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I am trying to understand why a cell might have minimal respiratory reserve capacity in the presence of unlimited substrate supply. This essentially means that the oxygen consumption rate (OCR) of the cell does not increase from its basal rate when oxidative phosphorylation is uncoupled — i.e. the reactions of the electron transport chain are uncoupled from ATP synthesis. What factors might conspire to cause this? I am thinking specifically of the photoreceptors1. I am interested in all logical possibilities here e.g.

(1) mitochondrial ATP production is barely meeting demands at basal level.

(2) oxidative phosphorylation may already be physiologically uncoupled.

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  • $\begingroup$ Is this a question about trouble shooting an experiment, or a theoretical question? $\endgroup$ – De Novo Jan 20 at 13:18
  • $\begingroup$ Welcome to SE Biology. I assume that you are trying to understand the results in the paper you cite. I do not wish to be discouraging, but few people will read that paper (questions here should be self-contained), and the key term it uses — respiratory reserve capacity — is one that I, as a biochemist, am unfamiliar with, and find difficult to understand from a brief perusal of the paper. If you understand it yourself it would be helpful if you could edit your question to expain it. $\endgroup$ – David Jan 20 at 14:30
  • $\begingroup$ Thanks for the responses. It's a theoretical question, the answer to which I was hoping might shed some light on the Warburg effect in the retina. I have some experience with metabolic assays but was hoping someone more experienced might be able to enlighten me. $\endgroup$ – Rob Casson Jan 21 at 10:08

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