Biochemistry of exercise-induced metabolic acidosis

American Journal of Physiology - Regulatory Integrative and Comparative Physiology - Tập 287 Số 3 - Trang R502-R516 - 2004
Robert A. Robergs1, Farzenah Ghiasvand, Daryl Parker
1Exercise Science Program, Department of Physical Performance and Development, Johnson Center, Rm. B143, The University of New Mexico, Albuquerque, NM 87131-1258, USA. [email protected]

Tóm tắt

The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and Pi, a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD+needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.

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Tài liệu tham khảo

10.1113/jphysiol.1990.sp018000

10.1097/00005768-199801000-00007

10.1152/physrev.1999.79.4.1127

10.1152/ajpregu.1984.246.4.R409

Clarence DH.The Handbook of Biochemistry and Biophysics. Cleveland, OH: World, 1966.

10.1046/j.1523-1755.2003.00177.x

Davis EJ, Bremer J, and Akerman KE.Thermodynamic aspects of translocation of reducing equivalents by mitochondria.J Biol Chem255: 2277–2283, 1980.

10.1016/0022-2828(91)91642-5

Finkel KWand DuBose TD.Metabolic acidosis. In:Acid-Base and Electrolyte Disorders: A Companion to Brenner and Rector's The Kidney, edited by DuBose TD and Hamm LL. Philadelphia, PA: Saunders, 2002, p. 55–66.

Fitts RHand Holloszy JO.Lactate and contractile force in frog muscle during development of fatigue and recovery.Am J Physiol231: 430–433, 1976.

10.1016/S0022-2828(77)80008-4

Gevers W.Generation of protons by metabolic processes other than glycolysis in muscle cells: a critical view [letter to the editor].J Mol Cell Cardiol11: 328, 1979.

10.1007/BF00585346

10.1152/jappl.2000.89.5.1793

Hill AV, Long CNH, and Lupton H.Muscular exercise, lactic acid, and the supply and utilization of oxygen.Proc R Soc Lond B Biol Sci16: 84–137, 1924.

10.1098/rspb.1926.0035

Hochachka PWand Mommsen TP.Protons and anaerobiosis.Science219: 1391–1397, 1933.

Holten CH, Muller A, and Rehbinder D.Lactic Acid: Property and Chemistry of Lactic Acid and Derivatives. Germany: Verlag Chemie, 1971.

10.1152/jappl.1999.87.5.1747

10.1152/ajpendo.00303.2003

10.1046/j.1365-201X.1996.206000.x

Juel C.Lactate-proton cotransport in skeletal muscle.Physiol Rev77: 321–358, 1977.

Juel C.Muscle pH regulation: role of training.Acta Physiol Scand162: 359–366, 1988.

10.1007/s002320010046

Karlsson J.Lactate and phosphagen concentrations in working muscle of man.Acta Physiol Scand Suppl358: 1–72, 1971.

10.1152/jappl.1988.65.2.509

10.1152/jappl.1988.65.5.2080

Laski MEand Wesson DE.Lactic acidosis. In:Acid-Base and Electrolyte Disorders: A Companion to Brenner and Rector's The Kidney, edited by DuBose TD and Hamm LL. Philadelphia, PA: Saunders, 2002, p. 835–108

Lehninger AL.The Principles of Biochemistry(2nd ed). New York: Worth, 1982.

Lusk G.The Elements of the Science of Nutrition. Philadelphia: Saunders, 1928.

10.1139/y91-038

10.1152/jappl.1995.78.2.758

Margaria R, Edwards HT, and Dill DB.The possible mechanisms of contracting and paying the oxygen debt and the role of lactic acid in muscular contraction.Am J Physiol106: 689–715, 1933.

10.1152/jappl.1993.75.4.1654

10.1097/00005768-199705000-00001

Raju TN.The Nobel Chronicles. 1922: Archilbald Vivian Hill (1886–1977), Otto Fritz Meyerfhoff (1884–1951).Lancet352: 1396, 1998.

Robergs RA.Exercise-induced metabolic acidosis: where do the protons come from?Sportscience5 [sportsci.org/jour/0102/rar. htm, 2001].

10.1016/0003-9861(90)90505-S

Sahlin K.Intracellular pH and energy metabolism in skeletal muscle of man.Acta Physiol Scand Suppl455: 7–50, 1978.

10.1007/BF00584099

10.1152/ajpcell.1981.240.3.C121

10.1152/ajpcell.1981.240.3.C121

10.1007/BF00585150

10.1111/j.1748-1716.1984.tb07517.x

10.1042/bj2450551

10.1046/j.1365-201X.1998.0298f.x

Sahlin K.Metabolic changes limiting muscle performance. In:Biochemistry of Exercise, edited by Saltin B. Champaign, IL: Human Kinetics, 1986, vol.16, p. 323–344.

10.4065/74.1.67

10.1113/jphysiol.1993.sp019932

10.1152/jappl.1987.62.2.611

10.1152/jappl.1987.62.2.616

10.1139/y92-023

10.1152/jappl.1994.76.4.1462

10.1152/jappl.1992.72.3.954

Stryer L.Biochemistry(4th ed). San Francisco: Freeman, 1995.

10.3109/10408369109106865

Trump BD, Mergner WJ, Kahng MW, and Saladino AJ.Studies on the subcellular pathophysiology of ischemia.Circulation53: I17–I26, 1976.

10.1016/0022-2828(79)90385-7

Webster’s Ninth New Collegiate Dictionary.Springfield: Merriam-Webster, 1984.

Westerblad H, Allen DG, and Lannergren J.Muscle fatigue: lactic acid or inorganic phosphate the major cause?News Physiol Sci17: 17–21, 2002.

10.1016/0022-2828(79)90446-2

10.1161/01.CIR.53.1.3

10.1074/jbc.273.26.15920

10.1177/000456327801500111

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American Journal of Physiology - Regulatory Integrative and Comparative Physiology

Tập 287 Số 3

R502-R516

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