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Glucose-induced decrease in glucagon and pinephrine responses to exercise in man

H Galbo, N J Christensen, J J Holst

    Journal of Applied Physiology: Respiratory, Environmental and Exercise Physiology
    |April 1, 1977
    PubMed
    Summary

    Beta-adrenergic blockade with propranolol accelerated exercise-induced drops in blood glucose and hormone levels. Maintaining normal blood glucose during exercise blunted these hormonal responses, suggesting glucose levels significantly influence glucagon and epinephrine secretion during prolonged physical activity.

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    Area of Science:

    • Exercise Physiology
    • Endocrinology

    Background:

    • Beta-adrenergic blockade impacts metabolic and hormonal responses during exercise.
    • Understanding substrate utilization and hormonal regulation during exercise is crucial for performance and health.

    Purpose of the Study:

    • To investigate the role of beta-adrenergic blockade and glucose levels on hormonal responses and substrate metabolism during prolonged exercise.
    • To determine the influence of decreased glucose concentrations on glucagon and epinephrine secretion.

    Main Methods:

    • Seven healthy men performed incremental exercise tests to exhaustion under two conditions: with propranolol (beta-adrenergic blockade) and without drugs (control).
    • Euglycemia was maintained using glucose infusion during beta-adrenergic blockade in a subset of experiments.
    • Measurements included plasma glucose, glucagon, epinephrine, norepinephrine, insulin, lactate, alanine, glycerol, and non-esterified fatty acids (NEFA). Muscle glycogen utilization was assessed in a subgroup.

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    Main Results:

    • Propranolol accelerated the decrease in plasma glucose and increased plasma glucagon and epinephrine concentrations during exercise compared to controls.
    • Maintaining euglycemia via glucose infusion during beta-adrenergic blockade markedly reduced, but did not abolish, exercise-induced glucagon and epinephrine responses.
    • The reduction in exercise-induced glucose decline correlated with reduced glucagon and epinephrine responses.
    • Glucagon response reduction did not alter NEFA or glycerol levels, indicating glucagon is not a primary driver of lipolysis during exercise.
    • Muscle glycogen utilization tended to decrease during glucose infusion, while carbohydrate combustion and other measured metabolites remained unchanged.

    Conclusions:

    • Decreased plasma glucose concentrations significantly stimulate glucagon and epinephrine secretion during prolonged exercise in humans.
    • Beta-adrenergic blockade influences glucose homeostasis and hormonal counter-regulation during exercise.
    • Glucagon's role in lipolysis during exercise appears limited, even when its response is diminished.