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Plasma catecholamines in exercise induced bronchoconstriction.

M Beil, H M Brecht, B Rasche

    Klinische Wochenschrift
    |June 15, 1977
    PubMed
    Summary
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    In patients with asthma, enhanced sympathetic activity during exercise does not directly cause exercise-induced bronchoconstriction (EIB). Plasma levels of nor-epinephrine (NE) and epinephrine (E) were analyzed in relation to EIB.

    Area of Science:

    • Cardiovascular Physiology
    • Respiratory Medicine
    • Neuroendocrinology

    Background:

    • Exercise-induced bronchoconstriction (EIB) is a common condition in asthma.
    • The role of sympathetic nervous system activity, specifically plasma catecholamines like nor-epinephrine (NE) and epinephrine (E), in EIB is not fully understood.

    Purpose of the Study:

    • To investigate plasma NE and E levels at rest and post-exercise in patients with asthma experiencing EIB.
    • To determine if enhanced sympathetic activity, indicated by NE and E levels, correlates with the severity of EIB.
    • To explore the potential involvement of adrenergic pathways in EIB.

    Main Methods:

    • Measurement of plasma NE and E levels at rest and immediately after exercise in 8 asthma patients and 7 healthy controls.

    Related Experiment Videos

  • Assessment of airway resistance before and after exercise.
  • Pharmacological blockade using phentolamine (alpha-adrenergic antagonist) and propranolol (beta-adrenergic antagonist) to elucidate adrenergic receptor involvement.

    • Main Results:

    • Asthma patients showed significantly higher increases in plasma NE post-exercise compared to controls, even after alpha-adrenergic blockade.
    • Plasma E levels did not differ significantly between groups or change notably with exercise, except in controls after beta-blockade.
    • No significant correlation was found between plasma NE levels and the degree of exercise-induced airway resistance increase.

    Conclusions:

    • Sympathetic nervous system activity appears enhanced during exercise in asthma patients.
    • The provocation of EIB in asthma is unlikely to be directly mediated by elevated plasma NE levels.
    • Adrenergic mechanisms, potentially involving pathways beyond simple NE increases, may play a role in EIB.