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Related Experiment Videos

Ventilatory control during exercise in calves with artificial hearts.

A Huszczuk1, B J Whipp, T D Adams

  • 1Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance 90509.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 1, 1990
PubMed
Summary

Cardiac reflexes do not cause exercise hyperpnea (increased breathing). Artificial hearts in calves showed ventilation matched metabolic needs, even when cardiac output was altered, refuting cardiac reflex involvement.

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Area of Science:

  • Physiology
  • Exercise Physiology
  • Cardiovascular Physiology

Background:

  • Exercise hyperpnea, the increase in ventilation during exercise, is essential for meeting metabolic demands.
  • The precise mechanisms triggering exercise hyperpnea, including the role of cardiac reflexes, remain incompletely understood.
  • Previous hypotheses suggested that increased cardiac output during exercise might stimulate cardiac receptors, leading to augmented ventilation.

Purpose of the Study:

  • To investigate the role of cardiac reflexes in mediating exercise hyperpnea.
  • To determine if changes in cardiac output directly influence ventilation during exercise.
  • To elucidate the relationship between cardiac function and respiratory regulation during physical exertion.

Main Methods:

  • Utilized treadmill exercise protocols in calves equipped with artificial hearts (n=7) and compared them to control calves (n=7).

Related Experiment Videos

  • Monitored ventilatory responses, arterial blood gases (PCO2, PO2), blood lactate levels, and cardiac output.
  • Experimentally manipulated cardiac output in calves with artificial hearts to assess its impact on exercise hyperpnea.

    • Main Results:

    • Calves with artificial hearts maintained adequate ventilation for metabolic demands, regulating arterial PCO2 and pH despite absent cardiac output increase.
    • Experimental increases in cardiac output in implanted calves did not affect ventilation.
    • Experimental decreases in cardiac output significantly augmented exercise hyperpnea and increased blood lactate, while decreasing oxygen consumption.

    Conclusions:

    • Cardiac reflexes, mediated by increased cardiac output, are not the obligatory cause of exercise hyperpnea in calves.
    • Ventilatory control during exercise is not solely dependent on cardiac output-related feedback mechanisms.
    • These findings challenge the traditional understanding of cardiovascular influences on respiratory regulation during exercise.