The Validity of the Cardiodynamic Hypothesis for Exercise Hyperpnea in Man

Miyamoto, Yuri; Niizeki, Kyuichi; Sugawara, T.; Nakazono, Yoshimi; Kikuchi, Kôichi; Mussell, M. J.

doi:10.1007/978-1-4613-0529-3_5

Cited by 2 publications

(3 citation statements)

References 22 publications

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“…These tendencies were observed in passive movement, supporting the idea of Miyamoto et al (1982), who concluded that the cardiodynamic process could be ruled out as the origin of the initial ventilatory response and, instead, that other neurogenic mechanisms mediated either centrally or peripherally should be considered. Recent ®ndings made by simultaneous measurement of c and E at the onset of exercise are strongly against the concept that ventilation in phase I is causally linked to right ventricular output, while the cardiodynamic theory may be valid in the latter part of phase I, or in phase II and phase III (Banner et al 1988;Miyamoto et al 1989;Morikawa et al 1989;Pokoroski et al 1990). However, whether the similarity in the pattern of ventilatory and cardiovascular changes is linked to hyperpnoea in phase I remains to be resolved, as reported by Whipp and Ward (1991).…”

Section: Discussionmentioning

confidence: 96%

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

Miyamura

Ishida

Hashimoto

et al. 1997

European Journal of Applied Physiology

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The present study was performed to examine whether or not the ventilatory response at the onset of voluntary exercise and passive movement in endurance runners is the same as in untrained subjects. Twelve long-distance runners belonging to the varsity athletic club and 13 untrained subjects of our university participated as subjects in this study. Maximum oxygen uptake was significantly higher in the endurance runner group [mean (SD) 70.8 (4.7) ml.kg-1.min-1] than in the untrained group [49.8 (6.3) ml.kg-1.min-1]. Cardiorespiratory responses during voluntary exercise and passive movement of alternate flexion-extension of the right and left legs for about 15 s at a frequency of about 60 rpm, were determined by means of breath-by-breath techniques. Minute inspiratory ventilation (VI), tidal volume (VT), respiratory frequency (fb), cardiac output (Qc), stroke volume (SV) and heart rate (HR) increased significantly immediately at the onset of voluntary exercise and passive movement. The incremental rate for VI was greater than that for Qc. Average values and standard deviations of changes in VI were calculated as the difference between the mean of the first and second breath and the mean of five breaths preceding the exercise or movement. The rates obtained in voluntary exercise and passive movement in the endurance runner group [2.34 (0.82) and 1.72 (0.71 l.min-1), respectively] were significantly (P < 0.05) lower than those in the untrained group [4.16 (2.66) and 2.71 (1.56 l.min-1), respectively]. Also changes in VT and HR were significantly lower in the endurance group than in the untrained group with regard to both voluntary exercise and passive movement. The results suggest that the magnitude of cardiorespiratory responses at the onset of voluntary exercise and passive movement in humans is influenced by chronic endurance training for long periods.

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Section: Discussionmentioning

confidence: 96%

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

Miyamura

Ishida

Hashimoto

et al. 1997

European Journal of Applied Physiology

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“…Humoral and cardiac factors related to exercise hyperpnea Figure 2 shows the relationships between VE and each of PETC0 2, Q, C02 flow (Qco2 = Q times CvC02), and Vco2 obtained from healthy subjects during the steadystates of mild to moderate exercise [42]. Q and CvC02 were determined using a new rebreathing method developed by MocHIzu I et al [44].…”

mentioning

confidence: 99%

“…[1] and MIYAMOTO et al [42] observed in humans that the ventilatory responses start to increase before appreciable changes in Q occur. The phenomenon should rather be ascribed to certain neural factors, probably mediated from the cerebral cortex, since it has been reported that the phase I response disappears in decerebrated animals [30], in electrically induced exercise [14,61] (but see [26]), and diminishes in amplitude when exercise is started from a low level of basal exercise [63].…”

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confidence: 99%

Neural and humoral factors affecting ventilatory response during exercise.

Miyamoto¹

1989

Jpn.J.Physiol

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The principle of feedback control is thought to be fundamental for maintaining homeostasis in biological systems. In the respiratory system, constancy of arterial Pcoz, Poz, and pH is also maintained essentially by means of a feedback control system. For the sake of simplicity, let's assume that the respiratory system is regulated by only one controlled variable, Pa~oz. According to control theory, the basic structure of a feedback control system may be represented by two components, a controller and a controlled system (plant) as shown in Fig. 1 a. The controller of the respiratory system consists of the medullary respiratory center, central and peripheral chemoreceptors and related sensory and motor nerve systems. The controlled system is the lung gas exchanger in which numerous alveoli, conductive airways, pulmonary capillaries, and respiratory muscles in the chest wall and the diaphragm are involved. The purpose of the respiratory feedback system is to keep the output of the controlled system, i.e. the controlled variable, within a relatively narrow range around the desired value or set point under any conditions. When CO2 is fed into the gas exchanger in excess of its resting level, the first step to take place in the respiratory system is the measurement of the controlled variable, Pa~oz, by means of the central and/or peripheral chemoreceptors. The measured value is then compared with the desired Pa~oz, and the controller generates a signal proportional to the difference between the measured and desired values of Pa~oz (error signal),which causes ventilation to increase. As a result of hyperpnea, excess CO2 accumulated in the lung gas exchanger is excreted, and Pa~oz returns to its initial level. Feedback control of the respiratory system has been well established as valid when CO2 is inhaled via the airways. However, it is difficult to explain ventilatory responses to exercise by the feedback principle, since during exercise below the anaerobic threshold, appreciable changes are observed neither in arterial Pa~oz nor in pH. Obviously, error-free control operates when metabolic CO2 is assumed to be a disturbance. In view of this, as noted by DEFARES [18], respiratory control during exercise has long been regarded as "forbidden territory"

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The Validity of the Cardiodynamic Hypothesis for Exercise Hyperpnea in Man

Cited by 2 publications

References 22 publications

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

Neural and humoral factors affecting ventilatory response during exercise.

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