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Marked reduction of forearm carbon dioxide production during states of decreased metabolism.

A F Wilson, R Jevning, S Guich

Physiology & Behavior 1987 DOI: 10.1016/0031-9384(87)90399-4 (opens in new tab)

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AI-extracted from the abstract
Characteristics Observational study Peer reviewed
Sample size 62
Population 62 subjects, 35 during transcendental meditation and 27 during unstylized rest
Intervention Transcendental meditation
Key findings During hypometabolic states the arterial-venous CO2 content difference declined and, during transcendental meditation, briefly disappeared, due to increased arterial CO2 and decreased venous CO2, with smaller opposite changes in O2 content. Respiratory quotient was low at all times and decreased during these states. The authors argue the results are consistent with the hypothesis that significant ketogenesis is induced and that fat beta-oxidation supplies energy while biochemical feedback inhibits the tricarboxylic acid cycle.

Abstract

We studied oxygen consumption, carbon dioxide production and acid/base changes in 62 subjects during two hypometabolic states (35 during transcendental mediation and 27 during unstylized rest). The results indicate that, during these hypometabolic states, arterial-venous CO2 content difference declines, and that during transcendental meditation, arterial-venous CO2 content difference briefly disappears. This change is due to both an increase of arterial CO2 content and a decrease of venous CO2 content. Similar, but opposite and smaller, changes occurred in arterial and venous O2 content. Respiratory quotient was low at all times and decreased during the hypometabolic states. These results are consistent with the hypothesis that, during hypometabolic states significant ketogenesis is induced, and provision of energy from the normally predominant process of beta-oxidation of fat becomes sufficient to provide energy for greatly reduced activity without entry of two carbon fragments into the tricarboxylic acid cycle; under these conditions, biochemical feedback mechanisms inhibit the tricarboxylic acid cycle. The net result of these metabolic changes could explain the major observations: absent carbon dioxide production while oxygen consumption declines but continues and the venous effluent contains more acid.

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