Circumstantial evidence suggests ergovaline is the putative toxin causing fescue toxicosis. However, several investigators suggest lysergic acid may be involved as well. Therefore, the purpose of this study was to (i) determine the metabolic fate of ergot alkaloids in ruminants, (ii) investigate gastric transport, and (iii) validate these findings in vivo. Ruminal metabolism of the alkaloids was determined by inoculating endophyte‐infected and endophyte‐free tall fescue [Lolium arundinaceum (Schreb.) Darbysh.] with viable and nonviable ruminal fluid using in vitro techniques. Total ergot alkaloid concentration increased with time due to microbial metabolism. The alkaloids were extracted, and ruminal and omasal transport investigated in vitro. Only lysergic acid crossed gastric barriers. To validate the findings, fistulated steers were allowed to graze endophyte‐infected or endophyte‐free tall fescue paddocks in a crossover study, and ruminal fluid and urine were analyzed for ergot alkaloids over time. Ergovaline was not found in ruminal fluid or urine. Urine was immunopurified from a steer grazing endophyte‐infected tall fescue and analyzed by high‐performance liquid chromatography. A peak with a signal consistent with lysergic acid was found. These results imply that lysergic acid may be involved in the fescue toxicosis syndrome.