OBJECTIVETo investigate the effects of chronic intermittent hypoxia (CIH) on electromyograph (EMG) and ultrastructure of genioglossus (GG) and the interventive effects with adiponectin supplement.

METHODSForty-two healthy male Wistar rats were randomly divided into normal control (A), CIH (B) and adiponectin treatment (C) groups with 14 rats in each. CIH was performed 8 hours per day for 5 weeks in both group B and C. In group C, transvenous injection of adiponectin of 10 microg dosage each time, twice a week for 5 weeks. While in group A and B, transvenous injection of saline was performed twice a week for 5 weeks. At the beginning of 6th week the GG EMG voltages were measured before, during and following hypoxia stimulation by inserted bipolar needle electrodes and compared among three groups. Transmission electron microscope was used for observation of ultrastructure of GG.

RESULTSThe serum adiponectin level in group B (1226.0 +/- 112.0) ng/ml (x(-) +/- s) was significantly lower than that in group A (2491.8 +/- 117.9) ng/ml, q = 38.2, P < 0.01), and adiponectin level in group C (1988.3 +/- 114.7) ng/ml was significantly higher than that in group B (q = 23.0, P < 0.01). Comparison of GG EMG activity showed that the baseline amplitude of GG EMG before hypoxia stimulation was significantly lower in group B than that in both group A and group C (all P < 0.01). At the 5th min of hypoxia stimulation the GG EMG activities were significantly enhanced among three groups (all P < 0.01). Such an enhancement was the most evident in group A but the least remarkable in group B, with a significant difference among three groups (q(ab) = 17.5; q(ac) = 8.9; q(bc) = 8.6, all P < 0.01). 15 min, 30 min and 45 min after hypoxia stimulation the amplitude of GG EMG remained at relative higher levels in group A and C, significantly higher than that in group B (all P < 0.01). CIH could cause significant ultrastructural pathological changes such as myofibril discontinuities, lysis of myofilament, edema of mitochondria and disruption of cristae, vacuoles and lysis of some mitochondria in group B. Venous supplement of adiponectin could improve pathological changes resulting from CIH.

CONCLUSIONSCIH could resulted in pathological changes in EMG and ultrastructure of GG, which might be associated with hypoadiponectinemia caused by CIH.