Breathing pattern and metabolic behavior during anticipation of exercise

Abstract

The mechanisms responsible for the marked increase in ventilation at the onset of exercise are incompletely defined. A conditioned response to exercise anticipation has been suggested as an influencing factor, but systematic measurements have not been made during the transition from rest to the time when exercise is anticipated but has not yet commenced. We tested the hypothesis that cortical activity associated with the anticipation of exercise causes hyperpnea, which is at least partly responsible for the increased ventilation at the onset of exercise. To assess the influence of continuous cortical activity in the absence of exercise anticipation the subjects performed mental arithmetic tasks. Fifteen subjects performed the two experiments in a random order. Ventilation was measured noninvasively using a calibrated respiratory inductive plethysmograph and end-tidal CO2 concentration (FETCO2) was monitored at the nasal vestibule. Both exercise anticipation and mental arithmetic caused an increase in minute ventilation (VI) (P less than 0.01) and mean inspiratory flow (VT/TI, P less than 0.01), which reflects respiratory center drive, although the derivation differed in that the former was volume based, whereas the latter was due to alteration in timing. Despite the increase in VI, FETCO2 remained constant in both instances. In a complementary study the constant FETCO2 in the face of increased VI was shown to be due to increased CO2 output. The results show that the mere anticipation of exercise causes an increase in ventilation. The mechanism responsible for this hyperpnea cannot be due solely to respiratory center activation because of the constancy of FETCO2 and the associated alterations in cardiac and metabolic behavior.

Specific neural substrate linking respiration to locomotion

“…Respiratory increases were found to occur before the onset of movement (increase by 10.4 ± 10.0%; 1.55 ± 0.30 Hz vs. 1.42 ± 0.38 Hz in control; one-tailed paired t test, P < 0.05; n = 9, locomotor bouts; measured 6 s before movement) and became more important during movement (2.09 ± 0.48 Hz; one-tailed paired t test, P < 0.001; n = 9 locomotor bouts). These results reproduce well what was previously shown in mammals (10)(11)(12)(13)(14). We then isolated the brainstem and spinal cord in vitro to see whether feedback from the contracting muscles was necessary for the respiratory increases ( Fig.…”

“…It is well documented that mental simulation of physical effort and preparation for effort in humans induce respiratory and heart rate increases (10,11). Furthermore, it was shown by using functional MRI that the MLR is activated in human subjects in similar tasks (40).…”

“…For instance, sensory feedback from the contracting muscles could play a role (8,9). However, respiratory increases also occur during mental simulation of movement as well as before the onset of exercise in humans (10,11). Furthermore, it was shown that the stimulation of the forebrain and brainstem regions controlling locomotion increases respiratory activity in the absence of movement-related feedback in animal models (12)(13)(14).…”

Effect of Resistive Loading on Variational Activity of Breathing

“…Because even the highest resistive load, 6 cm H 2 O/L/s, evoked a smaller compensatory peak airway pressure than either of the elastic loads of 9 and 18 cm H 2 O/L (7), and because the level of dyspnea did not exceed moderate (3 on a modified Borg scale of 1 to 10), respira- V · V · tory discomfort may have exerted a less important influence on the control of breathing in the present study. The increase in the random variability of TI may reflect the overriding influence of behavioral factors over the automatic control of respiration resulting in a new breathing pattern under loaded conditions (7); this new pattern can be modulated by anticipatory influences (30), personality (31), and genetic trait (32). Because behavioral influences on respiratory control are multifactorial, they may be reflected by the random (unpredictable) fraction of variational activity, whereas the automatic regulation of respiration may be reflected by the correlated (predictable) fraction, in that predictability is a marker of automatic neural reflexes dictated by vital needs (2,5).…”

Reprint of “Learning to breathe? Feedforward regulation of the inspiratory motor drive”

“…Anticipatory changes in breathing behavior have been documented for chemical perturbations, but studies on mechanical perturbations are sparse. An instance of the former may be the anticipatory increase in breathing when an increase in metabolism (CO 2 production) as a result of exercise is expected, the so-called "exercise hyperpnoea" (Fink et al, 1995;Mitchell et al, 1990;Tobin et al, 1986;Wood et al, 2003). During exercise, ventilation increases in proportion to O 2 consumption and CO 2 production, thus allowing a stabilization of blood gases.…”