Effects of high-energy and low-energy diets during late lactation on the subsequent dry period and lactation of Holstein dairy cows.

Our primary objective was to investigate the effect of 2 dietary treatments differing in energy density during late lactation on body reserves and the subsequent effects on the next dry period and lactation of high-producing Holstein cows. At 150 d of gestation, 66 multiparous lactating Holstein dairy cows were blocked by expected calving date and then randomly assigned to 2 dietary treatment groups that were fed either a high-energy diet (HE; 1.74 Mcal NEL kg DM) or a low-energy diet (LE; 1.50 Mcal NEL kg DM) to achieve a high or normal BCS at dry-off, respectively. Thereafter, both groups were fed identical diets. At dry-off, the HE group had higher BCS (3.69 ± 0.08 vs. 3.25 ± 0.05) and backfat thickness (BFT; 43.9 ± 2.5 vs. 37.1 ± 1.3 mm) compared with the LE group. Subsequently, during the dry period, LE cows had increased BFT and increased daily rumination time by 20 min compared with the HE group. During the last 10 d of gestation and the first 21 DIM, LE cows had increased DMI compared with HE cows. De novo fatty acid (FA; <C FA) content in milk relative to total FA concentrations (preformed FA and mixed FA) was lower in the HE group during the first 21 d of lactation, averaging 18.6% versus 20.2% ± 0.3% compared with LE cows. No differences in energy balance or milk production were detected during the first 3 wk of lactation or during the first 90 DIM. Circulating nonesterified fatty acid concentrations tended to differ between treatments (0.51 and 0.46 ± 0.01 mmol/L for HE and LE, respectively); however, no differences in BHB were detected between groups. In summary, dietary energy manipulation during late lactation led to differences in body reserves at dry-off, which were followed by distinct changes in body reserves during the dry period and early lactation. These patterns may reflect adjustments in feed intake in response to internal cues related to body fat, suggesting a possible regulatory mechanism toward an individual adiposity setpoint.