TY - JOUR
T1 - Short-term potentiation of breathing in humans
AU - Fregosi, R. F.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1991
Y1 - 1991
N2 - The purpose of this study was to determine if the increase in ventilation induced by hypoxic stimulation of the carotid bodies (CB) persists after cessation of the stimulus in humans. I reasoned that a short-term potentiation (STP) of breathing, sometimes called an 'afterdischarge,' could be unmasked by combining hypoxia with exercise, because ventilation increases synergistically under these conditions. Seven young healthy men performed mild bicycle exercise (30% peak power) while breathing O2 for 1.5 min ('control' state), and their CB were then stimulated by 1.5 min of hypoxic exercise (10% O2 - balance N2). CB stimulation was then terminated by changing the inspirate back to O2 as exercise continued. Inspiratory and expiratory duration (TI and TE) and inspiratory flow and its time integral [tidal volume (VT)] were measured with a pneumotachometer. Inspired minute ventilation (V̇I) and mean inspiratory flow (VT/TI) declined exponentially after the cessation of CB stimulation, with first-order time constants of 28.6 ± 6.7 and 24.6 ± 1.6 (SD) s, respectively. The slow decay of V̇I was due primarily to potentiation of both TI and TE, although the effect on the latter predominated. Additional experiments in six subjects showed that brief intense CB stimulation with four to five breaths of N2 during mild exercise induced STP of similar magnitude to that observed in the hypoxic exercise experiments. Finally, the imposition of hyperoxia during air breathing exercise at a level of respiratory drive similar to that induced by the hypoxic exercise did not change V̇I significantly. These data indicate that systems governing primarily the rate, but also the depth, of automatic ventilation in humans are capable of memory-like retention and expression of information arising from prior CB stimulation (i.e., STP or respiratory afterdischarge).
AB - The purpose of this study was to determine if the increase in ventilation induced by hypoxic stimulation of the carotid bodies (CB) persists after cessation of the stimulus in humans. I reasoned that a short-term potentiation (STP) of breathing, sometimes called an 'afterdischarge,' could be unmasked by combining hypoxia with exercise, because ventilation increases synergistically under these conditions. Seven young healthy men performed mild bicycle exercise (30% peak power) while breathing O2 for 1.5 min ('control' state), and their CB were then stimulated by 1.5 min of hypoxic exercise (10% O2 - balance N2). CB stimulation was then terminated by changing the inspirate back to O2 as exercise continued. Inspiratory and expiratory duration (TI and TE) and inspiratory flow and its time integral [tidal volume (VT)] were measured with a pneumotachometer. Inspired minute ventilation (V̇I) and mean inspiratory flow (VT/TI) declined exponentially after the cessation of CB stimulation, with first-order time constants of 28.6 ± 6.7 and 24.6 ± 1.6 (SD) s, respectively. The slow decay of V̇I was due primarily to potentiation of both TI and TE, although the effect on the latter predominated. Additional experiments in six subjects showed that brief intense CB stimulation with four to five breaths of N2 during mild exercise induced STP of similar magnitude to that observed in the hypoxic exercise experiments. Finally, the imposition of hyperoxia during air breathing exercise at a level of respiratory drive similar to that induced by the hypoxic exercise did not change V̇I significantly. These data indicate that systems governing primarily the rate, but also the depth, of automatic ventilation in humans are capable of memory-like retention and expression of information arising from prior CB stimulation (i.e., STP or respiratory afterdischarge).
KW - carotid bodies
KW - control of breathing
KW - exercise
KW - hypoxia
KW - memory
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U2 - 10.1152/jappl.1991.71.3.892
DO - 10.1152/jappl.1991.71.3.892
M3 - Article
C2 - 1757326
AN - SCOPUS:0025764697
VL - 71
SP - 892
EP - 899
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 3
ER -