Sustained hypoxia depresses sensory processing of respiratory resistive loads.
BACKGROUND
The combination of acute hypoxia and increased respiratory load is encountered in several respiratory diseases including acute life-threatening asthma and sleep apnea. Hypoxia has been shown to inhibit respiratory load perception in healthy and asthmatic subjects, and could contribute to treatment delays and impaired function of protective reflexes.


OBJECTIVE
Using respiratory-related evoked potentials (RREPs) this study aimed to determine the sensory processes mediating hypoxia-induced suppression of respiratory load sensation.


METHODS
EEG was measured over the central and parietal cortical regions in 14 healthy subjects. RREPs were elicited by 500-ms midinspiratory resistive load stimuli during and after isocapnic normoxia or hypoxia (blood arterial O2 saturation approximately 80%). On a separate occasion, subjects rated the perceived magnitude of five externally applied inspiratory resistive loads (range, 8.6-43.7 cm H2O x L(-1) x s) under similar experimental conditions. In both experiments subjects voluntarily ventilated approximately 90% above baseline to match ventilatory output between gas conditions.


RESULTS
RREP stimulus was matched between gas conditions in 11 subjects (minimum mask pressure -9.7 +/- 0.6 versus -9.2 +/- 0.4 cm H2O). P1 and P2 amplitudes were reduced during isocapnic hypoxia compared with normoxia (maximal at Cz: P1, 2.5 +/- 1.1 versus 3.9 +/- 1.2 microv, p = 0.03; P2, 10.0 +/- 2.2 versus 12.4 +/- 2.1 microv, p < 0.01, respectively). Perceived magnitude of externally applied resistive loads was also reduced during hypoxia compared with normoxia (17.1 +/- 1.1 versus 19.0 +/- 1.1 au, p < 0.01).


CONCLUSIONS
These data confirm that isocapnic hypoxia suppresses respiratory load sensation. Decreased amplitude of the earlier (P1) RREP component suggests that this is mediated, at least in part, by suppression of respiratory afferent information before its arrival at the primary sensory cortex.
Eckert
Danny J
DJ
Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia. danny.eckert@rgh.sa.gov.au
Catcheside
Peter G
PG
McDonald
Rachel
R
Adams
Amanda M
AM
Webster
Kate E
KE
Hlavac
Michael C
MC
McEvoy
R Doug
RD
D000208:Acute Disease; D000328:Adult; D000344:Afferent Pathways; D000403:Airway Resistance / Q000502:physiology*; D000704:Analysis of Variance; D001249:Asthma / Q000150:complications; D001784:Blood Gas Analysis; D015986:Confounding Factors, Epidemiologic; D004569:Electroencephalography; D005073:Evoked Potentials, Somatosensory; D005260:Female; D006801:Humans; D006985:Hyperventilation / Q000150:complications; D000860:Hypoxia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D016014:Linear Models; D008297:Male; D011930:Reaction Time; D012132:Respiratory Muscles / Q000378:metabolism / Q000503:physiopathology*; D012677:Sensation / Q000502:physiology*; D012891:Sleep Apnea Syndromes / Q000150:complications; D013990:Tidal Volume; D013997:Time Factors; D014939:Work of Breathing / Q000502:physiology*