Prior to the formation of the lactate shuttle hypothesis, lactate had long been considered a byproduct resulting from glucose breakdown through glycolysis in times of anaerobic metabolism.   As a means of regenerating oxidized NAD, lactate dehydrogenase catalyzes the conversion of pyruvate to lactate in the cytosol, oxidizing NADH to NAD, regenerating the necessary substrate needed to continue glycolysis.  Lactate is then transported from the peripheral tissues to the liver by means of the Cori Cycle where it is reformed into pyruvate through the reverse reaction using lactate dehydrogenase.  By this logic, lactate was traditionally considered a toxic metabolic byproduct that could give rise to fatigue and muscle pain during times of anaerobic respiration.  Lactate was essentially payment for ‘oxygen debt’ defined by Hill and Lupton as the ‘total amount of oxygen used, after cessation of exercise in recovery therefrom’.