Heat stress is a health and economic issue in every dairy-producing area in North America. The economic impact of heat stress on American animal agriculture ...
TechTalk Scientific Update From Elanco Animal Health
The Effects of Heat Stress on Production and its Nutritional Implications Lance H. Baumgard, PhD, and Robert P. Rhoads, PhD, The University of Arizona Chel E. Moore, PhD, Elanco Animal Health
Introduction Figure 1. Temperature-Humidity Index
Heat stress is a health and economic issue in every dairy-producing area in North America. The economic impact of heat stress on American animal agriculture is almost $2 billion annually and the dairy industry is the most susceptible. Conservative estimates have the impact at $897 million/year in the dairy industry alone.1 This results from the combination of lost milk, poor reproductive performance, a decrease in milk quality (primarily due to an increase in somatic cell count; SCC; and incidence in mastitis), increased health-care costs and reduced heifer growth.
Temperature
The effect of ambient heat on dairy-cattle maintenance and milk production is well known and heavily influenced by relative humidity. A combination of the two variables (temperature-humidity index; THI; Figure 1)2 is a better predictor of whether or not cows are “stressed”. As an example, the THI in southern Minnesota (an area of relatively high humidity) during the 2006 Memorial Day weekend was in the mid 90s but only in the low 80s in Phoenix Arizona (an area of low humidity).
Relative Humidity
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A THI >72 is the point at which a dairy cow starts to decrease productivity. A THI of 72 can be achieved at moderate temperatures if relative humidity is high. Unabated heat stress can decrease feed intake more than 35 percent. Even on well-managed and well-cooled dairies, heat stress decreases feed intake by 10 to 15 percent.3,4
Elanco Animal Health • A Division of Eli Lilly
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72 22.2 72 73 22.8 72 73 74 23.3 72 73 74 75 23.9 NO 72 73 74 75 76 24.4 STRESS 77 25.0 72 73 74 75 76 78 25.6 73 74 75 76 77 79 26.1 72 73 74 76 76 78 80 26.7 72 73 74 75 76 77 79 81 27.2 72 73 75 76 77 78 80 82 27.8 73 74 75 77 78 79 81 83 28.3 72 73 75 76 78 79 80 82 84 28.9 74 75 77 78 80 81 83 73 MILD 72 73STRESS 85 29.4 75 76 78 79 81 82 84 72 74 75 77 78 80 81 83 84 86 30.0 73 74 76 77 79 81 82 84 84 87 30.6 88 31.1 72 73 75 76 78 80 81 83 85 85 89 31.7 72 74 75 77 79 80 82 84 86 86 90 32.2 72 74 76 78 79 81 83 85 86 87 91 32.8 73 75 76 78 80 82 84 86 87 88 92 33.3 73 75 77 79 81 83 85 86 88 89 93 33.9 74 76 78 80 81HEAT 83 85 87 89 90 94 34.4 74 76 78 80 82 84 86 88 90 91 STRESS 95 35.0 75 77 79 81 83 85 87 89 91 92 96 35.6 75 77 79 81 83 86 88 90 92 93 97 36.1 76 78 80 82 84 86 88 91 93 94 98 36.7 76 78 80 83 85 87 89 91 94 95 99 37.2 76 79 81 83 85 88 90 92 94 96 100 37.8 77 79 82 84 86 88 91 93 95 97 101 38.3 77 80 82 84 87 89 92 94 96 98 92 95 97 99 102 38.9 78 80 83 85 87 90SEVERE 103 39.4 78 81 83 86 88 91 93 96 94 96 104 40.0 79 81 84 86 89 91STRESS 105 40.6 79 82 84 87 89 92 95 97 106 41.1 80 82 85 88 90 93 95 98 107 41.7 80 83 85 88 91 94 96 108 42.2 81 83 86 89 92 94 97 109 42.8 81 84 87 89 92 95 98 110 43.3 81 84 87 90 93 96 DEAD 111 43.9 82 85 88 91 94 96 112 44.4 82 85 88 91 94 97 COWS 113 45.0 83 86 89 91 95 98 114 45.6 83 86 89 92 96 115 46.1 84 87 90 93 96 116 46.7 84 87 90 94 97 117 47.2 85 88 91 94 98 118 47.8 85 88 92 95 119 48.3 85 89 92 96 120 48.9 86 89 93 96 121 86 90 93 97 122 87 90 94 97 123 87 91 94 98 124 88 91 95 125 88 91 96 126 89 92 96 127 89 92 97 128 90 93 97 129 90 93 98 and Company 130 90 94 •98Greenfield, Indiana 131 91 94 132 91 95 133 92
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Another easily recognized factor of heat stress is a significant reduction in milk yield. Even in well-cooled dairies, heat stress typically decreases milk yield by 10 to 15 percent and in non-cooled management systems milk yield can decrease by 40 to 50 percent during severe conditions.3,4 In addition to the immediate effects (milk yield and feed intake), cows will typically lose body weight and condition during prolonged periods of heat stress. Furthermore, the negative effects of heat stress on reproductive indices are not only immediately obvious, but linger/persist well into the fall months, even after cows have returned to more comfortable environmental conditions.5,6
increases the risks of rumen acidosis and indirectly enhances the risk of negative side effects of an unhealthy rumen environment (i.e. laminitis, milk fat depression, etc.).
Metabolic Adaptations to Reduced Nutrient Intake The early lactation cow is a classic example of lactation-induced negative energy balance (NEBAL) resulting from an inability of the cow to consume enough feed to meet the energy demands of lactation and maintenance requirements.8 Negative energy balance is associated with a variety of metabolic changes that are implemented to support the dominant physiological condition of lactation.9 Marked alterations in both carbohydrate and lipid metabolism ensure partitioning of dietary derived and tissue-originating nutrients towards the mammary gland, and not surprisingly, many of these changes are mediated by endogenous somatotropin which is naturally increased during periods of NEBAL.9 One characteristic response is a reduction in circulating insulin coupled with a reduction in systemic insulin sensitivity. Compared to a well-fed cow in positive energy balance (Figure 2), the reduction in insulin action allows for adipose lipolysis and mobilization of non-esterified fatty acids (NEFA).9 Increased circulating NEFA are typical
Effect of Heat Stress on Rumen Health Heat stress has long been known to adversely affect rumen health. One way cows dissipate heat is via panting, and this increased respiration rate results in enhanced CO2 (carbon dioxide) being exhaled. In order to be an effective blood pH buffering system, the body needs to maintain a 20:1 HCO3- (bicarbonate) to CO2 ratio. Due to the hyperventilation-induced decrease in blood CO2, the kidney secretes HCO3- to maintain this ratio. This reduces the amount of HCO3- that can be used (via saliva) to buffer and maintain a healthy rumen pH. In addition, panting cows often drool which reduces the quantity of saliva that would normally been deposited in the rumen. The reductions in saliva HCO3- content and the decreased amount of saliva entering the rumen make the heat stressed cow much more susceptible to subclinical and acute rumen acidosis.7
Figure 2. Postabsorptive metabolism in a well-fed cow in positive energy balance
To compensate for the reduced feed intake caused by heat stress and the metabolic heat load associated with fermenting forages, nutritionists typically increase the energy density of the ration. This is normally accomplished with extra concentrates and reductions in forages. However, this needs to be conducted with care as this type of diet can be associated with a lower rumen pH. The combination of a “hotter” ration and the cows reduced ability to neutralize the rumen (because of the reduced saliva HCO3- content and increased drooling) directly
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in “transitioning” cows and represent a significant source of energy (and precursor for milk fat synthesis) for cows in NEBAL (Figure 3). Post-absorptive carbohydrate metabolism is also altered by the reduced insulin action during NEBAL with the net effect of reduced glucose uptake by systemic tissues (i.e. muscle and adipose). The reduced nutrient uptake coupled with the net release of nutrients (i.e. amino acids and NEFA) by systemic tissues (Figure 3) are key homeorhetic (an acclimated response vs. an acute/homeostatic response) mechanisms implemented by cows in NEBAL to support lactation.9
Figure 3. Postabsorptive metabolism in a cow during negative energy balance
Bovine Somatotropin Somatotropin (bST) administration consistently increases milk yield in almost all management systems10 and has been U. S. Food and Drug Administration (FDA)-approved for use in the United States for over 12 years. Physiological effects of bST result from activation of the GH receptor (direct actions) or from GH-dependent stimulation of insulin-like growth factor-I (IGF-I) synthesis (indirect actions).10 Examples of direct actions are homeorhetic adaptations that promote nutrient trafficking away from adipose tissue (reduced lipogenesis, enhanced sensitivity to lipolytic signals, etc.) towards the mammary gland. A second target of GH is skeletal muscle where it decreases glucose utilization and may favor export of amino acids by inducing insulin resistance.11,12 These direct actions are coordinated systemic homeorhetic responses which are responsible for partitioning critical precursors and nutrients towards the mammary gland for milk synthesis.12
Taken together, these observations indicate that the bST-dependent increase in circulating IGF-I is a potent stimulator of milk synthesis (Figure 4). Furthermore, bST enhances liver gluconeogenesis (Figure 4) which is necessary to meet the mammary glands increased need for glucose. The combination of increased hepatic glucose output with a reduction in systemic insulin action, coupled with the mammary glands increased capacity (via IGF-I) to synthesize milk, are key mechanisms by which bST safely and consistently increases milk yield.10 Despite the fact that producing additional milk results in extra metabolic heat production, bST has demonstrated to be effective in a variety of management and environmental conditions.14 The mechanism by which bST remains effective during heat stress is due to its homeorhetic properties as it causes increased milk production via coordinating metabolism in almost all body tissues.10 This coordination includes an increased capacity to sweat and thus an enhanced ability to dissipate heat.15 However, despite the wealth of evidence demonstrating the effectiveness of bST during heat stress, some still question its usefulness and recommend limiting its employment during the summer months.
An additional mechanism by which bST is thought to increase milk yield occurs indirectly via increased liver secretion of insulin-like growth factor-I.10 Several lines of evidence support this notion13: first, mammary epithelial cells possess functional IGF-I receptors. Second, infusing IGF-I in lactating goats results in increased milk synthesis. Third, assays fail to detect significant specific GH binding in the bovine mammary gland. Fourth, mammary epithelial cells appear to produce little IGF-I.
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Figure 4. Mechanism of action for bST
Production Adaptations to Heat Stress
Metabolic Adaptations to Heat Stress
Heat stress reduces both feed intake and milk yield and the decline in nutrient intake has been identified as a major cause of reduced milk synthesis.5 However, the exact contribution of declining feed intake to the overall reduced milk yield remains unknown. To evaluate this question, we used a group of thermal neutral pair-fed animals to eliminate the confounding effects of nutrient intake. Lactating Holstein cows in mid-lactation were either cyclically heat stressed (THI = ~80 for 16 hours/day) for 9 days or remained in constant thermal neutral conditions (THI = ~64 for 24 hours/day) but pair-fed with heat-stressed cows to maintain similar nutrient intake.16 Cows were housed at the University of Arizona’s ARC facility and individually fed a total mixed ration (TMR) consisting primarily of alfalfa hay and steam flaked corn to meet or exceed nutrient requirements.17 Heat-stressed cows had an average rectal temperature of ~105° F during the afternoons of the treatment implementation. Heat-stressed cows had an immediate reduction (~11 lb/day) in dry matter intake (DMI) with the decrease reaching nadir at ~ day 4 and remaining stable thereafter. As expected and by design, thermal neutral pair-fed cows had a feed intake pattern similar to heat-stressed cows. Heat stress reduced milk yield by ~31 lbs/day with production steadily declining for the first 7 days before reaching a steady state. Thermal neutral pair-fed cows also had a reduction in milk yield of approximately 13 lbs/day, but milk production reached its nadir at day 2 and remained relatively stable thereafter. This indicates the reduction in DMI can only account for ~40 percent of the decrease in production when cows are heat stressed and that ~60 percent can be explained by other heat-stressed induced changes.
Due to the reductions in feed intake and increased maintenance costs,17 and despite the decrease in milk yield, heat-stressed cows enter into NEBAL.8 It is not unusual for heat-stressed cows to experience NEBAL of -4 to -6 Mcal/day.18 However, unlike NEBAL in thermal neutral conditions, heat-stressed induced NEBAL doesn’t result in elevated plasma NEFA (Figure 5). In addition, using a glucose tolerance test, we demonstrated that glucose disposal (rate of glucose entry into cells) is greater in heatstressed cows compared to thermal neutral pairfed cow.18 Both the decrease in plasma NEFA and the increased glucose disposal rate can be explained by increased insulin effectiveness. Insulin is a potent antilipolytic signal (blocks fat break down) and the primary driver of cellular glucose entry. Therefore, it appears that the heat-stressed cow becomes hypersensitive to the effects of insulin. Well-fed ruminants primarily oxidize (burn) acetate (a rumen-produced volatile fatty acid; VFA) as their principal energy source. However, during NEBAL cows also largely depend on NEFA for energy (Figure 3). Therefore, it appears the post-absorptive metabolism of the heat-stressed cow markedly differs from that of a thermal neutral cow, even though they are in a similar negative energetic state (Figure 3 vs. Figure 5). The apparent switch in metabolism and the increase in insulin sensitivity is probably a mechanism by which cows decrease metabolic heat production. Oxidizing fatty acids for energy generates more heat (~2 kcal/g or 13 percent on an energetic basis) compared to glucose (Figure 6). Therefore, during heat stress, preventing or blocking adipose mobilization/breakdown and increasing glucose “burning” is presumably a strategy to minimize metabolic heat production.
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The mammary gland requires glucose to synthesize milk lactose, and lactose production is the primary osmoregulator and thus determinant of milk yield. However, in an attempt to generate less metabolic heat, the body (primarily skeletal muscle) starts utilizing glucose at an increasing rate (Figure 5). As a consequence, the mammary gland may not receive adequate amounts of glucose and thus mammary lactose production and subsequent milk yield is reduced. This may be the primary mechanism which accounts for the additional reductions in milk yield that are not explained by decreased feed intake. Increasing hepatic glucose production should help alleviate the “shortage” that heat-stressed cows are experiencing.
Figure 6. Bioenergetics and metabolic heat production from oxidizing either glucose or fatty acids (i.e. stearic acid)
In addition to heat-stressed cows requiring special attention with regards to heat abatement and other dietary considerations (i.e. concentrate:forage ratio, HCO3- etc.), they also have an extra requirement for dietary or rumenderived glucose precursors. Of the three main rumen-produced volatile fatty acids, propionate is the one primarily converted into glucose by the liver. Highly fermentable starches such as grains increase rumen propionate production, and although propionate is the primary glucose precursor, feeding additional grains can be risky as heat-stressed cows are already susceptible to rumen acidosis.
Monensin Mode of Action Monensin has long been known to alter rumen fermentation and improve energy retention (Figure 7). Specifically, monensin increases propionate production and reduces rumen methane (CH4) synthesis.19 The increase in rumen-derived propionate explains the increased glucose production (turnover) in monensin-fed ruminants.19 Therefore, utilizing monensin during heat stress is a good management and nutritional decision to enhance liver glucose production.
Figure 5. Postabsorptive metabolism in a heat-stressed cow
In addition to monensin aiding the postabsorptive glucose “shortage” situation, it also has an important rumen function in heat-stressed cows. As stated earlier, heatstressed cows are predisposed to rumen acidosis and this is further complicated by additional concentrate feeding. Monensin reduces rumen lactate (the primary culprit in rumen acidosis) concentrations and increases rumen pH in stressed animals19 while providing more propionate for glucose production by the liver. 5
Conclusions and Recommendations
Figure 7. Usable energy derived from rumen fermentation
• Heat stress affects every region of the U.S. dairy industry
FORAGE S CONCENTR ATES
Usable energy derived per mole of glucose (kcal)20
• Heat stress reduces milk yield and thus limits profitability even on well-cooled and managed dairies
Methane & CO2 (wasted energy)21
419 ACETIC ACID
• Heat-stressed cows are susceptible and prone to rumen acidosis due to decreased buffering capacity
OR
524 BUTYRIC ACID OR
734 PROPIONIC ACID
• Heat-stressed cows switch metabolism to prevent adipose mobilization and fatty acid oxidation • Heat-stressed cows have increased need for glucose production
Heat Stress and Somatotropin 2% to 4% As stated earlier, despite the backing of scienmore energy perthat pound heat-stressed tific literature, some believe of feed with cows do not respond to bST. To evaluate this, Rumensin we used lactating Holstein cows in mid-lactation that were either cyclically heat stressed (THI = ~80 for 16 hours/day) for 7 days or remained in constant thermal neutral conditions (THI = ~64 for 24 hours/day) but pair-fed with heat-stressed cows to maintain similar nutrient intake. On the 7th day, both heatstressed and underfed cows received bST (supplemental bST was provided through administration of POSILAC®, 500 mg dose) and remained either heat-stressed or pair-fed for an additional 7 days. Similar to our previous experiments, feed intake, milk yield and daily NEFA data indicate marked differences that were independent of feed intake. Despite being extensively heat-stressed (average afternoon rectal temperature of ~105° F), and underfed, bST increased milk yield by ~10 and 15 percent in heat-stressed and thermal-neutral cows, respectively.18 CO FOR A NC EN GES TR AT ES
• Monensin alters rumen fermentation, increasing propionate synthesis • Propionate is the primary precursor to liver glucose production • Similar to thermal-neutral conditions, in heat-stressed cows bST reduces insulin sensitivity, increases glucose production and partitions nutrients toward the mammary gland to support increased milk yield
References 1. St. Pierre, NR, B Cobanov and G Schnitkey. Economic losses from heat stress by U.S. livestock industries. J. Dairy Sci. 86:E52-E77, 2003. 2. Smith, J, J Harner, D Dunham, J Stevenson, J Shirely, G Stokka and M Meyer. Coping with Summer Weather: Dairy Management Strategies to Control Heat Stress. Kansas State University Agricultural Experimental Station and Cooperative Extension Service (MF-2319), 1998.
Similar to thermal-neutral cows,10 evaluating daily blood bioenergetic variables (NEFA, PUN, glucose, etc.) and using a range of metabolic challenges, we have demonstrated that bST reduces systemic insulin sensitivity in heatstressed cows. Comparable to thermal-neutral cows, this reduction in insulin action partially explains the partitioning of nutrients to the mammary gland to support increased milk synthesis during heat stress.
3. Collier, RJ, DK Beede, WW Thatcher, LA Israel and CJ Wilcox. Influences of environment and its modification on dairy animal health and production. J. Dairy Sci. 65: 2213-2227, 1982.
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4. West, JW. Effects of heat-stress on production in dairy cattle. J. Dairy Sci. 86:21312144, 2003. 5. Fuquay, JW. Heat stress as it affects animal production. J. Anim. Sci. 52:164-174, 1981. 6. Roth, Z, A Bor, R Braw-Tal and D Wolfenson. Carry-over effect of summer thermal stress on characteristics of the preovulatory follicle of lactating cows. J. Thermal Bio. 29:681-685, 2004. 7. Kadzere, CT, MR Murphy, N Silanikove and E Maltz. Heat stress in lactating dairy cows: a review. Livestock Prod. Sci. 77:59-91, 2002 8. Moore, CE, JK Kay, MJ VanBaale, RJ Collier and LH Baumgard. Effect of conjugated linoleic acid on heat stressed Brown Swiss and Holstein cattle. J. Dairy Sci. 88:1732-1740, 2005. 9. Bauman, DE and WB Currie. Partitioning of nutrients during pregnancy and lactation: a review of mechanisms involving homeostasis and homeorhesis. J. Dairy Sci. 63:15141529, 1980. 10. Bauman, DE. Bovine somatotropin and lactation: from basic science to commercial application. Domest. Anim Endocrinol. 17:101-116, 1999. 11. Bauman, DE and RG Vernon. Effects of exogenous bovine somatotropin on lactation. Annu Rev Nutr. 13: 437-461, 1993. 12. Bell, AW and DE Bauman. Adaptations of glucose metabolism during pregnancy and lactation. J. Mammary Gland Bio. Neoplasia 2:265-278, 1997.
14. Collier, RJ, LH Baumgard, AL Lock and DE Bauman. Physiological Limitations: nutrient partitioning. Chapter 16. In: Yields of farmed Species: constraints and opportunities in the 21st Century. Proceedings: 61st Easter School. Nottingham, England. J. Wiseman and R. Bradley, eds. Nottingham University Press, Nottingham, U.K. 351377, 2005. 15. Manaulu, W, HD Johnson, R Li, BA Becker and RJ Collier. Assessment of thermal status of somatotropin injected lactating Holstein cows maintained under controlledlaboratory thermo-neutral, hot and cold environments. J. Nutr. 121:2006-2019, 1991. 16. Baumgard, LH, MJ VanBaale, RP Rhoads, ML Rhoads and RJ Collier. Strategies to reduce heat stress in semi-arid climates. Reunioin Internacional Sobre Produccion De Carne Y Leche En Climas Calidos. Mexicali, Baja California pp. 3-15, 2005. 17. National Research Council. Nutrient Requirements of Dairy Cattle, 7th rev. ed. Nat. Acad. Press, Washington, DC, 2001. 18. Wheelock, JB, SR Sanders, G Shwartz, LL Hernandez, SH Baker, JW McFadden, LJ Odens, R Burgos, SR Hartman, RM Johnson, BE Jones, RJ Collier, RP Rhoads, MJ VanBaale and LH Baumgard. Effects of heat stress and rbST on production parameters and glucose homeostasis. J. Dairy Sci. 89. Suppl. (1):290-291, 2006. 19. Schelling, GT. Monensin mode of action in the rumen. J. Anim. Sci. 58:1518-1527, 1984. 20. Handbook of Chemistry and Physics.
13. Rhoads, RP, ML Rhoads and YR Boisclair. Implications of a dysfunctional somatotropic axis during the transition period in dairy cattle. Pages 197-208 in Proc. 20th Annu. Southwest Nutr. & Mgmnt. Conf., Tempe, AZ, 2005.
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21. Hungate, RE. The rumen and its microbes. Academic Press, New York, 1966.
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