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Journal article

Contribution of Respiratory Muscle Oxygen Consumption to Breathing Limitation and Cyspnea

Abstract

During exercise, the sustainable activity of large muscle groups is limited by oxygen delivery. The purpose of this study was to see whether the oxygen consumption of the respiratory muscles reaches a similar critical value under maximal resistive loading and hyperventilation. A secondary objective was to see whether dyspnea (estimated discomfort experienced with breathing using the Borg 0‐10 scale) and the oxygen consumption of the respiratory muscles are closely related across conditions. This would be expected if intramuscular sensory nerve fibres stimulated as a consequence of metabolic events contributed to this sensation. In six normal subjects the respiratory muscles were progressively activated by the addition of incremental inspiratory resistive loads to a maximum of 300 cm H 2 0×s/L (SD=66.4), and incremental dead space to a maximum of 2638 mL (SD=452), associated with an increase in ventilation to 75.1 L/min (SD=29.79). Each increment was maintained for 5 mins to allow the measurement of oxygen uptake in a steady state. During resistive loading total oxygen consumption increased from 239 mL/min (SD=38.2) to 299 mL/min (SD=52.3) and dyspnea increased to "very severe" (Borg scale 7.5, SD=1.55). During dead space loading total oxygen consumption increased from 270 mL/min (SD=20.2) to 426 mL/min (SD=81.9) and dyspnea increased to "very severe" (7.1, SD=0.66). Oxygen cost of inspiratory muscle power was 25 mL/watt (95% confidence limits 16.7 to 34.3) with dead space loading and 91 mL/watt (95% confidence limits 54 to 128) with resistive loading. Oxygen consumption did not reach a critical common value in the two types of loading, 60 mL/min (SD 22.3) during maximal resistive loading and 156 mL/min (SD 82.4) during maximal dead space loading (P<0.05). Physiological factors limiting the respiratory muscles are not uniquely related to oxygen consumption and appear to be expressed through the activation of sensory structures, perceptually manifested as dyspnea.

Authors

Casan P; Villafranca CC; Kearon C; Campbell EJ; Killian KJ

Journal

Canadian Respiratory Journal, Vol. 4, No. 2, pp. 101–107

Publisher

Wiley

Publication Date

January 1, 1997

DOI

10.1155/1997/863215

ISSN

1198-2241

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