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First published online July 6, 2005
Journal of Experimental Biology 208, 2641-2652 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01686
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Does intracellular metabolite diffusion limit post-contractile recovery in burst locomotor muscle?

Stephen T. Kinsey1,*, Pragyansri Pathi2, Kristin M. Hardy1, Amanda Jordan2 and Bruce R. Locke2

1 Department of Biology and Marine Biology, University of North Carolina Wilmington, 601 South College Road, Wilmington, NC 28403-5915, USA
2 Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Tallahassee, FL 32310-6046, USA



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Fig. 1. Representative 31P-NMR spectra collected from perchloric acid extracts of large light levator muscle fibers that demonstrate the changes in relative concentrations of AP and Pi during a contraction–recovery cycle. Spectra were collected from crabs at rest and after 0, 30 and 60 min of recovery from burst exercise. Chemical shifts are in units of parts per million.

 


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Fig. 2. Relative changes in (A) AP and (B) Pi concentrations in small (filled symbols) and large (open symbols) light levator fibers during a contraction–recovery cycle. N≥5 for every point.

 


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Fig. 3. Model output for small (A,C) and large (B,D) light levator fibers using parameters in Table 1. The small fibers were modeled assuming a uniform distribution of mitochondria, while the large fibers were modeled assuming only subsarcolemmal mitochondria (Boyle et al., 2003Go). The temporally and spatially resolved concentrations of AP and ATP during a contraction–recovery cycle are shown. The arrows indicate where mild gradients exist in the large fibers. For AP, the gradients are not obvious due to the scaling of the concentration axis, but they are of a magnitude similar to that seen in ATP. ADP, Arginine and Pi are not shown, but the concentrations change in reciprocal fashion to that of AP.

 


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Fig. 4. Measured AP recovery (symbols) compared with the volume-averaged model of AP recovery (solid line) in small (A) and large (B) fibers. The measured AP data have been normalized to a resting concentration of 34.3 mmol l–1 to coincide with that of the model. In the model, the myosin ATPase was activated long enough to cause a decrease in AP that was comparable to the measured data. The dotted line indicates the resting concentration.

 


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Fig. 5. The effect of increasing the rate of mitochondrial ATP production in large fibers on the temporal and spatial concentration profiles of AP (left panels) and ATP (right panels). All parameters are the same as in Fig. 3B,D, except that the Vm,mito has been increased over the value used in Fig. 3 by 2-fold (A), 10-fold (B) and 100-fold (C).

 





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