Abstract

How central and peripheral chemoreceptor drives to breathe interact in humans remains contentious. We measured the peripheral chemoreflex sensitivity to hypoxia (PChS) at various isocapnic CO2 tensions ( ) to determine the form of the relationship between PChS and central . Twenty participants (10F) completed three repetitions of modified rebreathing tests with end-tidal ( ) clamped at 150, 70, 60 and 45mmHg. End-tidal ( ), , ventilation ( E ) and calculated oxygen saturation (SC O2 ) were measured breath-by-breath by gas-analyser and pneumotach. The E - relationship of repeat-trials were linear-interpolated, combined, averaged into 1mmHg bins, and fitted with a double-linear function ( E S, L min-1 mmHg-1 ). PChS was computed at intervals of 1mmHg of as follows: the difference in E between the three hypoxic profiles and the hyperoxic profile (∆ E ) was calculated; three ∆ E values were plotted against corresponding SC O2 ; and linear regression determined PChS (Lmin-1 mmHg-1 %SC O2 -1 ). These processing steps were repeated at each to produce the PChS vs. isocapnic relationship. These were fitted with linear and polynomial functions, and Akaike information criterion identified the best-fit model. One-way repeated measures analysis of variance assessed between-condition differences. E S increased (P<0.0001) with isoxic from 3.7±1.5 L min-1 mmHg-1 at 150mmHg to 4.4±1.8, 5.0±1.6 and 6.0±2.2 Lmin-1 mmHg-1 at 70, 60 and 45mmHg, respectively. Mean SC O2 fell progressively (99.3±0%, 93.7±0.1%, 90.4±0.1% and 80.5±0.1%; P<0.0001). In all individuals, PChS increased with , and this relationship was best described by a linear model in 75%. Despite increasing central chemoreflex activation, PChS increased linearly with indicative of an additive central-peripheral chemoreflex response. KEY POINTS: How central and peripheral chemoreceptor drives to breathe interact in humans remains contentious. We measured peripheral chemoreflex sensitivity to hypoxia (PChS) at various isocapnic carbon dioxide tensions ( ) to determine the form of the relationship between PChS and central . Participants performed three repetitions of modified rebreathing with end-tidal fixed at 150, 70, 60 and 45mmHg. PChS was computed at intervals of 1mmHg of end-tidal ( ) as follows: the difference in E between the three hypoxic profiles and the hyperoxic profile (∆ E ) was calculated; three ∆ E values were plotted against corresponding calculated oxygen saturation (SC O2 ); and linear regression determined PChS (Lmin-1 mmHg-1 %SC O2 -1 ). In all individuals, PChS increased with , and this relationship was best described by a linear (rather than polynomial) model in 15 of 20. Most participants did not exhibit a hypo- or hyper-additive effect of central chemoreceptors on the peripheral chemoreflex indicating that the interaction was additive.

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