The decrease in productivity caused by fescue toxicosis has been estimated to cost the United States livestock industry more than $1 billion per year due to reduced growth and diminished reproductive efficiency. This goal of the research presented in this dissertation is to enhance the knowledge base concerning the underlying physiological changes that occur during fescue toxicosis that lead to reduced intake and weight gain in cattle. As one of the factors associated with fescue toxicosis is a reduction in feed intake, achieving a consistent and adequate intake of toxins can be a complication. Results from experiment 1demonstrate that ruminal dosing of ground seed and a seed extract are able to mimic the classic symptoms of fescue toxicosis in cattle. This model whereby seed or extract is directly dosed into the rumen eliminates the possibility of reduced alkaloid intake due to refusal of feed by the animal. This model allows for more precise and repeatable dosing of alkaloids in fescue research. Experiment 2 results indicate that ingestion of endophyte-infected tall fescue leads to decreased fasting heat production in cattle. This is indicative of a reduction in maintenance energy requirements and may be related to a decrease in liver size or other metabolic activity in animals grazing endophyte-infected pastures. In addition, a reduction in basal metabolic rate may cause the compensatory gain often observed in cattle entering the feedlot after grazing endophyte-infected pastures. Data from experiment 3 provides evidence that whole body nitrogen and energy metabolism are not altered by fescue alkaloid ingestion. Experiment 3 also addresses the rate of feed degradation and ruminal passage rates in cattle ingesting endophyte infected fescue. While ruminal VFA profile is altered, this is likely due to reduced absorption, not increased production. The data from this experiment indicate that the reduction in weight gain and productivity seen during fescue toxicosis is primarily a function of reduced intake and not secondary effects of alkaloid ingestion.