There is an ongoing debate attempting to determine whether lactic acid buildup during exercise is an advantage that improves performance or a disadvantage that results in muscle fatigue occurring sooner. While there is evidence to support both sides of the argument, the data supporting lactic acid accumulation being a disadvantage during muscle activity is more compelling.
A brief intro into what lactate is and why it is produced in the first place: lactate metabolism is necessary to produce the required energy to continue exercising, but its role in the production of hydrogen ions depresses muscle function. So while the lactate is being produced to satisfy high energy demands, it must be cleared from the muscles and sent to the liver to be metabolized (or sent to the muscles to be used as an energy source) if the activity is to continue. In general, adrenaline causes a decrease in the clearance of lactate and fast twitch fibers produce the most lactate [1].
The first crucial data supporting lactic acid’s role in muscle fatigue is that when the lactate concentration of the blood is elevated, there is a reduction in overall performance. These studies take into account the potential fatigue factor by exercising one part of the body to increase the lactate levels, and then while the blood had these increased levels, they exercise another part of the body until fatigue. It has been done over and over again, with all the studies producing the same results: increased blood lactate levels promote muscle fatigue. The performance reduction was associated with a lower release of lactate, a lower muscle pH, and a greater potassium release. These factors work together to result in a potassium buildup in the muscle interstitium, which leads to fatigue [2].
Another study that has been done to test the effects of lactate on muscle fatigue involved incubating the muscle in lactic acid. These studies have found that when the muscles are incubated in lactic acid, force development is reduced and fatigue is achieved faster. The studies also found that lactate mostly affects the function of the muscle membrane and that the effect of lactate can be linked back to the pH-induced changes, such as the potassium balance [2].
Lactate does not just affect the pH balance and potassium concentrations. It also has been found to affect the intracellular calcium, which is responsible for muscle activation. The lactate affects the sarcoplasmic reticulum’s calcium release channels, affecting calcium’s ability to bind to the troponin, providing a binding site on the actin filament for the myosin head to bind to, causing a muscle contraction. Since this process is inhibited, muscle contraction is limited [2].
Lactic acid is not necessarily what is causing the fatigue. Lactic acid is dissociated into lactate anions and hydrogen ions under normal internal body conditions, so it is the lactate anions and hydrogen ions that are accumulating in the muscle, not ‘lactic acid’. It is believed that the hydrogen ion accumulation is what truly influences muscle fatigue, as opposed to the lactate anions. Studies support the earlier claims that the decline in exercise performance is due to the decrease in sarcoplasmic reticulum function, increase in hydrogen ions, and inhibiting the calcium, which inhibits the myofibrillar ATPase thereby inhibiting the maximal shortening velocity [1].
When these factors work together (the potassium accumulation, low pH, the calcium release channels), muscle fatigue is inevitable. So while lactate may not directly cause fatigue, it induces enough changes within the normal pathways to affect the process and cause fatigue.
(FYI: Based on the articles I found during my research, I am more on the lactate is advantageous bandwagon.)
References:
[1] Aldeam Facey, Rachael Irving, and Lowell Dilworth, “Overview of Lactate Metabolismand the Implications for Athletes.” American Journal of Sports Science and Medicine 1, no. 3 (2013): 42-46.
[2] Point:Counterpoint, “Lactic acid accumulation is an advantage/disadvantage during muscle activity.” Journal of Applied Physiology, 100 (2006): 1410-1414.
