Respiratory Control During Exercise

Wasserman, Karlman; Whipp, Brian J.; Casaburi, Richard

doi:10.1002/cphy.cp030217

Cited by 98 publications

(97 citation statements)

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“…They assumed that this process might be involved in the mechanism eliciting the very early ventilatory response at the onset of exercise (phase I). A close linkage between the kinetics of Q and VE during the early period of exercise onset can be expected from the observation showing a constancy in both PETco2 and gas exchange ratio during this period [57]. However, direct measurement of Pa~o2 in humans has demonstrated slight hypocapnia in rest-to-exercise transitions [22].…”

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confidence: 79%

“…HUMORAL STIMULI FOR EXERCISE HYPERPNEA Cardiodynamic hyperpnea WASSERMAN et al [57,59] postulated that C02 flow from venous blood to the lungs, i.e. the product of cardiac output (Q) and mixed venous C02 content (Cvc02), is a prime determinant of hyperpnea during exercise.…”

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confidence: 99%

“…The impedance technique has recently been proved to be valid as an appropriate method for estimating stroke volume during exercise in comparison with dilution [45] and C02 rebreathing methods [19]. Although the mechanism linking C02 flow to the ventilatory response is unsettled, WASSERMAN et al [57] seemed to assume a mechanism based on a feedback principle, in which the respiratory controller is thought to track the PaC02 error signal continually.…”

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confidence: 99%

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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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Neural and humoral factors affecting ventilatory response during exercise.

Miyamoto¹

1989

Jpn.J.Physiol

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“…2e of Cunningham et al 1986). This is also the case when minute ventilation is measured at the start of exercise (Wasserman et al 1986;Duffin & McAvoy, 1988), when temperature has not yet risen detectably, and is also the case when attempts are made to simulate the increase in COµ production with venous COµ loading at constant temperature in rats (Yamamoto & Edwards, 1960), dogs (Stremel et al 1978) and sheep (Phillipson et al 1981). Thus the line shifts upwards but in parallel on the ventilation axis and the intercept on the Pa,COµ axis (the apnoeic threshold) falls to a lower Pa,COµ level.…”

Section: Surgical Preparationmentioning

confidence: 99%

A Respiratory Drive in Addition to the Increase in Co₂ Production at Raised Body Temperature in Rats

Boden

Harris

Parkes

2000

Experimental Physiology

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Mammals that use the ventilatory system as the principal means of increasing heat loss, i.e. that pant, show two fundamental changes in the control of breathing at raised temperatures. First, alveolar ventilation increases by more than, rather than in proportion to, the increase in CO2 production. Second, hypocapnia no longer causes apnoea. Rats do not use the ventilatory system as the principal means of increasing heat loss, so we have investigated whether rats also show these two changes at raised temperatures. Breathing was detected from diaphragmatic electromyogram (EMG) activity. Anaesthesia and hyperoxia were used to minimise behavioural and hypoxic drives to ventilation and arterial PCO2 (Pa,CO2) was controlled using mechanical ventilation. At 36.6 ± 0.1 °C, breathing was absent as long as Pa,CO2 was held below a threshold level of 32.9 ± 0.7 mm Hg (n= 14) under steady‐state conditions. When body temperature in rats was raised above 37 °C, both fundamental changes in the control of breathing became apparent. First, at 39 °C the mean Pa,CO2 level during spontaneous breathing (39.6 ± 5.4 mm Hg, n= 4) fell by 3.9 ± 1.4 mm Hg (P < 0.05, Student's paired t test). Second, at 39.9 ± 0.1 °C breathing was present when mean Pa,CO2 levels were only 18.2 ± 1.5 mm Hg (n= 14), the lowest mean Pa,CO2 level we could achieve with mechanical ventilation. We calculate, however, that at 39.9 °C, the drive to breathe from the increased CO2 production alone would not sustain breathing below a Pa,CO2 level of 27.8 ± 1.4 mm Hg (n= 13). In rats at raised body temperatures therefore a respiratory drive exists that is in addition to that related to the increase in CO2 production.

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“…This hyperventilatory response is considered to be respiratory compensation to minimize a decrease in blood pH (Kowalchuk et al 1988;Rausch et al 1991;Ward 2007;Wasserman et al 1986;Yunoki et al 1999), and the decrease in blood pH per se has been regarded as an important factor enhancing ventilation during exercise above the lactate threshold (Stringer et al 1992;Wasserman et al 1975). However, by using a glycogen-reduction procedure (Gollnick et al 1974;Heigenhauser et al 1983; Sabapathy et al 2006), which can manipulate the degree of metabolic acidosis, we found that hyperventilatory response to IE is not dependent on blood pH but is associated with effort sense of exercising muscle (Yamanaka et al 2011;Yamanaka et al 2012).…”

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confidence: 99%

Relationship between motor corticospinal excitability and ventilatory response during intense exercise

et al. 2016

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2 Abstract PurposeEffort sense has been suggested to be involved in the hyperventilatory response during intense exercise (IE). However, the mechanism by which effort sense induces an increase in ventilation during IE has not been fully elucidated. The aim of this study was to determine the relationship between effort-mediated ventilatory response and corticospinal excitability of lower limb muscle during IE. MethodsEight subjects performed 3 min of cycling exercise at 75-85% of maximum workload twice (IE 1st and IE 2nd ). IE 2nd was performed after 60 min of resting recovery following 45 min of submaximal cycling exercise at the workload corresponding to ventilatory threshold. Vastus lateralis muscle response to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs), effort sense of legs (ESL, Borg 0-10 scale), and ventilatory response were measured during the two IEs. ResultsThe slope of ventilation (l/min) against CO 2 output (l/min) during IE 2nd (28.0 ± 5.6) was significantly greater than that (25.1 ± 5.5) during IE 1st . Mean ESL during IE was significantly higher in IE 2nd (5.25 ± 0.89) than in IE 1st (4.67 ± 0.62). Mean MEP (normalized to maximal M-wave) during IE was significantly lower in IE 2nd (66 ± 22%) than in IE 1st (77 ± 24%). The difference in mean ESL between the two IEs was significantly (p < 0.05, r = -0.82) correlated with the difference in mean MEP between the two IEs. ConclusionsThe findings suggest that effort-mediated hyperventilatory response to IE may be associated with a decrease in corticospinal excitability of exercising muscle.

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Respiratory Control During Exercise

Cited by 98 publications

References 186 publications

Neural and humoral factors affecting ventilatory response during exercise.

Neural and humoral factors affecting ventilatory response during exercise.

A Respiratory Drive in Addition to the Increase in Co₂ Production at Raised Body Temperature in Rats

Relationship between motor corticospinal excitability and ventilatory response during intense exercise

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Respiratory Control During Exercise

Cited by 98 publications

References 186 publications

Neural and humoral factors affecting ventilatory response during exercise.

Neural and humoral factors affecting ventilatory response during exercise.

A Respiratory Drive in Addition to the Increase in Co2 Production at Raised Body Temperature in Rats

Relationship between motor corticospinal excitability and ventilatory response during intense exercise

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A Respiratory Drive in Addition to the Increase in Co₂ Production at Raised Body Temperature in Rats