The effect of volitional breathing on the breathlessness-ventilation relationship during progressive exercise in healthy subjects

Abstract

The current hypothesis about the generation of breathlessness sensation is that a conscious awareness of reflex activation in the brainstem, rather than sensory feedback from peripheral receptors, is the major factor that gives rise to this sensation. This hypothesis was based on work that showed subjects and patients were less breathless when volitionally copying a hypercapnic breathing pattern [1]. However, later studies have shown no effects of volitional breathing on breathlessness [2]. To investigate the contribution of the cortical drive on modulation of the reflex drive, experiments on volitional breathing per se were conducted during progressive exercise. Sixteen subjects undertook a progressive exercise test on a bicycle ergometer, to a symptom-limited maximum during the course of which breathlessness was estimated each minute using the Visual Analogue Scale (VAS). All subjects had completed control exercise experiments to reach reproducible breathlessness estimations. A control study was followed, 7–10 days later, by a study of volitional breathing. The subjects (all males) had a mean age of 29.6 years (SD ± 9.3). The breathing pattern of a control exercise test (control) was recorded. Following this, an 'appropriate volitional tracking' experiment was conducted in which the subjects attempted to copy the previous control breathing pattern during another control exercise test. The subjects were told to follow the breathing pattern by adjusting a cursor, which was driven by flow through a pneumotachograph (PK Morgan, UK). In control and volitional tracking experiments, ventilation (VE), tidal volume (VT) and respiratory frequency (fR) were plotted against time. Breathlessness estimations were plotted against ventilation, from which slope and intercept values were derived. Mean changes in the saturation of oxygen in arterial blood (SaO2) found at the end of each exercise test were also recorded (Biox IIA, USA). Comparisons were made using a paired t-test. All t-tests were two-tailed and the level of probability taken as significant was 5% (P < 0.05) (Table 1). Table 1 Control Volitional Breathlessness index (mean ± SEM) (mean ± SEM) P VAS/VE slope (mmmin l-1) 0.86 ± 0.10 0.97 ± 0.11 P = 0.307 VAS/VE Intercept (lmin-1) 45.50 ± 4.29 54.34 ± 4.91 P = 0.009 The mean slope and intercept of VE/time, VT/time and fR/time relationships for both experiments were not significantly different. Mean SaO2 levels also showed no significant changes. Mean slopes of the VAS/VE relationship were also not significantly different. However, the mean intercept of the volitional experiment was significantly increased relative to control. The major finding in this study was that the onset of breathlessness was significantly delayed, though there were no significant changes in any objective physiological data set between control and volitional experiments. We postulate that this delay is due to cortical drive bypassing the medullary rhythm generator, with possible inhibition of the reflex efferent drive projecting to the sensory cortex. This is consistent with the hypothesis that the medullary reflex activity is responsible for the genesis of breathlessness sensation.