“Lactate is now recognized for its important metabolic functions and is a key substance used to provide energy, produce blood glucose and liver glycogen and promote survival in stressful situations. Oxidation of lactate is one of our most important energy sources. In highly oxidative muscle fibers, lactate is the preferred fuel source.” Brooks GA 1988
而McArdle, Katch, and Katch在他們的運動生理學課本清楚的說明了這解釋是基於假設：
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“The usual explanation for a lactate increase is based on an assumed relative tissue hypoxia during heavy exercise.”(1)
對於乳酸增加的常見解釋是基於組織在高強度運動時缺氧的假設。”
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儘管這個想法沒有被證實，但我們還是需要知道，這麼多年以來，科學社群以及一般大眾已把它視為一個事實。
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不過，有很多專家努力的使用新技術來確定這個想法是，反而出現了相反結果：
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these data demonstrate that, during incremental exercise, skeletal muscle cells do not become anaerobic…since intracellular PO2 (the oxygen pressure in the muscles) is well preserved at a constant level, even at maximal exercise.”(2)
如果肌肉不會進入無氧狀態，那為什麼乳酸水平會在強度漸進時會增加呢？乳酸到底是不是無氧狀態下的產物呢？事實上，乳酸是碳水化合物代謝的產物，與氧氣沒有關係。而這個答案在Tim Noakes教授的Lore of Running做出了的回答：
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“As the exercise intensity increases, so does the rate of carbohydrate use. When high exercise intensities (greater than 85% to 95% VO2max) are achieved, virtually all the energy comes from carbohydrate oxidation (G.A. Brooks and Mercier 1994; Brooks 1998). This means that the rate of energy flow through the glycolytic pathways increases steeply with increasing exercise intensity. The result is that the rate of lactate production increases inside the muscles.”(3)
當運動強度增加時，碳水化合物的使用也會隨著增加。當運動到達高強度時（高於85～95%VO2max），實質上所有能量都來自於碳水化合物的氧化(G.A. Brooks and Mercier 1994; Brooks 1998)。這表示當提升運動強度時，大部分能量來源是來自於糖酵解，這就導致肌肉裡的乳酸增加。
“This mistaken conclusion resulted from at least 2 errors. First, too few blood samples were measured. For example, if only 4 blood samples had been drawn at running speeds of 10, 14, 16, and 20 km per hour, then a fictitious anaerobic threshold would have been identified at 15.5 km per hour. But measuring blood lactate concentrations repeatedly – for example every km per hour – shows that blood lactate concentrations rise exponentially without any evidence of a threshold phenomenon.”
“It is clear that the blood lactate concentrations do not show a clearly defined, abrupt threshold response during exercise of progressively increasing intensity. Rather, blood lactate concentrations begin to rise as soon as progressive exercise commences. However, at low intensities, the rate of the increase is so low that it is barely noticeable. Only when the exercise becomes more intense does the rise become apparent, which perhaps explains the erroneous impression that blood lactate concentrations increase abruptly when the lactate threshold is reached.”
“In contrast to the often suggested role for acidosis as a cause of muscle fatigue, it is shown that in muscles where force was depressed by high (potassium), acidification by lactic acid produced a pronounced recovery of force. Since intense exercise is associated with increased (potassium), this indicates that acidosis may protect against fatigue rather than being a cause of fatigue.”(6)
What they are saying in the above quote is that lactic acid in the muscles is likely to protect against fatigue, allowing the muscle to work longer and/or harder before fatigue sets in.
“…lactic acid is more than 99% dissociated at physiological pH. This has led to the incorrect notion that the donation of a proton by each lactic acid molecule causes a decreased pH during conditions such as exercise.(7)
“In addition, many textbooks report that muscle fatigue is mainly the result of a decrease in pH within the muscle cell due to a rise in hydrogen ion concentration ([H+]) resulting from anaerobic metabolism and the accumulation of lactic acid. Recent literature, however, contradicts this assertion.”(8)
“…the increase in H+ (i.e. reduced pH or acidosis) is the classic cause of skeletal muscle fatigue. However, the role of reduced pH as an important cause of fatigue is now being challenged, and several recent studies show that reduced pH may have little effect on contraction in mammalian muscle at physiological temperatures.”(9)
“For much of the 20th Century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage…
The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional, and whole body metabolism.”(6)
McArdle, Katch, Katch, Exercise Physiology: energy, nutrition, and human performance, 4th edition, 1996, pg. 123
Richardson R, Noyszewski E, Leigh J, Wagner P. Lactate efflux from exercising human skeletal muscle: role of intracellular PO2, J Appl Phsiol 1998, 85(2), 627-634
Noakes, T Lore of Running, 4th edition, 2004, pg 160
Noakes, T Lore of Running, 4th edition, 2004, pg 158-159
Noakes, T Lore of Running, 4th edition, 2004, pg 163
Nielsen O, Paoli F, Overgaard K. Protective Effects of lactic acid on force production in rat skeletal muscle J of Physiol 2001, 536.1, 161-166
Gladden L. B., Lactate Metabolism: a new paradigm for the third millennium J Physiol 2004 558(1), 5-30
Stackhouse SK, Reisman DS, Binder-Macleod SA., Challenging the role of pH in skeletal muscle, Phys Ther 2001, 81(12), 1897-903
Westerblad H, Allen D, Jannergren J. Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause? News Physiol Sci 2002, 17, 17-21
