Lactatemia might be caused by CO2 poisoning during acute ruminal acidosis (ARA).

Lactatemia might be caused by CO2 poisoning and no ruminal lactate during acute ruminal acidosis (ARA).

Carbophilic lactate producing bacteria might outgrowth lactate utilising bacteria under low pH/high dCO2 concentrations (Prescott and Stutts, 1955, Dain et al., 1956, Counotte and Prins, 1978, 1981). Lactic acid concentration during ARA can reach 50 mM at values closer to the pKa 3.8 (50% equilibrium). But, lactatemia might not be present (Nagaraja et al., 1985).

Huber suggested that ruminal lactate production was unlikely to overcome kidney’s clearance, he argued instead that lactatemia had an internal origin (Huber, 1969, 1976). This hypothesis mirrors lactic acidosis in other species (Gladden, 2004), where hypoxia drives glycolysis in peripheral tissues and lactate clearance by the liver via gluconeogenesis is reduced (The Cori Cycle). Hence, how does ARA influence The Cori Cycle?

Here some hypotheses,

During ARA the exposure to high dCO2 concentrations might enhance CO2 absorption (Whitelaw et al., 1972, Veenhuizen et al., 1988), overwhelm the cellular buffering system, and reach the liver via the portal vein leading to intracellular hepatocyte acidification (Mommsen et al., 1988). Intracellular acidification might impair hepatic LDH function (Firth et al., 1995), with the concomitant lactatemia.

Alternatively, low intracellular HCO3- signal by cellular acidification might impair the lactate shuttle function (Gladden, 2004, Brooks, 2018). This might be caused by reducing Na-HCO3- cotransporter (NBC1) or an indirect effect on MTC by interfering with Thiamine pyrophosphate (TPP) a cofactor for MTC and HCO3- dependent (Espiritu et al., 2002, Kirat et al., 2007). Together they might reduce translocation of blood lactate by hepatic HCO3-, leading to lactatemia.

Likewise, high blood CO2 might lead to hypoxemic glycolysis in peripheral tissues (Gladden, 2004, Brooks, 2018). However, the low affinity of haemoglobin to oxygen, the reliance on the chlorine shift to transport HCO3- by RBC, and the concomitant hyperkalaemia observed in ruminants speaks against this mechanism (Bunn, 1981, Gustin et al., 1994, Kurbel, 2011), high blood HCO3- is usually observed during ruminal acidosis (Gianesella et al., 2010). Instead, HIF-1 response to hypoxia might be HCO3- dependent (Pastorekova et al., 2008) and the lactate shuttle activation in peripheral tissues might lead to lactatemia. In fact, lactatemia might enhance lactate metabolism is lungs (Johnson et al., 2012, Brooks, 2018) with the concomitant increase in CO2 excretion under ruminal acidosis.

Thus, ARA might be caused by CO2 poisoning and monitoring dCO2 might help us to reduce the prevalence of ruminal acidosis.