Abstract
In some organisms and cells, oxygen availability influences oxygen consumption. In this review, we examine this phenomenon of hypoxic hypometabolism (HH), discussing its features, mechanisms, and implications. Small mammals and other vertebrate species exhibit “oxyconformism,” a downregulation of metabolic rate and body temperature during hypoxia which is sensed by the central nervous system. Smaller body mass and cooler ambient temperature contribute to a high metabolic rate in mammals. It is this hypermetabolic state that is suppressed by hypoxia leading to HH. Larger mammals including humans do not exhibit HH. Tissues and cells also exhibit reductions in respiration during hypoxia in vitro, even at oxygen levels ample for mitochondrial oxidative phosphorylation. The mechanisms of cellular HH involve intracellular oxygen sensors including hypoxia-inducible factors, AMP-activated protein kinase (AMPK), and mitochondrial reactive oxygen species (ROS) which downregulate mitochondrial activity and ATP utilization. HH has a profound impact on cardiovascular, respiratory, and metabolic physiology in rodents. Therefore, caution should be exercised when extrapolating the results of rodent hypoxia studies to human physiology.
Highlights
Hypoxia is defined as reduced oxygen (O2) in the environment or in an organism [1]
The thermoneutral zone (TNZ) is the range of ambient temperatures where basal metabolic rate (BMR) is determined, since thermogenic energy expenditure is at a minimum [13]
“room temperature” (22◦C) approximates the TNZ for clothed humans but is far below TNZ for mice; the metabolic rate of a mice housed at 22◦C will be 50% above its BMR [13]
Summary
Small mammals and other vertebrate species exhibit “oxyconformism,” a downregulation of metabolic rate and body temperature during hypoxia which is sensed by the central nervous system. Smaller body mass and cooler ambient temperature contribute to a high metabolic rate in mammals. It is this hypermetabolic state that is suppressed by hypoxia leading to HH. Larger mammals including humans do not exhibit HH. The mechanisms of cellular HH involve intracellular oxygen sensors including hypoxia-inducible factors, AMP-activated protein kinase (AMPK), and mitochondrial reactive oxygen species (ROS) which downregulate mitochondrial activity and ATP utilization. Caution should be exercised when extrapolating the results of rodent hypoxia studies to human physiology
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
