Ventilatory sensitivity to inhaled carbon dioxide around the control point during exercise

Cummin, A.R.C.; Alison, Jennifer; Jacobi, M. S.; Iyawe, V. I.; Saunders, K.B.

doi:10.1042/cs0710017

Cited by 25 publications

(13 citation statements)

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“…Together, these findings suggest that cerebrovascular responses during exercise, with or without accompanying elevated environmental temperature, are very different relative to that during passive heating. A number of studies have shown that, relative to resting conditions, ventilatory CO 2 sensitivity to a hypercapnic challenge (i.e., the change in ventilation in response to a change in PET CO 2 ) is increased during short-term aerobic exercise, independent of associated increases in core temperature (2,10,17,21,22,39). These studies support the hypothesis that exercise, independent of internal temperature, can alter responsiveness to CO 2 , although it is recognized that exercise-induced altered ventilatory responses to CO 2 are insufficient evidence to fully support the hypothesis that exercise itself can alter cerebrovascular responsiveness to CO 2 .…”

Section: Discussionmentioning

confidence: 99%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

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Section: Discussionmentioning

confidence: 99%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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“…During exercise a graphical technique to calculate PAco2was simulated by the computer program. We have previously compared PA,Co2 obtained graphically with arterial CO2 (Pa,CO,) (Cummin et al 1986) and subsequently validated the computed version against the original manual technique (Jacobi et Figs 3 and 5). During exercise, the steady-state response was significantly higher than the transient at both flow rates.…”

Section: A)mentioning

confidence: 99%

“…The apparatus for the constant inflow technique is more fully described elsewhere (Cummin et al 1986;Jacobi et al 1987 a). Essentially, pure CO2 is run at accurately controlled rates into a small mixing chamber in the inspiratory line of a breathing circuit (Fig.…”

Section: Apparatusmentioning

confidence: 99%

Transient, steady‐state and rebreathing responses to carbon dioxide in man, at rest and during light exercise.

Jacobi

Patil

Saunders

1989

The Journal of Physiology

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SUMMARY1. The transient ventilatory response to CO2, measured using short pulses at constant inflow, was compared with the steady-state response at rest and during exercise at 50 W, and with the rebreathing response at rest, in nine healthy subjects. At rest CO2 was given at flow rates of 0-2 and 0-41 min-' and during exercise, to compensate for the smaller inhaled CO2 fraction as ventilation increased, at flow rates of 0 4 and 0-8 1 min-'.2. We calculated two indexes of gain for the transient response: the ratio of the peaks of the ventilation and Pco2 pulses, and the ratio of their integrals.3. The steady-state response was greater than the transient response at rest and during exercise, but there was no correlation between the two. The rebreathing response was greater than both. Both the transient and the steady-state responses were greater during exercise than at rest.4. To assess alinearity, the steady-state responses to the two CO2 flow rates were compared. At rest, there was no significant difference. During exercise, the response was greater to 0 4 than 0-8 1 min-', indicating alinearity concave downwards.5. We conclude that the transient response as we calculate it is not representative of steady-state gain, and that the CO2 response in light exercise is steeper, and concave downwards in shape. The rebreathing technique overestimates CO2 sensitivity near the control point.

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“…On the other hand, Cummin, Alison, Jacobi, Iyawe & Saunders (1986), using CO2 administration, have reported an increased slope of the VE-alveolar PcO2 (PA, C02) relation close to the eucapnic point even in light exercise in euoxia. However, their timing of the crucial determinations was such as to straddle the peak of the early change of blood lactic acid (Cunningham & Douglas, 1987); such small transient changes of lactic acid during the early determinations would be capable of producing small lateral displacements of PA, c2' When the exercise intensity is well below the anaerobic threshold, as in the experiments to be reported here, the effects of any early rise of blood lactic acid have passed within about the initial 10 min.…”

Section: Introductionmentioning

confidence: 99%

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

Macfarlane¹,

Cunningham²

1992

The Journal of Physiology

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SUMMARY1. Four human subjects exercised in hypoxia (end-tidal partial pressure Of 02 (PET, 02) ca 55 Torr; heart rate ca 100-130 beats min-), and the contribution to the respiratory drive of the peripheral and central chemoreflex pathways have been separated on the basis of the latencies and the time courses of the responses to sudden changes of stimulus.2. The subjects were exposed to repeated end-tidal step changes in PCO2 of ca 3-3 5 Torr (at nearly constant PET, 02 ) and P02 (between ca 55 and 230 Torr) at three regions along the expiratory ventilation VE-PET°2 response line (hypocapnia, eucapnia, hypercapnia). The dynamics of the ventilatory responses were calculated using a two-compartment non-linear least-squares optimization method.3. The component of the response attributable to the peripheral chemoreflex loop may in some subjects contribute up to 75% of the ventilatory drive during mild hypocapnic hypoxic exercise and ca 72 % of the total gain following steps Of PET, CO, during hypoxic exercise. These data support the notion that the effectiveness of the peripheral chemoreceptor pathway is enhanced in moderate exercise.4. During hypoxic exercise, the time delays and time constants attributed to the peripheral chemoreflex pathways (ca 3-5 and 9 s respectively) and to the central chemoreflex pathways (ca 9-5 and 47 s respectively) are some of the shortest reported.5. The dynamics of the peripheral and central chemoreflex pathways appeared to be largely independent of each other.6. There was a notable absence of systematic change of inspiratory and expiratory durations during the step-induced transients.

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Ventilatory sensitivity to inhaled carbon dioxide around the control point during exercise

Cited by 25 publications

References 0 publications

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Transient, steady‐state and rebreathing responses to carbon dioxide in man, at rest and during light exercise.

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

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