Journal of Applied Physiology
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J Appl Physiol (January 18, 2002). doi:10.1152/japplphysiol.01132.2001
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Articles in PresS, published online ahead of print January 18, 2002
J Appl Physiol, 10.1152/jap.01132.2001
Submitted on November 13, 2001
Accepted on January 12, 2002

Increased concentrations of Pi and lactic acid reduce creatine stimulated respiration in muscle fibers

Brandon Walsh1, Toomas Tiivel2, Michail Tonkonogi1, and Kent Sahlin1*

1 Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Institute of Chemical Physics and Biophysics, Tallin, Estonia
2 Department of Sport and Health Science, Stockholm University College of Physical Education and Sports, Stockholm, Sweden

* To whom correspondence should be addressed. E-mail: kent.sahlin{at}fyfa.ki.se.

We tested the hypothesis that the respiratory function in skeletal muscle mitochondria is impaired by lactic acidosis and elevated concentrations of inorganic phosphate (Pi). The respiration of chemically skinned fiber bundles from rat soleus muscle was measured at [Pi] and pH similar to those at rest (3 mM Pi, pH 7.0) and high intensity (HI) exercise (20 mM Pi, pH 6.6). Respiration was measured in the absence of ADP (V0) and after sequential additions of 0.1 mM ADP (Vsubmax), 20 mM creatine (Cr; Vcreatine), and 4 mM ADP (Vmax). Cr increased submaximally [ADP] stimulated respiration in all conditions but Vcreatine was 23% lower (P<0.05) during HI conditions than during resting conditions. Vcreatine was also reduced when Pi or H+ were increased separately (P<0.05). V0, Vsubmax, and Vmax were not affected by changes in [Pi] or [H+]. The response was similar irrespective of when acidosis was induced (i.e. quiescent or actively respiring mitochondria). In conclusion, Cr stimulated respiration is impaired by increases in [H+] and [Pi] corresponding to those in exercising muscle. Although the reduced Cr stimulated respiration could be compensated for by increased [ADP] this might have implications on intracellular homeostasis.




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