Abstract

ABSTRACT The reduction of productivity and efficiency of nutrient utilization in heat-stressed dairy cattle is mediated by physiological and molecular alterations. Heat stress impairs the digestive and absorptive capacity of the gastrointestinal tract, and this effect is independent of nutrient intake. The shift in blood flow away from the splanchnic tissues to the skin reduces nutrient delivery to the small intestine and increases mucosal cell damage. The translocation of individual AA and the availability of total and individual AA to peripheral tissues is impaired during heat stress. In addition, heat stress alters tissue-specific demands for individual AA, protein synthesis, and whole-body protein degradation. For example, heat stress and the associated systemic inflammatory response alters the use of AA in metabolic tissues, increasing their demand. Glutamate, Gln, Arg, and Leu appear to ameliorate the inflammatory state of the intestine by preventing villi atrophy and improving synthesis of tight junction proteins and the intestinal barrier function. Moreover, heat stress increases the synthesis of acute phase proteins and heat-shock proteins and appears to promote hepatic removal of individual AA to sustain augmented protein synthesis. The fractional rates of extraction of total AA that reach the liver increase during systemic inflammation. An increase in intestinal and hepatic utilization of AA alters the net supply and the pattern of AA available to peripheral tissue. Whole-body protein breakdown and synthesis of urea increases in heat-stressed animals. This result suggests that AA are mobilized to meet the animal needs. Finally, local effects of heat stress may impair the synthesis of proteins in the mammary glands and reduce α-S2 casein and whey fractions, milk protein content, and milk protein yield, probably via reduced signaling activity. Collectively, heat stress alters the use of AA in absorptive and postabsorptive tissues, reducing AA availability to sustain animal production.

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