Metabolic acidosis is an imbalance between proton-releasing and proton-consuming reactions of catabolism during high intensity exercise, which can cause fatigue. Fatigue refers to the inability to continue exercise at a given intensity. Various exercise training and nutritional strategies appear to be effective at delaying the onset of metabolic acidosis.
Lactic acid build up was the classical explanation for the cause of fatigue, denoted by sensations of pain and muscle burn experienced during intense exercise. Many coaches, athletes, exercise professionals, and scientists alike have traditionally linked lactic acidosis with an inability to continue exercise at a given intensity. Lactic acid has a long history. For centuries it has been known that if milk is allowed to spoil, then something that formed in the milk caused a sour taste. In 1780, Carl Scheele, a Swedish chemist, documented that this “something” was lactic acid. In fact, the crude isolation of this substance from sour milk led to the name lactic acid (“lactic,” meaning of, or related to, milk). By the 1830s, scientists had also discovered the presence of lactic acid in muscle from stressed animals, fresh milk, and blood. By this time, pure samples of lactic acid had also been isolated, and the chemical formula verified. Research on lactic acid continued as an indirect output to the main area of chemical interest—fermentation. In fact, this early research on lactic acid established the connection between cellular lactic-acid production, anaerobiosis (a lack of oxygen), and acidosis.
Lactate is formed from the reduction of pyruvate and catalyzed by the enzyme lactate dehydrogenase. The lactate dehydrogenase reaction regenerates NAD+ and consumes a proton. Both of these contribute to a continued rapid rate of ATP regeneration (Figure 1). In glycolysis, a key step involves a reaction whereby 2 molecules of NAD+ are reduced to NADH. This step precedes the reactions from which 4 ATP are produced. Under steady state exercise intensity conditions the electrons and protons from NADH are passed into the mitochondria and NAD+ is regenerated; however, at higher exercise intensities this does not occur. Consequently, NADH begins to accumulate in the cytosol, while NAD+ becomes limited. If NAD+ were not regenerated in the lactate dehydrogenase reaction, glycolytic flux would be compromised, and ATP regeneration would be reduced. The consumption of a proton is beneficial in that it combats the development of metabolic acidosis. Proton accumulation contributes most to muscle fatigue, and hence, lactate production should be perceived as fatigue-countering rather than fatigue-inducing. Lastly, lactate can be used for fuel elsewhere. In fact, it has been shown that most of the lactate produced during high-intensity exercise is shuttled out of the cell via monodecarboxylate transporters (MCTs) (Figure 1) and taken up elsewhere by less metabolically active skeletal muscle. The lactate is subsequently converted back to pyruvate, moved into the mitochondria, and oxidized to regenerate large quantities of ATP.
Proton accumulation contributes to a decreased cellular pH (acidosis), which interferes with normal skeletal muscle contraction through a number of mechanisms:
Various exercise training and nutritional strategies appear to be effective at partially mitigating these untoward events, delaying the onset of metabolic acidosis and fatigue, and increasing overall exercise performance. One of those is improving the buffering-capacity system of the cellular environment to permit better tolerance of increased metabolic acidosis, and hence, delay fatigue when performing short-term intense exercise. Interestingly, past research has shown that eliciting metabolic acidosis (i.e., high concentrations of protons) is a requisite training stimuli. To elicit favorable muscle-buffering-capacity adaptations, high-intensity interval training (HIIT) has been recommended. A sample HIIT workout includes six to ten interval bouts of two minutes each at a workload, corresponding to 90%–95% maximal heart rate with one-minute rest. To optimize improvements to the buffering capacity of skeletal muscle, the specific exercise intensity of the HIIT sessions are critical. In particular, it has been noted that intensities below 80%–85% or intensities near/at 100% maximal heart rate will be inadequate for beneficial training adaptations to occur.
Given the fact that increased concentrations proton (H+) molecules within the muscle cell are detrimental to skeletal muscle performance, it makes logical sense that the cell has a means for removing this fatigue-inducing product of metabolism. MCTs are proteins found on the cell membranes that facilitate the flow of proton (H+) molecules from inside the cell into the blood. The MCT is in fact a cotransporter because it collectively transports a molecule each of proton (H+) and lactate out of the cell. Exercise training leads to an increased MCT concentration, and therefore, a greater capacity for removal of excessive protons (H+) from the cell. This adaptation provides a mechanism for quicker recovery from metabolic acidosis. HIIT improves MCT concentrations.
In addition to exercise training, the muscle buffering capacity of skeletal muscle can also be augmented by nutritional strategies. Alkalizing agents have been studied extensively for their potential to enhance performance by attenuating the extent to which metabolic acidosis contributes to fatigue during high-intensity exercise performance. One such alkalizing substance that has been found to improve tolerance to metabolic acidosis by increasing the muscle-buffering capacity is sodium bicarbonate. Taking sodium bicarbonate enhances the muscle-buffering capacity of skeletal muscle by promoting proton (H+) removal from the skeletal muscle. Because increased concentrations of proton (H+) molecules within the muscle cell are detrimental to skeletal muscle performance, an increased rate of proton (H+) removal from skeletal muscle will result in better tolerance of intense exercise and a more rapid recovery from high-intensity exercise. The main drawback to sodium bicarbonate use is that some individuals experience gastrointestinal distress. The recommended dosage of sodium bicarbonate is between 0.2 to 0.4 grams per kilogram of body weight. It is recommended that sodium bicarbonate be taken with approximately one quart (1 L) of water and consumed between one to two hours before intense exercise. Sodium bicarbonate can either be taken in capsule form or in a beverage, such as water.
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American Council on Exercise, 4851 Paramount Dr., San Diego, CA, 92123, (858) 576-6500, (888) 825-3636, ext. 782, Fax: (858) 576-6564, https://www.acefitness.org .
Lance C. Dalleck, PhD