| Summary: | 博士 === 國立臺灣大學 === 物理治療學研究所 === 96 === Obstructive sleep apnea (OSA) is associated with higher inflammatory markers. It has been reported that skeletal muscle dysfunction is common in systemic inflammatory diseases. However, whether skeletal muscle dysfunction developed in OSA is still unknown. The present study was designed to investigate the skeletal muscle dysfunction, nerve conduction delay, and metabolic abnormalities in patients with OSA. The men whose ages ranged 40-65 years and with normal pulmonary function were recruited.
The purpose of the first part was to investigate the inspiratory muscle function in patients with different severity of OSA. Eighty-eight participants firstly underwent polysomnography assessments were recruited. The measurements included Epworth sleepiness scale, strength and endurance of inspiratory muscles, and fatigue test during either maximal voluntary efforts or in response to cervical magnetic stimulation (CMS) with simultaneously sEMG recordings. The parameters of sEMG included root mean square, median power frequency, compound muscle action potential (CMAP) amplitude and latency, which represented phrenic nerve conduction time (PNCT). The results showed there were 20 subjects without OSA, 13 mild OSA, 21 moderate OSA, and 34 severe OSA. Patients with severe OSA had significantly lower levels of muscle strength and endurance, and higher fatigability than the subjects in the other three groups. Furthermore, the performance and sEMG parameters of inspiratory muscles and knee extensors were compared in a subgroup consisted of 15 pairs of patients with severe OSA and without OSA matched for age-, and body mass index (BMI). The participants received performance tests for vastus lateralis (VL) with simultaneous sEMG recording. It was shown that patients in OSA group had significantly lower strength and endurance of knee extensors, but no significant difference in fatigability than those of the controls. CMAP amplitude and latency for VL in OSA group were not significantly different from those in the control group. It indicated that different adaptations might play an important role on skeletal muscle dysfunction in severe OSA.
The second part was designed to examine the metabolic characteristics of lower extremity in patients with OSA. Twenty pairs of patients with severe OSA and non-OSA controls matched with age and BMI volunteered to this part of study. Blood samples were drawn and proton magnetic resonance spectroscopy was used to detect intramyocellular and extramyocellular lipid contents (IMCL and EMCL). It was shown significantly lower values of IMCL and EMCL, higher inflammatory markers and insulin resistance, and worse lipid profiles in severe OSA group than the control group after controlling for age and BMI. There was no significant correlation between the biochemistrical variables and IMCL or EMCL. It seemed that metabolic properties changed in OSA patients; however, the mechanisms were needed to be further studied.
The third part determined the exercise capacity with simultaneous sEMG recordings for diaphragm and VL during the exercise testing. Twenty patients with severe OSA and 20 matched controls participated in this study. The results showed that significantly lower values of oxygen consumption at peak exercise and at anaerobic threshold in OSA group. The major limiting factors were abnormal heart rate response to exercise and peripheral muscle fatigue. The sEMG results showed that knee extensors fatigued at the relatively lower exercise intensity in patients with OSA, but their inspiratory muscles fatigued only at the peak phase of exercise.
Interrelationships among skeletal muscle dysfunction, nerve conduction delay, and metabolic properties in OSA showed that only PNCT correlated significantly with apnea-hypopnea index. Skeletal muscles performance, electromyographic properties, and metabolic properties were correlated significantly with exercise capacity.
In summary, skeletal muscle dysfunction, nerve conduction delay, and metabolic abnormalities were observed in patients with severe OSA than their age-, and BMI-matched controls. Muscle adaptation to chronic increased activation might play an obvious role than the systemic oxidative stress in the effect of OSA on skeletal muscles. Future studies are needed to investigate the effect of intervention on skeletal muscle function in OSA populations, and to explore the possible mechanisms.
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