ISSUE FOCUS FEED & ADDITIVE MAGAZINE June 2022 39 low producers, as they require a higher metabolism, creating more heat. For example, cows producing 35L/day tolerate threshold temperatures for HS 5°C higher than cows producing 45L/day. OBSERVING HEAT STRESS IN DAIRY Recognizing the signs of HS is the first step to implementing practical mitigation strategies. When suffering from HS, cows change their behavior to reduce the amount of heat produced or increase heat dissipation. Mechanisms such as increased respiration rate and panting, open-mouth breathing, reduced feed intake (FI) and rumination time, reduced activity and lying time, and seeking shade and water… can then be detected. Regular observation of cows, coupled with records of FI and milk production in parallel to THI, help alleviate HS early on. Indeed, the FI drop is responsible for the decreased performance witnessed during HS, but only partially, as demonstrated in studies using heatstressed cows pair-fed to cows in normal conditions (i.e., restricted FI). It is estimated that FI reduction accounts for 50% of the milk drop, the rest being linked to the evolution of the cow's metabolism. EFFECT OF HEAT STRESS ON DAIRY COWS Ruminal acidosis is closely related to HS as the FI behavior of the cows is switched toward fewer but bigger meals, while rumination time decreases, and bicarbonate is redirected to the bloodstream, all leading to an acidification of the rumen. The rumen pH drop is observed both in the case of high fiber or high concentrate diets, together with an increase of the rumen temperature, leading to impaired rumen functions. Along with rumen acidosis, some metabolic-related diseases appear, such as gut lesions, lameness & laminitis due to massive endotoxins (LPS) production, oxidative stress (OS), inflammation, etc. Indeed, the higher CBT, responsible for lower blood flow in the small intestine, triggers the production of reactive species from oxygen and nitrogen, thus damaging the intestinal mucosa. This, in turn, facilitates the passage of LPS and pathogens through the gut wall via loose, tight junctions, further compromising the resilience of the cows: LPS induce a systemic immune reaction through the release of pro-inflammatory cytokines and acute-phase proteins such as haptoglobin. What's more, LPS challenges are always followed by increased SCC and mastitis. In parallel, the inflammatory state generates a higher energy demand while its supply is reduced because of decreased FI. Additionally, OS causes the production of heat shock proteins, which activate the immune system and further increase the energy demand for reaching the "back-to-normal" state. This is achieved by switching the energy metabolism and activating the endocrine and immune systems. All these physiological adaptations and responses to HS-related challenges can have long-lasting effects on the cows and directly affect the economic performance of the dairy operation (cf. Figure 2).
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