Tissue-specific responses to oxidative fuel source preference during heat stress in lactating dairy cows

Graphical Abstract

Summary: Heat stress (HS) lowers milk yield and alters milk component concentration independently of concurrent reduction in dry matter intake. The physiological mechanisms mediating this profit-lowering response to HS are not well defined. It is hypothesized that HS alters metabolism in a tissue-specific manner, altering glucosesparing mechanisms to increase dependency on glucose as a fuel source. The objective of this work was to elucidate the effects of HS on the metabolic flexibility (i.e., substrate adaptability) of muscle, liver, and mammary tissue in lactating dairy cattle. Heat stress reduced energy substrate adaptability in skeletal muscle but did not alter metabolic flexibility in mammary or liver tissue. Reduced metabolic flexibility in skeletal muscle was due to decreased lipid oxidation, resulting in an increased dependency on pyruvate oxidation. Altered metabolic flexibility may contribute to decreased milk yield and warrants further investigation.

Highlights

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  Four days of HS lowered metabolic flexibility in skeletal muscle.

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  HS did not affect metabolic flexibility of mammary or liver tissue.

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  HS reduced total milk and milk component yields.

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  Respiration rates and rectal temperatures were elevated in response to HS.

Abstract

Prolonged exposure to high environmental temperatures results in an accumulated heat load that induces a heat stress (HS) response in dairy cattle. Heat stress compromises dairy farm profitability by reducing milk yield, altering milk composition, and hindering reproductive performance. The ability to alternate between carbohydrate and lipid sources for energy production is termed metabolic flexibility (Met Flex). The objective of this study was to evaluate the Met Flex of mammary, muscle, and liver tissue in lactating dairy cows under HS and thermoneutral (TN) conditions. Sixteen Holstein cows were assigned to 1 of 2 treatment groups: pair-feeding in TN conditions (PFTN) or HS conditions. All cows experienced a 4-d TN period with ad libitum intake followed by a 4-d treatment period. Heat stress cows were exposed to a temperature-humidity index (THI) ranging from 76 to 80 and the PFTN cows were exposed to a THI of 64. Milk production and health data were recorded twice daily. Semitendinosus biopsies were obtained on d 4 of each period and postmortem mammary and liver samples were obtained on d 4 of period 2. All tissue samples were assayed for Met Flex. Activity of mitochondrial (Mit) enzymes were assessed in skeletal muscle only. Four days of HS decreased milk yield, altered milk composition, and increased respiration rate and rectal temperatures. No differences in Met Flex were observed in mammary or liver tissue during period 2. However, HS, but not PFTN conditions, lowered Met Flex of skeletal muscle by 18.3% when compared with TN ad libitum feed intake conditions of period 1. No treatment differences were observed in skeletal muscle Mit enzyme activity indicating the decrease in Met Flex occurred independently of changes in Mit function. The reduction in Met Flex of skeletal muscle during HS may contribute to reduced milk yield and warrants further investigation.