Environmental-induced hyperthermia compromises efficient animal production and jeopardizes animal welfare. Reduced productive output during heat stress was traditionally thought to result from decreased nutrient intake. Our observations challenge this dogma and indicate that heat-stressed animals employ novel homeorhetic strategies to direct metabolic and fuel selection priorities independent of nutrient intake or energy balance. Alterations in systemic physiology support a shift in carbohydrate metabolism, evident through changes such as basal and stimulated circulating insulin levels. Hepatocyte and myocyte metabolism also show clear differences in glucose production and use during heat stress. Perhaps most intriguing, given the energetic shortfall of the heat-stressed animal, is the apparent lack of fat mobilization from adipose tissue coupled with a reduced responsiveness to lipolytic stimuli. Thus, the heat stress response markedly alters postabsorptive carbohydrate, lipid, and protein metabolism independently of reduced feed intake through coordinated changes in fuel supply and utilization by multiple tissues.

Accurately quantifying activated immune system energy requirements in vivo is difficult, but a better understanding may advance strategies to maximize animal productivity. Study objectives were to estimate whole-body glucose utilization following an i.v. endotoxin challenge. Lactating Holstein cows were jugular catheterized and assigned 1 of 3 bolus treatments: control (CON; 5 mL of saline; n = 6), lipopolysaccharide (LPS)-administered (LPS-C; 1.5 μg/kg of body weight; Escherichia coli 055:B5; n = 6), and LPS + euglycemic clamp (LPS-Eu; 1.5 μg/kg of body weight; 50% glucose solution infusion; n = 6). After LPS administration, blood glucose was determined every 10 min and glucose infusion rates were adjusted in LPS-Eu cows to maintain euglycemia for 720 min. Blood samples were obtained 180, 360, 540, and 720 min postbolus for further analysis. Cows were milked 360 and 720 min postbolus. Blood glucose was increased 84% in LPS-administered cows for up to 150 min postbolus; thereafter, circulating glucose was decreased 30% in LPS-C relative to LPS-Eu and CON cows. Mild hyperthermia (+0.5°C) occurred between 30 and 90 min postbolus in LPS-administered relative to CON cows; thereafter, rectal temperature did not differ between treatments. Milk yield and lactose percentage were decreased 80 and 11%, respectively, in LPS-administered relative to CON cows. Circulating insulin was increased 4 fold and nonesterified fatty acids, β-hydroxybutyrate, and ionized Ca were decreased ∼50% in LPS-administered compared with CON cows. Plasma l-lactate, haptoglobin, and serum amyloid A increased ∼160, 260, and 75%, respectively, in LPS-administered relative to CON cows. Overall, LPS-binding protein was increased 87% in LPS-administered relative to CON cows; however, at 720 min, it was decreased 25% in LPS-Eu compared with LPS-C cows. White blood cell count decreased ∼90% in LPS-administered cows at 180 min and progressively increased to ∼50% of CON values by 720 min. Total glucose deficit during the 720 min following LPS administration was calculated as the decrease in the amount of glucose required to synthesize milk (due to the decrease in milk yield relative to prebolus levels) plus the amount of glucose infused to maintain euglycemia (in LPS-Eu cows only) and was 461, 1,259, and 1,553 g for CON, LPS-C, and LPS-Eu cows, respectively. Our data indicate an acutely activated immune system uses >1 kg of glucose within 720 min and maintaining euglycemia did not rescue milk synthesis.

Heat stress (HS) jeopardizes pig health, reduces performance variables, and results in a fatter carcass. Whether HS directly or indirectly (via reduced feed intake) is responsible for the suboptimal production is not known. Crossbred gilts (n = 48; 35 ± 4 kg BW) were housed in constantly climate-controlled rooms in individual pens and exposed to 1) thermal-neutral (TN) conditions (20°C; 35% to 50% humidity) with ad libitum intake (n = 18), 2) HS conditions (35°C; 20% to 35% humidity) with ad libitum intake (n = 24), or 3) pair-fed [PF in TN conditions (PFTN), n = 6, to eliminate confounding effects of dissimilar feed intake (FI)]. Pigs in the TN and HS conditions were sacrificed at 1, 3, or 7 d of environmental exposure, whereas the PFTN pigs were sacrificed after 7 d of experimental conditions. Individual rectal temperature (T_r), skin temperature (T_s), respiration rates (RR), and FI were determined daily. Pigs exposed to HS had an increase (P < 0.01) in Tr (39.3°C vs. 40.8°C) and a doubling in RR (54 vs. 107 breaths per minute). Heat-stressed pigs had an immediate (d 1) decrease (47%; P < 0.05) in FI, and this magnitude of reduction continued through d 7; by design the nutrient intake pattern for the PFTN controls mirrored the HS group. By d 7, the TN and HS pigs gained 7.76 and 1.65 kg BW, respectively, whereas the PFTN pigs lost 2.47 kg BW. Plasma insulin was increased (49%; P < 0.05) in d 7 HS pigs compared with PFTN controls. Compared with TN and HS pigs, on d 7 PFTN pigs had increased plasma NEFA concentrations (110%; P < 0.05). Compared with TN and PFTN controls, on d 7 circulating N^τ-methylhistidine concentrations were increased (31%; P < 0.05) in HS pigs. In summary, despite similar nutrient intake, HS pigs gained more BW and had distinctly different postabsorptive bioenergetic variables compared with PFTN controls. Consequently, these heat-induced metabolic changes may in part explain the altered carcass phenotype observed in heat-stressed pigs.

The progression from gestation into lactation represents the transition period, and it is accompanied by marked physiological, metabolic, and inflammatory adjustments. The entire lactation and a cow's opportunity to have an additional lactation are heavily dependent on how successfully she adapts during the periparturient period. Additionally, a disproportionate amount of health care and culling occurs early following parturition. Thus, lactation maladaptation has been a heavily researched area of dairy science for more than 50 yr. It was traditionally thought that excessive adipose tissue mobilization in large part dictated transition period success. Further, the magnitude of hypocalcemia has also been assumed to partly control whether a cow effectively navigates the first few months of lactation. The canon became that adipose tissue released nonesterified fatty acids (NEFA) and the resulting hepatic-derived ketones coupled with hypocalcemia lead to immune suppression, which is responsible for transition disorders (e.g., mastitis, metritis, retained placenta, poor fertility). In other words, the dogma evolved that these metabolites and hypocalcemia were causal to transition cow problems and that large efforts should be enlisted to prevent increased NEFA, hyperketonemia, and subclinical hypocalcemia. However, despite intensive academic and industry focus, the periparturient period remains a large hurdle to animal welfare, farm profitability, and dairy sustainability. Thus, it stands to reason that there are alternative explanations to periparturient failures. Recently, it has become firmly established that immune activation and the ipso facto inflammatory response are a normal component of transition cow biology. The origin of immune activation likely stems from the mammary gland, tissue trauma during parturition, and the gastrointestinal tract. If inflammation becomes pathological, it reduces feed intake and causes hypocalcemia. Our tenet is that immune system utilization of glucose and its induction of hypophagia are responsible for the extensive increase in NEFA and ketones, and this explains why they (and the severity of hypocalcemia) are correlated with poor health, production, and reproduction outcomes. In this review, we argue that changes in circulating NEFA, ketones, and calcium are simply reflective of either (1) normal homeorhetic adjustments that healthy, high-producing cows use to prioritize milk synthesis or (2) the consequence of immune activation and its sequelae.

Heat stress compromises efficient animal production by marginalizing nutrition, management, and genetic selection efforts to maximize performance endpoints. Modifying farm infrastructure has yielded modest success in mitigating heat stress-related losses, yet poor production during the summer remains arguably the costliest issue facing livestock producers. Reduced output (e.g., milk yield and muscle growth) during heat stress was traditionally thought to result from decreased nutrient intake (i.e., a classic biological response shared by all animals during environmental-induced hyperthermia). Our recent observations have begun to challenge this belief and indicate heat-stressed animals employ novel homeorhetic strategies to direct metabolic and fuel selection priorities independently of nutrient intake or energy balance. Alterations in systemic physiology support a shift in carbohydrate metabolism, evident by increased basal and stimulated circulating insulin concentrations. Perhaps most intriguing given the energetic shortfall of the heat-stressed animal is the apparent lack of basal adipose tissue mobilization coupled with a reduced responsiveness to lipolytic stimuli. Thus, the heat stress response markedly alters postabsorptive carbohydrate, lipid, and protein metabolism independently of reduced feed intake through coordinated changes in fuel supply and utilization by multiple tissues. Interestingly, the systemic, cellular, and molecular changes appear conserved amongst different species and physiological states. Ultimately, these changes result in the reprioritization of fuel selection during heat stress, which appears to be primarily responsible for reduced ruminant animal productivity during the warm summer months.

Heat stress is a major environmental issue negatively affecting animal welfare and production efficiency in almost every livestock sector (Baumgard and Rhoads, 2013). When animals are exposed to environmental conditions that exceed their thermoneutral zone, production efficiency is compromised because the hierarchy of nutrient utilization is reprioritized to maintain euthermia, and consequently productivity is deemphasized. Heat stress is not an issue limited to tropical regions, as temperate countries are also affected during warm summer months (Renaudeau et al., 2012a). In fact, estimated annual losses due to heat stress in the U.S. livestock industry alone is US$1.5 billion for dairy and nearly US$1 billion for swine (Pollmann, 2010; Key and Sneeringer, 2014). Furthermore, increased genetic selection for production traits (i.e., lean tissue accretion, milk yield, and fecundity) leads to reduced heat stress tolerance as these phenotypes are associated with increased metabolic heat production (Renaudeau et al., 2012a; Baumgard and Rhoads, 2013).