The onset of acidosis during periods of intense exercise is commonly attributed to accumulation of hydrogens that are dissociated from lactate. Previously, lactic acid was thought to cause fatigue.  From this reasoning, the idea of lactate production being a primary cause of muscle fatigue during exercise was widely adopted.  A closer, mechanistic analysis of lactate production under “anaerobic” conditions shows that there is no biochemical evidence for the production of lactate through LDH contributing to acidosis.  While LDH activity is correlated to muscle fatigue, the production of lactate by means of the LDH complex works as a system to delay the onset of muscle fatigue. George Brooks and Colleagues at UC Berkeley where the lactate shuttle was discovered showed that lactate was actually a metabolic fuel not a waste product or the cause of fatigue.
LDH works to prevent muscular failure and fatigue in multiple ways.  The lactate-forming reaction generates cytosolic NAD+, which feeds into the glyceraldehyde 3-phosphate dehydrogenase reaction to help maintain cytosolic redox potential and promote substrate flux through the second phase of glycolysis to promote ATP generation.  This, in effect, provides more energy to contracting muscles under heavy workloads.  The production and removal of lactate from the cell also ejects a proton consumed in the LDH reaction- the removal of excess protons produced in the wake of this fermentation reaction serves to act as a buffer system for muscle acidosis.  Once proton accumulation exceeds the rate of uptake in lactate production and removal through the LDH symport, muscular acidosis occurs.