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Laboratory and Animal Investigations |

Effects of Chronic Intermittent Asphyxia on Rat Diaphragm and Limb Muscle Contractility*

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. 2003;123(3):875-881. doi:10.1378/chest.123.3.875
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Objective: In obstructive sleep apnea (OSA), there is intermittent upper airway (UA) collapse due to an imbalance between the collapsing force generated by the diaphragm and the stabilizing force of the UA muscles. This results in chronic intermittent asphyxia (CIA). We have previously shown that CIA affects UA muscle fatigue, but little is known about the effects of chronic hypoxia on diaphragm or on limb muscle contractile properties and structure.

Design: Rats were exposed to asphyxia and normoxia twice per minute for 8 h/d for 5 weeks to simulate the intermittent asphyxia of OSA in humans. Isometric contractile properties were determined from strips of isolated diaphragm, extensor digitorum longus (EDL), and soleus muscles in Krebs solution at 30°C. EDL and soleus type 1 (slow, fatigue resistant), type 2A (fast, fatigue resistant), and type 2B (fast, fatigable) fiber distribution was determined using adenosine triphosphatase staining.

Results: CIA caused a significant increase in diaphragm, EDL, and soleus fatigue, and reduced recovery from fatigue. Most of the other contractile properties were unaffected aside from a small reduction in diaphragm half-relaxation time and EDL twitch tension and a small shift to the left in the EDL force-frequency curve. There was no change in soleus fiber-type distribution and a small increase in EDL type 2A fibers (46.1 ± 1.2% vs 49.9 ± 1.4%, control vs CIA [mean ± SD]).

Conclusions: CIA increases diaphragm, EDL, and soleus muscle fatigue. We speculate that if this also occurs in OSA, it would contribute to the pathophysiology of the condition.

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