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1 Department of Medicine, University of California San Diego, San Diego, CA, USA
2 Lab of Cardiac Energetics, National Institutes of Health/National Heart, Lung and Blood Institute, Bethesda, MD, USA
3 Light Microscopy Facility, National Institutes of Health/National Heart, Lung and Blood Institute, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: combsc{at}nhlbi.nih.gov.
The blue autofluorescence (351nm excitation, 450nm emission ) of single skeletal muscle fibers was characterized to be originating from mitochondrial NAD(P)H based on morphological and functional correlations. This fluorescence signal was used to estimate the oxygen availability to isolated single Xenopus muscle fibers during work level transitions using confocal microscopy. Fibers were stimulated to generate two contractile periods that were only different in the oxygen partial pressure of the solution perfusing the single fibers (PO2 of 30 or 0-2 Torr; pH=7.2). During contractions, mean cellular NAD(P)H increased significantly from rest in the low PO2 condition with the core (inner 10%) increasing to a greater extent than the periphery (outer 10%). Following the cessation of work, NAD(P)H decreased in a manner consistent with oxygen tensions sufficient to oxidize the surplus NAD(P)H. In contrast, NAD(P)H decreased significantly with work in 30 Torr PO2. However, the rate of NAD(P)H oxidation was slower and significantly increased with the cessation of work in the core of the fiber when compared to the peripheral region, consistent with a remaining limitation in oxygen availability. These results suggest that the blue autofluorescence signal in Xenopus skeletal muscle fibers is from mitochondrial NAD(P)H and that the rate of NAD(P)H oxidation within the cell is influenced by extracellular PO2 even at high extracellular PO2 during the contraction cycle. These results also demonstrate that although O2 availability influences the rate of NAD(P)H oxidation, it does not prevent NAD(P)H from being oxidized through the process of oxidative phosphorylation at the onset of contractions.
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