Explore the vast range of titles available.

Heat stress has an enormous economic impact on the global dairy industry, but the mechanisms by which hyperthermia negatively affect systemic physiology and milk synthesis are not clear. Study objectives were to evaluate production parameters and metabolic variables in lactating dairy cows during short-term heat stress or pair-fed conditions coupled with bST administration. Twenty-two multiparous Holstein cows were subjected to 3 experimental periods: 1) thermoneutral conditions with ad libitum intake for 7 d (P1); 2) heat stress (HS) with ad libitum intake (n=10) or pair-fed (PF) in thermoneutral conditions (n=12) for 7 d (P2), and 3) 7 d of HS or PF in conditions as described in P2 with recombinant bovine somatotropin administered on d 1 (P3). All cows received an intravenous glucose tolerance test (GTT) on d 5 of each period. Heat stress conditions were cyclical and temperatures ranged from 29.4 to 38.9°C. Rectal temperatures and respiration rates increased during heat stress (38.6–40.4°C and 44–89 breaths/min, respectively). Heat stress reduced dry matter intake by 30% and by design PF cows had similar intake reductions (28%). During heat stress and pair-feeding, milk yield decreased by 27.6% (9.6kg) and 13.9% (4.8kg), respectively, indicating that reduced feed intake accounted for only 50% of the decreased milk production. Milk yield increased with recombinant bovine somatotropin in both HS (9.7%) and PF (16.1%) cows. Cows in both groups were in positive energy balance (3.95 Mcal/d) during P1 but entered negative energy balance during P2 and P3 (−5.65 Mcal/d). Heat stress and pair-feeding treatments decreased (9.3%) basal glucose concentrations. Heat stress conditions had no effect on basal NEFA levels during P2; however, PF cows (despite a similar calculated energy balance) had a 2-fold increase in basal NEFA concentrations. Both groups had increased plasma urea nitrogen levels during P2 and P3 compared with P1. Basal insulin levels increased (37%) during P2 and P3 in HS cows but did not differ between periods in PF cows. During P2 and compared with P1, PF cows had a decreased rate of glucose disposal, whereas HS cows had a similar disposal rate following the GTT. During P2 and compared with P1, PF cows had a reduced insulin response whereas HS cows had a similar insulin response to the GTT. In summary, reduced nutrient intake accounted for only 50% of heat stress-induced decreases in milk yield, and feed intake-independent shifts in postabsorptive glucose and lipid homeostasis may contribute to the additional reduction in milk yield.

Environmentally induced periods of heat stress decrease productivity with devastating economic consequences to global animal agriculture. Heat stress can be defined as a physiological condition when the core body temperature of a given species exceeds its range specified for normal activity, which results from a total heat load (internal production and environment) exceeding the capacity for heat dissipation and this prompts physiological and behavioral responses to reduce the strain. The ability of ruminants to regulate body temperature is species- and breed-dependent. Dairy breeds are typically more sensitive to heat stress than meat breeds, and higher-producing animals are more susceptible to heat stress because they generate more metabolic heat. During heat stress, ruminants, like other homeothermic animals, increase avenues of heat loss and reduce heat production in an attempt to maintain euthermia. The immediate responses to heat load are increased respiration rates, decreased feed intake and increased water intake. Acclimatization is a process by which animals adapt to environmental conditions and engage behavioral, hormonal and metabolic changes that are characteristics of either acclimatory homeostasis or homeorhetic mechanisms used by the animals to survive in a new ‘physiological state’. For example, alterations in the hormonal profile are mainly characterized by a decline and increase in anabolic and catabolic hormones, respectively. The response to heat load and the heat-induced change in homeorhetic modifiers alters post-absorptive energy, lipid and protein metabolism, impairs liver function, causes oxidative stress, jeopardizes the immune response and decreases reproductive performance. These physiological modifications alter nutrient partitioning and may prevent heat-stressed lactating cows from recruiting glucose-sparing mechanisms (despite the reduced nutrient intake). This might explain, in large part, why decreased feed intake only accounts for a minor portion of the reduced milk yield from environmentally induced hyperthermic cows. How these metabolic changes are initiated and regulated is not known. It also remains unclear how these changes differ between short-term v. long-term heat acclimation to impact animal productivity and well-being. A better understanding of the adaptations enlisted by ruminants during heat stress is necessary to enhance the likelihood of developing strategies to simultaneously improve heat tolerance and increase productivity.

Heat stress is detrimental to dairy production and affects numerous variables including feed intake and milk production. It is unclear, however, whether decreased milk yield is primarily due to the associated reduction in feed intake or the cumulative effects of heat stress on feed intake, metabolism, and physiology of dairy cattle. To distinguish between direct (not mediated by feed intake) and indirect (mediated by feed intake) effects of heat stress on physiological and metabolic indices, Holstein cows (n = 6) housed in thermal neutral conditions were pair-fed (PF) to match the nutrient intake of heat-stressed cows (HS; n = 6). All cows were subjected to 2 experimental periods: 1) thermal neutral and ad libitum intake for 9 d (P1) and 2) HS or PF for 9 d (P2). Heat-stress conditions were cyclical with daily temperatures ranging from 29.7 to 39.2°C. During P1 and P2 all cows received i.v. challenges of epinephrine (d 6 of each period), and growth hormone releasing factor (GRF; d 7 of each period), and had circulating somatotropin (ST) profiles characterized (every 15 min for 6 h on d 8 of each period). During P2, HS cows were hyperthermic for the entire day and peak differences in rectal temperatures and respiration rates occurred in the afternoon (38.7 to 40.2°C and 46 to 82 breaths/min, respectively). Heat stress decreased dry matter intake by greater than 35% and, by design, PF cows had similar reduced intakes. Heat stress and PF decreased milk yield, although the pattern and magnitude (40 and 21%, respectively) differed between treatments. The reduction in dry matter intake caused by HS accounted for only approximately 35% of the decrease in milk production. Both HS and PF cows entered into negative energy balance, but only PF cows had increased (approximately 120%) basal nonesterified fatty acid (NEFA) concentrations. Both PF and HS cows had decreased (7%) plasma glucose levels. The NEFA response to epinephrine did not differ between treatments but was increased (greater than 50%) in all cows during P2. During P2, HS (but not PF) cows had a modest reduction (16%) in plasma insulin-like growth factor-I. Neither treatment nor period had an effect on the ST response to GRF and there was little or no treatment effect on mean ST levels or pulsatility characteristics, but both HS and PF cows had reduced mean ST concentrations during P2. In summary, reduced nutrient intake accounted for just 35% of the HS-induced decrease in milk yield, and modest changes in the somatotropic axis may have contributed to a portion of the remainder. Differences in basal NEFA between PF and HS cows suggest a shift in postabsorptive metabolism and nutrient partitioning that may explain the additional reduction in milk yield in cows experiencing a thermal load.

Multiparous, lactating Holstein cows (n = 23; 120 ± 30 d in milk, 690 ± 67 kg of body weight) housed in climatic chambers were randomly assigned to 1 of 2 dietary treatments: a diet containing a novel yeast culture formulation (YC) for heat stress (n = 12, 10 g/d) or a control diet (n = 11). The trial length was 28 d and consisted of a 7-d thermal neutral period (TN; 18°C, 20% humidity) followed by 21 d of heat stress (HS; cyclical daily temperatures ranging from 29.4 to 37.8°C and 20% humidity). Cows were individually fed a total mixed ration consisting primarily of alfalfa hay and steam-flaked corn. During TN, the YC feeding had no effect on production variables or most body temperature indices. During HS, all body temperature indices increased and YC had no effect on rump surface temperature, respiration rate, or sweating rates. Cows fed YC had lower rectal temperatures at 1200 and 1800 h (40.29 vs. 40.02°C and 40.35 vs. 40.12 ± 0.07°C, respectively) compared with control-fed cows. Cows fed both diets lost body weight (42 kg) during HS, but there were no differences between diets. Control-fed cows had increased dry matter intake (DMI) and milk yield (19.1 vs. 17.9 ± 0.5 kg/d and 32.15 vs. 29.15 ± 0.02 kg/d, respectively) compared with YC-fed cows, but intake and milk production were similar between diets when evaluated on a body weight basis. Heat stress progressively decreased DMI (29%) and milk yield, with milk production reaching a nadir (33%) in the third week. Heat stress decreased milk protein (7%) and lactose (5%) levels, but did not alter milk fat content. Heat-stressed cows were in calculated negative energy balance (-1.91 ± 0.70 Mcal/d) and this was unaffected by diet. Independent of diet, HS decreased plasma glucose (11%), but neither diet nor HS altered basal nonesterified fatty acid levels. Heat stress increased plasma urea N concentrations (11.5 vs. 14.8 ± 0.4 mg/dL). Despite YC-fed cows having slightly reduced body temperatures indices, feeding YC did not prevent the negative effects of HS.

Scoring body condition and assessing changes in the body condition of dairy cattle have become strategic tools in both farm management and research. Consequently, body condition score (BCS) is being researched extensively throughout the world. However, international sharing, comparing, and use of data generated are limited because different BCS systems exist. In the United States and Ireland a 5-point BCS system is used for dairy cows, whereas Australia and New Zealand use 8- and 10-point scales, respectively. The New Zealand 10-point scale was compared with the scoring systems in the United States, Ireland, and Australia by trained assessors. Cows were assessed visually in the United States and Australia, and in Ireland, cows were assessed by palpating key areas of the cow's body (n = 154, 110, and 120, respectively). Data were analyzed by regression. Significant positive linear relationships were found between the New Zealand 10-point scale and the other scoring systems: US 5-point scale, r2 = 0.54; Irish 5-point scale, r2 = 0.72; and Australian 8-point scale, r2 = 0.61. Those relationships must be interpreted cautiously because respective BCS within a given country were by just one experienced evaluator in each country in comparison to a separate evaluator scoring all cows in all counties using the New Zealand 10-point scale. Also, few very thin or very fat cows limit evaluation across extremes of BCS. However, differences between systems were not accurately predicted by simple mathematical calculations. The relationship may be closer for New Zealand and Ireland (r2 = 0.72) because both of those scoring systems include palpation of individual body parts, whereas visual evaluation is done in Australia and the United States. The current study is the first to examine relationships among differing BCS systems. These results may be useful for comparing/extrapolating research findings from different countries.

Heat stress (HS) is a multibillion-dollar problem for the global dairy industry, and reduced milk yield is the primary contributor to this annual economic loss. Feed intake declines precipitously during HS but accounts for only about 35% of the decreased milk synthesis, indicating that the physiological mechanisms responsible for decreased milk production during HS are only partly understood. Thus, our experimental objectives were to characterize the direct effects of HS on the somatotropic axis, a primary regulator of metabolism and milk yield. We recently reported no differences in mean growth hormone (GH) concentrations, GH pulsatility characteristics, or GH response to growth hormone releasing factor in HS versus pair-fed (PF) thermoneutral controls. Despite similarities in circulating GH characteristics, plasma insulin-like growth factor (IGF)-I concentrations were reduced during heat stress conditions but not in PF animals, suggesting that uncoupling of the hepatic GH-IGF axis may occur during HS. We investigated this possibility by measuring proximal indicators of hepatic GH signaling following a GH bolus. Heat stress but not PF decreased abundance of the GH receptor and GH-dependent signal transducer and activator of transcription (STAT)-5 phosphorylation. Consistent with reduced GH signaling through STAT-5, basal hepatic IGF-I mRNA abundance was lower in HS cows. Thus, the reduced hepatic GH responsiveness (in terms of IGF-I gene expression) observed during HS appears to involve mechanisms at least partially independent of reduced nutrient intake. The physiological significance of reduced hepatic GH receptor abundance during HS is unclear at this time. Aside from reducing IGF-I production, it may reduce other GH-sensitive bioenergetic processes such as gluconeogenesis.

Heat stress (HS) jeopardizes livestock health and productivity and both may in part be mediated by reduced intestinal integrity. Dietary zinc improves a variety of bowel diseases, which are characterized by increased intestinal permeability. Study objectives were to evaluate the effects of supplemental zinc amino acid complex (ZnAA) on intestinal integrity in heat-stressed growing pigs. Crossbred gilts (43±6 kg BW) were ad libitum fed one of three diets: (1) control (ZnC; 120 ppm Zn as ZnSO4; n=13), (2) control+100 ppm Zn as ZnAA (Zn220; containing a total of 220 ppm Zn; n=14), and (3) control+200 ppm Zn as ZnAA (Zn320; containing a total of 320 ppm Zn; n=16). After 25 days on their respective diets, all pigs were exposed to constant HS conditions (36°C, ∼50% humidity) for either 1 or 7 days. At the end of the environmental exposure, pigs were euthanized and blood and intestinal tissues were harvested immediately after sacrifice. As expected, HS increased rectal temperature (P⩽0.01; 40.23°C v. 38.93°C) and respiratory rate (P⩽0.01; 113 v. 36 bpm). Pigs receiving ZnAA tended to have increased rectal temperature (P=0.07; +0.27°C) compared with ZnC-fed pigs. HS markedly reduced feed intake (FI; P⩽0.01; 59%) and caused BW loss (2.10 kg), but neither variable was affected by dietary treatment. Fresh intestinal segments were assessed ex vivo for intestinal integrity. As HS progressed from days 1 to 7, both ileal and colonic transepithelial electrical resistance (TER) decreased (P⩽0.05; 34% and 22%, respectively). This was mirrored by an increase in ileal and colonic permeability to the macromolecule dextran (P⩽0.01; 13- and 56-fold, respectively), and increased colonic lipopolysaccharide permeability (P⩽0.05; threefold) with time. There was a quadratic response (P⩽0.05) to increasing ZnAA on ileal TER, as it was improved (P⩽0.05; 56%) in Zn220-fed pigs compared with ZnC. This study demonstrates that HS progressively compromises the intestinal barrier and supplementing ZnAA at the appropriate dose can improve aspects of small intestinal integrity during severe HS.

The cellular heat stress (HS) response is one component of the acute systemic response to HS. Gene networks within and across cells and tissues respond to environmental heat loads above the thermoneutral zone with both intra- and extracellular signals that coordinate cellular and whole-animal metabolism. Activation of these systems appears to be initiated at skin surface temperatures exceeding 35°C as animals begin to store heat and rapidly increase evaporative heat loss (EVHL) mechanisms. Gene expression changes include 1) activation of heat shock transcription factor 1 (HSF1); 2) increased expression of heat shock proteins (HSP) and decreased expression and synthesis of other proteins; 3) increased glucose and amino acid oxidation and reduced fatty acid metabolism; 4) endocrine system activation of the stress response; and 5) immune system activation via extracellular secretion of HSP. If the stress persists, these gene expression changes lead to an altered physiological state referred to as \"acclimation,\" a process largely controlled by the endocrine system. In the acclimated state, metabolism is adjusted to minimize detrimental effects of increased thermal heat load. The role of secreted HSP in feedback regulation of the immune and endocrine system has not yet been investigated. The variation in EVHL among animals and the central role that HSF1 has in coordinating thermal tolerance suggest that there is opportunity to improve thermal tolerance via gene manipulation. Determining the basis for altered energy metabolism during thermal stress will lead to opportunities for improved animal performance via altered nutritional management.

Supplementing a high dose of dietary conjugated linoleic acid (CLA) inhibits milk fat synthesis in dairy cows immediately postpartum. During negative net energy balance (EBAL), it appears that moderate CLA-induced milk fat depression causes a positive response in milk yield; however, as milk fat depression becomes more severe, the milk yield response diminishes. Multiparous Holstein cows (n = 31) were randomly assigned to 1 of 3 treatments beginning 9 ± 6 d before expected calving and ceased at 40 d in milk (DIM): 1) 578 g/d of a rumen-inert (RI) palm fatty acid distillate (control), 2) 600 g/d of RI-CLA for the entire trial period (CLA-1), and 3) 600 g/d of RI-CLA until 10 DIM followed by 200 g/d for the remainder of the trial (CLA-2). Each dose provided equal amounts of fatty acids by replacing and balancing each treatment with a RI palm fatty acid distillate. Doses provided a total of 522 g of fatty acids/ d and 0, 174, or 58 (depending upon DIM) g of CLA (mixed isomers)/d. To improve palatability, doses were mixed with 600 g/d of dried molasses; one-half of the supplement was fed at 0800 h, and the remainder at 1900 h. Individual milk yield, dry matter intake, and body weight were recorded daily and milk composition determined every other day. There was no overall CLA effect on either the content or yield of milk protein or lactose. Both CLA treatments decreased overall milk fat content (26.0 and 18.3%) and yield (22.5 and 17.3%) with CLA-induced milk fat depression becoming significant by d 8. The CLA-induced milk fat depression increased in magnitude with progressing DIM until reaching a plateau on d 18 for CLA-1 (43%) and on d 14 for CLA-2 (33%), although neither milk fat trans-10, cis-12 CLA content (1.8 mg/g) nor its transfer efficiency (6.3%) changed over time. Treatments had no effect on overall dry matter intake or milk yield, but there was a treatment x time interaction for milk production, as cows fed either CLA treatment had increased milk yield after the second week of lactation. Cows fed either CLA treatment had a significant improvement in overall EBAL (-5.1 vs. -1.8 Mcal/d), a decrease in nonesterified fatty acid levels (12%), and an increase in glucose levels (11%). A dietary supplement containing trans-10, cis-12 CLA markedly improves EBAL and bioenergetic variables and increases milk yield in the total mixed ration-fed transitioning dairy cow.

Serotonin (5-HT), a neurotransmitter synthesized from tryptophan, has been proposed as a feedback inhibitor of lactation. We determined that the gene coding for tryptophan hydroxylase 1, the rate-limiting enzyme for 5-HT synthesis, is expressed in bovine mammary epithelial cells in vitro and is upregulated by prolactin. In addition, 5-HT reduced the expression of α-lactalbu-min and casein genes in vitro. Furthermore, inhibiting 5-HT synthesis with p-chlorophenylalanine or blocking the 5-HT receptor with methysergide (METH) increased milk protein gene expression. We then evaluated effects of intramammary 5-HT or METH infusion on production and milk composition in 6 multiparous Holstein cows. Cows were assigned to a repeated measures design of contralateral intramammary infusions of METH (20 mg/quarter per d) or saline for 3 d followed by a 7-d washout period before administering 5-HT (50 mg/quarter/d) or SAL for 3 d. For each udder half, milk yield was recorded twice and composition was determined once per day. Blood samples were harvested each day for plasma to determine glucose and nonesterified fatty acid concentrations. Evaporative heat loss, respiration rate, left and right udder temperatures, and rectal temperatures were obtained after each milking to evaluate possible systemic effects of infusions. During METH and saline infusions milk yield increased 10.9%. During 5-HT and saline infusion milk yield decreased 11.1%. Milk yield and physiological responses suggested intramammary 5-HT and METH doses were high enough to cause systemic effects. Infusing saline, METH, and 5-HT increased milk SCC. Infusing 5-HT tended to reduce mean lactose concentration (4.3 vs. 4.6%) relative to saline. Milk protein content was decreased by METH and SAL (2.0%) and was increased (5.8%) by 5-HT followed by a 33% decrease postinfusion. Infusion of METH increased evaporative heat loss 11%, which decreased 11% postinfusion. Infusions of 5-HT or METH did not affect plasma nonesterified fatty acid or glucose concentrations, respiration rate, or milk fat content. We conclude 5-HT infusion reduced milk synthesis, whereas blocking the 5-HT receptor with METH increased milk synthesis. Doses of 5-HT and METH used in this study likely resulted in systemic effects. These data support the concept that 5-HT is a feedback inhibitor of lactation in the bovine.