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Laboratory and Animal Investigations |

The Effects of Chronic Episodic Hypercapnic Hypoxia on Rat Upper Airway Muscle Contractile Properties and Fiber-Type Distribution*

Michelle McGuire, PhD; Mary MacDermott, PhD; Aidan Bradford, PhD
Author and Funding Information

*From the Department of Physiology, Royal College of Surgeons in Ireland, Dublin, Ireland.

Correspondence to: Aidan Bradford, PhD, Department of Physiology, Royal College of Surgeons in Ireland, St. Stephen’s Green, Dublin 2, Ireland; e-mail: abradfor@rcsi.ie



Chest. 2002;122(4):1400-1406. doi:10.1378/chest.122.4.1400
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Objective: Obstructive sleep apnea (OSA) is caused by episodes of upper airway (UA) obstruction due to an inability of UA muscles such as the geniohyoids and sternohyoids to maintain airway patency. This results in chronic episodic hypercapnic hypoxia. Chronic continuous hypoxia and episodic hypocapnic hypoxia affect skeletal muscle structure and function, but the effects of chronic episodic hypercapnic hypoxia on UA muscle structure and function are unknown.

Design: Rats breathed air and hypercapnic hypoxic gas twice per minute for 8 h/d for 5 weeks in order to mimic the intermittent hypercapnic hypoxia of OSA in humans. Isometric contractile properties were determined using strips of isolated geniohyoid and sternohyoid muscles in physiologic saline solution at 30°C. Fiber-type distribution was determined by adenosine triphosphatase staining.

Results: For both muscles, chronic episodic hypercapnic hypoxia had no significant effect on twitch or tetanic tension, twitch/tetanic tension ratio, and tension-frequency relationship. There was a significant (p < 0.05) increase in geniohyoid fatigue (50.5 ± 6.6% vs 43.6 ± 5.8% of initial tension), but sternohyoid fatigue was reduced (31.5 ± 5.2% vs 37.8 ± 6.0% of initial tension). Geniohyoid type 1 fibers were reduced and type 2B fibers increased, whereas sternohyoid muscle had an increase in type 1 and 2A fibers and a decrease in type 2B fibers.

Conclusions: Chronic episodic hypercapnic hypoxia alters UA muscle structure and function, changes that may affect the regulation of UA patency.

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