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  • Edgar Desautels

Etiology of Heat Stress in Dairy

Updated: Sep 4, 2019




In order to reduce economic losses due to heat stress, we must first understand what causes dairy cattle to become heat stressed. The biological mechanism by which heat stress leads to decreased production and reproduction is partly explained by reduced feed intake. It also includes, however, altered endocrine status, reduction in rumination and nutrient absorption, and increased maintenance requirements (Collier et al., 2005), which results in decreased nutrients and energy available for production. Due to the reduction in feed intake during heat stress, a majority of dairy cows enter into negative energy balance (NEBAL) (Baumgard et al., 2008). This is similar to the NEBAL observed in early lactation but not to the same extent. In addition to decreased feed intake, the thermoregulation process leads to an increase in blood flow to the skin to bring heat up from the body core to dissipate that heat via evaporation from the skin and respiratory tract. Thus, there is decreased blood flow to internal organs (i.e., digestive tract), therefore less movement of water and nutrients via the portal system that would have been used to support milk production (Finch 1986). Even though both early lactation and heat stressed cows are in NEBAL, there are major differences between the 2 groups (Baumgard et al., 2008).

In early lactation, dry matter intake (DMI) is insufficient to support peak milk production, causing cows to enter into NEBAL because they simply cannot consume enough energy to meet their requirements for milk production. For this reason, these cows begin to mobilize body fat in order to meet their energy requirements. Changes in both carbohydrate and lipid metabolism help ensure partitioning of dietary and tissue derived nutrients towards the mammary gland (Bauman and Currie et al., 1980). In the early lactation cow, circulating insulin levels are reduced; insulin is an anti-lipolytic signal. Due to the reduction of insulin during early lactation, these cows are able to mobilize body fat to meet their energy needs. As a result of body fat mobilization, it is very common for early lactating cows to have increased non-esterified fatty acid (NEFA) levels in the blood. This allows glucose to be used by the mammary gland for milk production. If, however, the early lactation cow becomes heat stressed, changes in metabolism occur. In a recent study, 2 groups of early lactation cows were pair fed. One group was exposed to heat stress conditions while the pair fed group was housed under thermoneutral conditions. NEFA levels were similar for each group prepartum but the heat stressed group showed a significant reduction in NEFA levels postpartum, indicating impaired adipose tissue mobilization (Lamp et al., 2015). This would lead to increased glucose uptake by tissues (muscle) as an energy source, leaving less glucose available for the mammary gland, and thus decreasing milk output.

Similarly, heat stressed dairy cows also enter into NEBAL due to a reduction in DMI, but unlike early lactation cows, heat stressed induced NEBAL does not result in elevated plasma NEFA. Also, insulin levels do not decrease in heat stressed dairy cows like they do in early lactation cows. The greater levels of insulin sensitivity is likely a mechanism by which cattle decrease metabolic heat production, as oxidizing glucose is more efficient (Baldwin et al., 1980). This blocks the breakdown of fat, making the heat stressed dairy cow metabolically inflexible because of not being able to rely on adipose tissue to meet the energy needs of a cow that already is energy deficient due to a drop in DMI. The mammary gland requires glucose to synthesize the primary sugar in milk known as lactose. When an animal is heat stressed, it uses glucose as an energy source at a greater rate in an attempt to generate less metabolic heat. A major consequence of this is that less glucose is available for the mammary gland to produce lactose, leading to decreased milk production.

In a study done by Rhoads et al. (2009), the authors studied what percent decline in production could be attributed to decreased DMI and what percent was due to other factors. This was accomplished by pair feeding 2 groups of cows, 1 which was exposed to heat stress and the other which was kept under thermoneutral conditions. During the heat stress period under similar DMI between both groups, cows under heat stress had a milk yield of 21.5 kg/d while the pair-fed cows under thermoneutral conditions produced 29.0 kg/d. Thus, the authors reported that factors other than reduced DMI are responsible for 64% of the milk loss due to heat stress. These authors hypothesized that due to the fact that heat stressed dairy cows do not mobilize adipose tissue, glucose-sparing mechanisms that normally prevent severe reductions in milk yield during periods of inadequate intake are not present.

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