodes, although efficient, was no longer pursued due to technical reasons. Although the results of an external stimulation showed improvements regarding apneas and snoring, the findings were usually weakly pronounced. In a study ascertaining muscle training with transcutaneous electrical stimulation a significant improvement regarding snoring was achieved when compared to placebo. In general, no influence on sleep apnea syndrome could be accomplished, although there were individual cases showing a clinically relevant amelioration. A preceding study compared habitual snorers with control persons. It was shown that respiratory muscle training by means of normocapnic hyperpnea was accompanied by enlargement of the musculus genioglossus and reduced snoring. Moreover, an increased physical performance was observed. Thus, the question arises if training of the respiratory musculature by means of normocapnic hyperpnea leads to clinical and polysomnographical improvements in patients with mild to intermediate sleep apnea syndrome.
Investigators
Eligibility Criteria
Inclusion Criteria
- •Mild to intermediate sleep apnea syndrome with AHI of 10 - 30/h and clinical symptoms
- •Refusal of a primary nCPAP therapy
- •Epworth Sleepiness Scale (ESS) score ≥ 9
- •Signed informed consent form
Exclusion Criteria
- •Therapy with pharmaceuticals which can influence the musculature
- •Psychiatric disease which negatively influences compliance
- •Acute and chronic diseases of the lung and/or the respiratory passages
- •BMI ≥ 35 kg/m²
Outcomes
Primary Outcomes
Apnea-hypopnea index, Snoring
Time Frame: 5 weeks
Secondary Outcomes
- Polysomnography (PSG) with sleep stages, total arousal count and respiratory arousal count(5 weeks)
- Clinical symptoms according to self-assessment questionnaire (Epworth Sleepiness Scale)(5 weeks)
- Lung function test parameters (VC, FEV1, MVV, etc.)(5 weeks)
- Nocturnal partial pressure of oxygen and/or carbon dioxide in the blood (during PSG)(5 weeks)