Abstract
31P magnetic resonance spectroscopy (31P MRS) and near-infrared spectroscopy (NIRS) are combined to study interactions between oxidative ATP synthesis rate, perturbation of the creatine kinase equilibrium, and cellular oxygenation state in calf muscle of normal subjects and patients with muscle perfusion impaired by peripheral vascular disease.
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Chance B., J.S. Leigh Jr, B.J. Clark, J. Maris, J. Kent, S. Nioka & D. Smith. 1985. Control of oxidative metabolism and oxygen delivery in human skeletal muscle: a steady state analysis of the work/energy cost transfer function. Proc. Natl. Acad. Sci. USA 82: 8384–8388.
Conley, K.E., M.J. Kushmerick & S.A. Jubrias. 1998. Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo. J. Physiol. 511: 935–945.
Duhaylongsod, F.G., J.A. Greibel, D.S. Bacon, W.G. Wolfe & C.A. Piantadosi. 1993. Effects of muscle contraction on cytochrome a,a3 redox state. J. Appl. Physiol. 75: 790–797.
Harkema, S.J. & R.A. Meyer. 1997. Effect of acidosis on control of respiration in skeletal muscle. Am. J. Physiol. 272: C491-C500.
Haseler, L.J., M.C Hogan & R.S. Richardson. 1999. Skeletal muscle phosphocreatine recovery in exercise-trained humans is dependent on O2 availability. J. Appl. Physiol. 86: 2013–2018.
Hogan, M.C., R.S. Richardson & L.J. Haseler. 1999. Human muscle performance and PCr hydrolysis with varied inspired oxygen fractions: a 31P MRS study. J. Appl. Physiol. 86: 1367–1373.
Jeneson, J.A.L., H.V. Westerhoff & M.J. Kushmerick. 2000. A metabolic control analysis of kinetic controls in ATP free energy metabolism in contracting skeletal muscle. Am. J. Physiol. 279: C813-C832.
Jeneson, J.A.L., R.W. Wiseman, H.V. Westerhoff & M.J. Kushmerick, 1996. The signal transduction function for oxidative phosphorylation is at least second order in ADP. J. Biol. Chem. 271: 27995–27998.
Kemp, G.J. 1994. Interactions of mitochondrial ATP synthesis and the creatine kinase equilibrium in skeletal muscle. J. Theor. Biol. 170: 239–246.
Kemp, G.J. 2000. Studying metabolic regulation in human muscle. Biochem. Soc. Trans. 28: 100–103.
Kemp, G.J., D.J. Taylor & G.K. Radda. 1993. Control of phosphocreatine resynthesis during recovery from exercise in human skeletal muscle. NMR in Biomed. 6: 302–310.
Kemp, G.J., N. Roberts, W.E. Bimson, A. Bakran, P.L. Harris, G.L. Gilling-Smith, J. Brennan, A. Rankin & S.P. Frostick. 2001. Mitochondrial function and oxygen supply in normal and in chronically ischaemic muscle: a combined 31P magnetic resonance spectroscopy and near infra-red spectroscopy study in vivo. J. Vasc. Surg. 34: 1103–1110.
Korzeniewski B. 1998. Regulation of ATP supply during muscle contraction: theoretical studies. Biochem. J. 330: 1189–1195.
Meyer, R.A. 1988. A linear model of muscle respiration explains monoexponential phosphocreatine changes. Am. J. Physiol. 254: C548-C553.
Paganini, A.T., J.M. Foley & R.A. Meyer. 1997. Linear dependence of muscle phosphocreatine kinetics on oxidative capacity. Am. J. Physiol. 272: C501-C510.
Richardson, R.S. 1999. What governs skeletal muscle VO2max? New evidence. Med. Sci. Sports Exerc. 32: 100–107.
Richardson, R.S., J.S. Leigh, Jr., P.D. Wagner & E.A. Noyszewski. 1999. Cellular PO2 as a determinant of maximal mitochondrial O2 consumption in trained human skeletal muscle. J. Appl. Physiol. 87: 325–331.
Tran, T.K., N. Sailasuta, U. Kreutzer, R. Hurd, Y. Chung, P. Mole, S. Kuno & T. Jue. 1999. Comparative analysis of NMR and NIRS measurements of intracellular PO2 in human skeletal muscle. Am. J. Physiol. 276: R1682-R1690.
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Kemp, G., Roberts, N., Bimson, W. et al. Muscle Oxygenation and ATP Turnover When Blood Flow is Impaired by Vascular Disease. Mol Biol Rep 29, 187–191 (2002). https://doi.org/10.1023/A:1020325812680
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DOI: https://doi.org/10.1023/A:1020325812680