Respiratory Muscle Training in Obstructive Sleep Apnea Syndrome (OSAS) Patients
|Study Design:||Endpoint Classification: Efficacy Study
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment
|Official Title:||The Impact of Respiratory Muscle Training on the Therapy of Obstructive Sleep Apnea Syndrome (OSAS) Patients|
- Apnea-hypopnea index, Snoring [ Time Frame: 5 weeks ] [ Designated as safety issue: No ]
- Polysomnography (PSG) with sleep stages, total arousal count and respiratory arousal count [ Time Frame: 5 weeks ] [ Designated as safety issue: No ]
- Clinical symptoms according to self-assessment questionnaire (Epworth Sleepiness Scale) [ Time Frame: 5 weeks ] [ Designated as safety issue: No ]
- Lung function test parameters (VC, FEV1, MVV, etc.) [ Time Frame: 5 weeks ] [ Designated as safety issue: No ]
- Nocturnal partial pressure of oxygen and/or carbon dioxide in the blood (during PSG) [ Time Frame: 5 weeks ] [ Designated as safety issue: No ]
|Study Start Date:||January 2009|
|Study Completion Date:||March 2010|
|Primary Completion Date:||January 2010 (Final data collection date for primary outcome measure)|
|Experimental: Respiratory Muscle Training||
Respiratory muscle training with SpiroTiger device, 1 week training initiation and 4 weeks training period with 5 training days per week, training duration 30 min each. Respiratory bag volume set at 50% VC, respiratory frequency starting from 50% MVV. Weekly control trainings.
Other Name: SpiroTiger Medical
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00936286
|Wissenschaftliches Institut Bethanien e.V.|
|Solingen, Nordrhein-Westfalen, Germany, 42699|
|Study Chair:||Winfried J. Randerath, Prof. Dr.||Wissenschaftliches Institut Bethanien e.V|