The Influence of Heat Stress on Milk Yield, Gastrointestinal Permeability, and Nutrient Partitioning in Lactating Dairy Cattle

The US dairy industry loses approximately $1.2 billion due to heat stress related production losses annually. It was formerly believed that heat-stressed lactating dairy cattle produce less milk because they consume less feed. It has since been established that the reduction of feed intake is only responsible for about 50% of the reduced milk yield in HS cows. It is believed that HS increases gastrointestinal permeability (GIP), resulting in microbial components leaking from the lumen of the gastrointestinal tract into underlying tissue and stimulating an immune response. The immune response is suspected to alter overall metabolism, and milk production specifically, by diverting nutrients away from the mammary gland and other non-essential processes to support immune system activation. Topics examined herein focus on identifying markers to assess gastrointestinal permeability and the influence of heat stress on GIP and nutrient metabolism. The first study utilized an in vitro rumen fermentation system to determine if lactulose, sucralose, and D-mannitol could persist in an in vitro rumen culture. Lactulose could not be quantified in the rumen fluid matrix, D-mannitol was rapidly degraded, and sucralose concentrations did not change after 48 h of incubation, establishing sucralose as an indigestible marker in mature ruminants. The second study utilized a pair feeding design to directly assess the effect of HS on GIP, milk yield, and immune activation by lipopolysaccharide (LPS). HS cows (n=7) were exposed to a temperature-humidity index (THI) value of 74-80 for 4 d. The pair-fed thermoneutral cows (PFTN, n=8) were exposed to a constant THI of 64 with their intake matched to the HS cows. HS lowered milk yield without altering GIP, measured using orally dosed sucralose as a permeability marker, or eliciting an LPS related immune response. Jejunal mucosal scrapings were harvested from each cow, tight junction proteins were quantified, and no differences were detected. Lack of treatment responses in GIP marker recovery and tight junction protein abundance indicate that increased GIP may not be a driving force behind production losses in HS dairy cows. The third study focused on energy substrate utilization during HS with the objective of determining if tissue-level energy substrate metabolism could be influencing glucose sparing mechanisms. Metabolic flexibility of skeletal muscle, liver, and mammary tissue was assessed after 4 d of HS. It was determined that HS reduced skeletal muscle metabolic flexibility and did not alter liver and mammary metabolic flexibility. This indicates that skeletal muscle has a greater dependency on glucose as an energy substrate, which may decrease the pool of glucose available for lactose synthesis in lactating cows. Finally, the last study had the objective of assessing branched-chain amino acid (BCAA) requirements during HS. BCAA are oxidized for ATP synthesis in extrahepatic tissues and provide precursors for the biosynthesis of non-essential amino acids. They are also taken up by the mammary gland at a rate greater than what they are used in milk protein. Taken together, it was hypothesized that BCAA requirements may be increased during HS. BCAA entry rates into blood were assessed using a stable isotope approach and a 4-pool model. No differences were detected in daily entry rates or flux rates between pools indicating no change in requirements. When considering the results of all studies, reductions in milk yield are likely a result of altered macronutrient metabolism but further work is needed to confirm that hypothesis. Understanding the physiology behind HS related production losses is the first step in developing mitigation strategies.