Lactic Acid is not the cause of your cycling woes
One of the more pervasive myths in cycling is that lactic acid is responsible for the burn in your legs. It’s not. In fact, it’s almost the opposite of the truth. That so many people propagate this myth is amazing to me. An acid? It must cause burning.
Here’s the science (thanks to Jason), courtesy of Faria et al., Sports Medicine:Volume 35(4)2005pp 285-312.
It is apparent that when cycling at increasing power outputs, lactate accumulates in the vastus lateralis muscle. However, while the mechanisms responsible for its production, accumulation, use and disposal have been well investigated, they are misinterpreted by many athletes, coaches and some scientists. More importantly, there is a need to dispel the myths of ‘lactic acid’ so often voiced among cycling coaches and athletes. Included among the misnomers are such statements as: lactic acid is the primary factor in muscle soreness; lactic acid is the central cause of oxygen debt; lactic acid is the causative agent in muscle fatigue; lactic acid is the immediate energy donor for muscle contraction; and lactic acid is a dead-end waste product.
It should be evident that the production of lactate should not be viewed as a negative facet of increasing exercise intensity. Every aspect of lactate production is beneficial. Lactate production serves to maintain cytosolic redox, make new glucose, consume H+ from the cytosol, as well as allow transport of H+ from the cell. All of these reactions are advantageous to the exercise response. Therefore, it is better to conclude that high levels of lactate are not detrimental to cycling performance.
The more scientifically inclined can read more details after the jump…
“Most texts on physiology and biochemistry clearly demonstrate the importance of the lactate reaction in maintaining cytosolic redox (oxidation-reduction reaction) and allowing glycolysis to continue during intensive exercise. Furthermore, Donovan and Brookswere able to demonstrate the significance of lactate as a gluconeogenic substrate during exercise. The most striking finding was the observation that well trained individuals were better able to maintain blood glucose levels through the gluconeogenesis of lactate than were untrained individuals. Recall that gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors such as glycerol, ketoacids or amino acids. While many have come to accept these positive facets of lactate metabolism, some individuals continue to believe that these benefits come at the cost of increasing acidosis whose genesis is ‘lactic acid’.
“Nevertheless, there is no biochemical evidence to support the belief that lactate production during exercise releases a proton and causes acidosis.A review and comments by Robergs et al.clearly identifies that the intermediates of glycolysis are protonated in a physiological pH (measure of acidity/alkalinity) where ‘lactic acid’ would exist as lactate and not ‘lactic acid’. Moreover, the main form of ‘lactic acid’ in physiological systems is sodium lactate.Rather, Robergs et al. suggests an increased reliance on non-mitochondrial ATP turnover as the potential source of proton production that is associated with increased lactate creation and development of acidosis. Furthermore, when cell buffering capacity is exceeded, acidosis develops. Clearly, there are plausible mechanisms which explain that ‘lactic acid’ is not the likely source of protons during exercise. In this regard, Robergs et al.points to the evidence that lactate serves to lower hydrogen ion concentrations rather than raise them. The conversion of pyruvate to lactate not only oxidises the reduced form of nicotinamide-adenine dinucleotide (NADH) but also utilises an H+ from solution to attach to the middle carbon, thereby serving to lower the H+ concentration rather than contribute to its increase. In a recent investigation of professional cyclists (exercising at 90% V-dotO2max, 2 × 6-minute sessions), Santalla et al.demonstrated that despite a pH indicative of acidosis, there was no apparent acidosis-induced impairment in skeletal muscle function in the athletes. These results also suggest, indirectly, that the efficiency of muscle contraction was not altered significantly and adds further support that lactate production retards rather than contributes to acidosis.
“It should be evident that the production of lactate should not be viewed as a negative facet of increasing exercise intensity. Every aspect of lactate production is beneficial. Lactate production serves to maintain cytosolic redox, make new glucose, consume H+ from the cytosol, as well as allow transport of H+ from the cell. All of these reactions are advantageous to the exercise response. Therefore, it is better to conclude that high levels of lactate are not detrimental to cycling performance.”