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EFFECTS OF CHRONIC HYPOXIA ON UPPER AIRWAY AND DIAPHRAGM MUSCLE ENDURANCE IN THE DEVELOPING RAT
Author(s) -
O'Halloran Ken D,
Mitchell Gordon S,
Bradford Aidan,
Carberry Jayne
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1232.1
Subject(s) - hypoxia (environmental) , muscle fatigue , diaphragm (acoustics) , respiratory system , medicine , skeletal muscle , diaphragm muscle , airway , analysis of variance , endocrinology , anesthesia , anatomy , electromyography , chemistry , physical medicine and rehabilitation , oxygen , physics , organic chemistry , acoustics , loudspeaker
Chronic hypoxia (CH) is common in respiratory disease and is known to alter skeletal muscle structure and oxidative capacity. We hypothesized that CH in early development would alter respiratory muscle function. Wistar rats were reared in normobaric normoxia or hypobaric hypoxia (PB=450mmHg) for 7 days beginning at P1, P11, P21 or P31. Isolated muscle function studies were conducted at P19, P29 or P39. Fatigue was assessed in response to repeated tetanic contractions (40Hz, 300msec) every 2 sec for 5 minutes. Chronic hypoxia during early development (beginning P1 and P11) increased sternohyoid specific force but significantly reduced muscle endurance (fatigue index ie ratio of force at 5 min of fatigue to initial force, measured at P19 was 83+/−7% vs. 59+/−7%* and 63+/−4%*; control vs. P1 and P11 hypoxic groups, *P<0.05 ANOVA). CH in older animals did not affect sternohyoid endurance. CH increased diaphragm specific force but had no effect on muscle endurance (eg fatigue index at P19 was 81+/−6% vs. 76+/−4% and 88+/−4%; control vs. P1 and P11 hypoxic groups, P>0.05 ANOVA). We conclude that CH elicits plasticity in respiratory muscles with differential effects in diaphragm and upper airway muscles. Increased fatigue of the sternohyoid muscle may have important consequences for the control of upper airway patency in vivo.