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J Appl Physiol (1985). 2019 Oct 24. doi: 10.1152/japplphysiol.00569.2019. [Epub ahead of print]

Dissociating the effects of oxygen pressure and content on the control of breathing and acute hypoxic response.

Author information

1
Department of Kinesiology, University of Waterloo, Canada.
2
Department of Anesthesia and Perioperative Medicine, Mayo Clinic, United States.
3
Department of Anesthesiology, Mayo Clinic, United States.
4
Department of Cardiovascular Diseases, Mayo Clinic, United States.
5
Department of Cardiovascular Disease, Mayo Clinic, United States.
6
Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, United States.
7
Departments of Anesthesiology and Perioperative Medicine, Mayo Clinic, United States.
8
Department of Laboratory Medicine and Pathology, Mayo Clinic, United States.
9
School of Health and Exercise Science, University of British Columbia, Canada.

Abstract

Arterial oxygen tension and oxyhemoglobin saturation (SaO2) decrease in parallel during hypoxia. Distinguishing between changes in oxygen tension and oxygen content as the relevant physiological stimulus for cardiorespiratory alterations remains challenging. To overcome this, we recruited nine individuals with hemoglobinopathy manifesting as high-affinity hemoglobin (HAH) (partial pressure at 50% SaO2 (P50)= 16±0.4 mmHg) causing greater SaO2at a given oxygen partial pressure compared to control subjects (n=12, P50=26±0.4 mmHg). We assessed ventilatory and cardiovascular responses to acute isocapnic hypoxia, iso-oxic hypercapnia and twenty minutes of isocapnic hypoxia (arterial PO2=50 mmHg). Blood gas alterations were achieved with dynamic end-tidal forcing. When expressed as a function of the logarithm of oxygen partial pressure, ventilatory sensitivity to hypoxia was not different between groups. However, there was a significant difference when expressed as a function of SaO2. Conversely, the rise in heart rate was blunted in HAH subjects when expressed as a function of partial pressure, but similar when expressed as a function of SaO2. Ventilatory sensitivity to hypercapnia was not different between groups. During sustained isocapnic hypoxia, the rise in minute ventilation was similar between groups; however heart rate was significantly greater in the controls during minutes three to nine of exposure. Our results support the notion that oxygen tension, not content, alters cellular PO2 in the chemosensors and drives the hypoxic ventilatory response. Our study suggests that in addition to oxygen partial pressure, oxygen content may also influence the heart rate response to hypoxia.

KEYWORDS:

heart rate; high affinity hemoglobin; ventilation

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