What question did this study set out to answer?

To determine whether beta-adrenergic stimulation or parasympathetic withdrawal mediates the elevation in heart rate and cardiac output observed during hypoxic exercise in humans.

May 27, 2003The Journal of PhysiologyOpen Access

β‐Adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans

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Why the study?

Does beta-adrenergic or parasympathetic inhibition alter the increase in heart rate and cardiac output during acute hypoxic exercise in healthy humans?

Population

6 healthy subjects (5 male, 1 female), mean age 31.7 +/- 1.6 years

Comparison

Exercise during acute hypoxia with… vs Exercise during normoxia and control condition

Design

Other

Authors

SHSusan R. HopkinsUniversity of California, San Diego HBHarm Jan BogaardHeart Failure & Transplant KNKyuichi NiizekiYamagata University

Discussion

Member takes

Implication

Hypothesis-generating for non-autonomic drivers of HR and Qt in hypoxia; should not yet alter clinical practice or guidelines.

Key Points

To determine whether beta-adrenergic stimulation or parasympathetic withdrawal mediates the elevation in heart rate and cardiac output observed during hypoxic exercise in humans.
Assessed six healthy adults (5 male, 1 female; mean age 31.7 ± 1.6 years) during progressive exercise to maximal oxygen consumption under normoxia and acute hypoxia (fraction of inspired oxygen = 0.125).
Tested participants on separate days across three conditions: unblocked control, beta-adrenergic blockade via 8.0 mg intravenous propranolol, and parasympathetic blockade via 0.8 mg intravenous glycopyrrolate.
Measured cardiac output using open-circuit acetylene uptake alongside heart rate, oxygen consumption, and venous catecholamine concentrations.
Hypoxia significantly elevated venous adrenaline (P < 0.05) and noradrenaline (P < 0.01) at a given oxygen consumption, while dopamine concentrations remained unchanged (P = 0.2).
Heart rate and cardiac output relative to oxygen uptake increased significantly during hypoxia across all three conditions: control, propranolol, and glycopyrrolate (P < 0.05 for each).
The hypoxic increases in heart rate and cardiac output did not differ significantly from control conditions following either beta-adrenergic or parasympathetic inhibition.

Structured PICO

Does beta-adrenergic or parasympathetic inhibition alter the increase in heart rate and cardiac output during acute hypoxic exercise in healthy humans?

Population

6 healthy subjects (5 male, 1 female), mean age 31.7 +/- 1.6 years

Intervention

Exercise during acute hypoxia (inspired oxygen fraction=0.125) with beta-sympathetic inhibition (8.0 mg propranolol i.v.) or parasympathetic inhibition (0.8 mg glycopyrrolate i.v.)

Comparator

Exercise during normoxia and control condition (no autonomic blockade)

Outcome

Heart rate (HR) and cardiac output (Qt) at a given oxygen consumption (VO2)surrogate

The hypoxia-induced increase in heart rate and cardiac output during exercise does not require intact cardiac muscarinic or beta-adrenergic receptors.

Cite This Study

Hopkins et al. (2003) studied this question.

synapsesocial.com/papers/6a8157a1176d2ce03166186f https://doi.org/10.1113/jphysiol.2003.040568

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β‐Adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

β‐Adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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