Dynamics of ventilatory response to exercise in humans

Bennett, Frederick M.; Reischl, Peter; Grodins, Fred S.; Yamashiro, S. M.; Fordyce, Wayne E.

doi:10.1152/jappl.1981.51.1.194

Cited by 48 publications

(25 citation statements)

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“…Since the first component accounts for a relatively small portion of the total response, the over-all dynamics is mainly determined by the second component kinetics. A qualitatively similar dynamics has been observed in inspiratory ventilation volume (Vi) at transitions from a 25W basal exercise to a 100W impulse (BENNETT et al, 1981). WHIPP et al (1982) also observed similar responses in V02, and VE when a 10OW step work was given from loadless pedaling.…”

Section: Methodssupporting

confidence: 69%

“…CASABURI et al (1977) and BAKKER et al (1980) compared the kinetics of heart rate, ventilation, and gas exchange parameters to define the interrelationship among variables during exercise. Other investigators used impulse forcings which differ from sinusoidal work in that a scale of frequencies can be given simultaneously (BAKKER et a!.,1980;BENNETT et a!., 1981;FUJIHARA et al, 1973a, b). In a linear system both the types of forcings would provide essentially the same results.…”

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confidence: 99%

“…BENNETT et al (1981) have argued that to identify the rapid component it is necessary to excite the respiratory system with an input containing high frequency components. Impulse forcings would be a more sensitive method than sinusoidal forcings to demonstrate the fast component since it can excite the system over a higher range of frequencies which is difficult to attain by sinusoidal forcings because of the limitation of signal-to-noise ratio of measurements.…”

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confidence: 99%

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Cardiorespiratory dynamics during sinusoidal and impulse exercise in man.

Miyamoto

Nakazono

et al. 1983

Jpn.J.Physiol

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Dynamic characteristics of ventilation, cardiac output, and gas exchange during sinusoidally varying work rates for the periods from 1 to 12 min and impulse work rate with a duration of 10 sec were studied on five healthy men in an upright position. Changes in work rate were given by controlling externally the electromagnetic braking system of a bicycle ergometer. Stroke volume, heart rate, and cardiac output during exercise were determined continuously by using an automated impedance cardiograph. Breath by breath determination in minute ventilation, respiratory frequency, tidal volume, oxygen consumption, carbon dioxide output, end-tidal pressures of oxygen and carbon dioxide, and gas exchange ratio were conducted. From these and steady-state response data amplitude and phase relations between each variable and the input work loads were obtained utilizing the frequency analysis techniques. The response characteristics to sinusoidal stimuli were well represented by first-order models with time constants for VE, Vcoz, V o ,, and Q averaging 75, 67, 52, and 36 sec, respectively. The kinetics of HR closely resembled that of Q. There was a close link between both the dynamics of VE and Vco 2. On the other hand, the responses to impulse stimuli were better described by second-order models in which fast and slow response components were connected in parallel. However, the contribution of the fast component to total response was small. Although this response may support in its form the neurohumoral concept to explain exercise hyperpnea, a tight linkage was observed between VE and VCO2 responses to impulse stimuli. Thus, hyperpnea during the unsteady-state of exercise may be explained by the cardiodynamic hypothesis.

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Section: Methodssupporting

confidence: 69%

mentioning

confidence: 99%

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confidence: 99%

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Cardiorespiratory dynamics during sinusoidal and impulse exercise in man.

Miyamoto

Nakazono

et al. 1983

Jpn.J.Physiol

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“…A similar approach has been used to determine the dynamics of pulmonary gas exchange, namely, oxygen uptake (V O 2 ) and carbon dioxide excretion (V CO 2 ). TheV O 2 andV CO 2 responses to a constant moderate work load follow a pattern similar to that ofV E but with faster phase II kinetics of 30 to 35 s forV O 2 and 40 to 50 s forV CO 2 (37,63,66,343). Likė V E , theV O 2 andV O 2 time constants lengthen during heavy exercise and a steady state is never achieved.…”

Section: Characteristics Of the Exercise Hyperpneamentioning

confidence: 68%

“…4A), (37,63,66,343,347). The steady state is achieved within 3 min during light or moderate levels of exercise.…”

Section: Characteristics Of the Exercise Hyperpneamentioning

confidence: 99%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.

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Exercise Hyperpnea

Ward

2006

Wiley Encyclopedia of Biomedical Engineering

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Control schemes of ventilation during moderate exercise [i.e., below the lactate threshold ( θ L )] have classically incorporated both proportional humoral feedback (carotid and central chemoreflex) and neurogenic feed forward (central command, muscle, cardiocirculatory) to provide stability of arterial PCO 2 (PaCO 2 ) pH (pHa), and PO 2 (PaO 2 ). In response to a step work‐rate (WR) forcing from prior rest in the upright posture, increases abruptly for some 15–20 s, this being followed by a subsequent more‐prominent exponential component (consistent with first‐order kinetics). The lack of any sustained error signals in the mean levels of PaCO 2 , pHa, or PaO 2 , coupled with the dynamic matching of with pulmonary CO 2 output but not O 2 uptake or WR, suggests that the controller operates as if it incorporates an errorless humoral feedback element proportional to (or some close proxy). In addition, the controller seems to evidence considerable redundancy, with particular sensory deficits having little effect on the steady‐state response to exercise or the stability of PaCO 2 between rest and exercise. Above θ L , kinetics become markedly nonlinear, with steady states being either delayed or not attained, which reflects the influence of the developing metabolic acidemia (1) indirectly, via bicarbonate‐mediated body CO 2 stores washout, which augments ; and (2) directly, to effect respiratory compensation for the falling pHa (this being constrained by the falling PaCO 2 that results from increasing out of proportion to ). The carotid bodies are important in mediating this respiratory compensation, although with surprisingly slow kinetics, In conclusion, despite there now being general agreement regarding the overall characteristics of the response to exercise, the precise details of the control process(es) remain unresolved.

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Dynamics of ventilatory response to exercise in humans

Cited by 48 publications

References 0 publications

Cardiorespiratory dynamics during sinusoidal and impulse exercise in man.

Cardiorespiratory dynamics during sinusoidal and impulse exercise in man.

Control of Breathing During Exercise

Exercise Hyperpnea

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