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1008 PD: What’s behind heat-stress-induced milk depression?

Chel Moore Published on 30 June 2008

Heat stress is both a cow health and an economic issue wherever dairies exist in North America.

It’s estimated impact on American agriculture is nearly $2 billion annually, and the dairy industry is the most susceptible. The combination of lost milk, poor reproductive performance, rumen acidosis, decreases in milk quality, increased health care costs and reduced heifer growth adds up to a conservatively estimated total loss of about $897 million per year to the dairy industry.

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Ambient temperature is known to affect milk production, and its effect is heavily influenced by relative humidity. The temperature-humidity index (THI), a combination of relative humidity and ambient temperature, is a better predictor of whether a cow is “stressed.” A dairy cow’s productivity begins to decrease at a THI greater than 72. When relative humidity is high, this point can be achieved at moderate temperatures. This explains why all dairy regions in North America are affected by heat stress. Unabated heat stress can decrease dry matter intake (DMI) more than 35 percent and lower milk yield by 40 to 50 percent. Even on well-managed and well-cooled dairies, heat stress decreased feed intake and milk yield by 10 to 15 percent. In prolonged periods of heat stress, cows typically lose body condition and weight as well.

Reproduction is also negatively affected, both during the time of heat stress and well into the fall months, even after the return of more comfortable environmental conditions.

The cow’s metabolic response in early lactation
The early lactation cow is a classic example of lactation-induced negative energy balance (NEBAL). This results when the cow is unable to consume enough feed to meet the energy demands of lactation and her own maintenance.

NEBAL is associated with a number of metabolic changes that support lactation. Early lactation brings about changes in the cow’s carbohydrate and lipid metabolism to guarantee a supply of nutrients to the mammary gland. Circulated insulin is reduced as well as systemic insulin sensitivity. Compared to a well-fed cow in positive energy balance, the reduced insulin action allows increased circulating non-esterified fatty acids (NEFA), a significant source of energy (and precursor for milk fat synthesis) for cows in NEBAL. This action likewise reduces glucose uptake by systemic tissues (muscle and adipose), allowing the mammary gland to use this excess glucose for lactose and subsequent milk production.

A somewhat different metabolic response to heat stress
The decline in nutrient intake during heat stress has been identified as a major cause of lower milk yield. The exact contribution of lowered feed intake to reduced milk output was explored in research recently completed at the University of Arizona. In the study, a group of thermal-neutral cows were pair-fed with a group of heat-stressed cows to eliminate the confounding effect of dissimilar DMI. Cows were housed at the University of Arizona William J. Parker Agriculture Research Complex and individually fed a total mixed ration (TMR) consisting primarily of alfalfa hay and steam flaked corn to meet or exceed nutrient requirements.

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The heat-stressed cows were exposed to the typical conditions of Arizona in July. The environment of the thermal-neutral group was maintained at a near constant 64 THI. The heat-stressed cows had an immediate reduction in DMI of about 11 pounds per day with the decrease reaching its lowest point on Day 4 and remaining stable thereafter. As expected, the thermal-neutral pair-fed cows experienced a similar feed intake decrease.

Heat-stressed cows reduced milk yield by about 31 pounds per 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 pounds per day, but milk production leveled off after only two days. The differences observed between these two groups suggest that decreased DMI accounts for only about 40 percent of the decrease in production when cows are heat stressed and the other 60 percent must be attributed to other heat-stress-induced changes.

Due to reductions in feed intake and increased maintenance demands, heat-stressed cows enter into NEBAL similar to their thermal-neutral, underfed counterparts. Heat-stress-induced NEBAL does not, however, result in elevated plasma NEFA. The research also demonstrated that glucose clearance is greater in heat-stressed cows than in thermal neutral pair-fed cows. Both the lack of a plasma NEFA response and the increased glucose disposal rate can be explained by increased insulin action. Insulin is a potent antilipolytic signal that blocks fat breakdown and is the primary driver of glucose disposal. It appears, therefore, that the heat-stressed cow becomes hypersensitive to the effects of insulin.

Well-fed ruminants primarily oxidize acetate, a rumen-produced volatile fatty acid (VFA), as their principal energy source. When cows experience NEBAL during early lactation, however, they largely depend on NEFA for energy. The post-absorptive metabolism of the heat-stressed cow is then markedly different from that of a thermal-neutral early lactation cow, even though they are in a similar negative-energy state. The apparent switch in metabolism and the increase in insulin sensitivity may be a mechanism by which cows decrease metabolic heat production.

The mammary gland requires glucose to synthesize milk lactose, and lactose production is the primary determinant of milk yield. However, in an attempt to generate less metabolic heat, the body starts utilizing glucose at an increasing rate. As a result, the mammary gland may not receive adequate amounts of glucose, thus reducing mammary lactose production and subsequent milk yield. This may be the primary mechanism that accounts for the additional reductions in milk yield not explained by decreased feed intake. Increasing hepatic glucose production should help alleviate the “shortage” that heat-stressed cows are experiencing.

Heat-stressed cows also require more dietary or rumen-derived glucose precursors. Of the three main rumen-produced VFAs, propionate is the one primarily converted into glucose by the liver. Highly fermentable starches, such as grains, increase rumen propionate production, but feeding additional grains can be risky as heat-stressed cows are already susceptible to rumen acidosis. Therefore, during periods of heat stress, maximizing energy utilization and propionate production from feedstuffs becomes even more important.

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Conclusions and recommendations
1. Heat stress affects every region of the U.S. dairy industry.

2. Heat stress reduces milk yield and thus limits profitability even on well-cooled, well-managed dairies.

3. Heat-stressed cows switch metabolism to prevent adipose mobilization and fatty acid oxidation.

4. Heat-stressed cows have increased need for glucose production.

5. Propionate is the primary precursor to liver glucose production. PD

References omitted but are available upon request at

Chel Moore for Progressive Dairyman

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