Heifer rearing represents one of the largest costs of commercial dairying because these animals do not begin to produce milk until approximately 2 yr of age. The objectives of this study were to characterize milk production, growth, reproduction, and herd life after induced lactation in healthy 15-mo-old heifers. We further wanted to quantify their lactation response to bovine somatotropin (bST), and compare survival rate and profitability of heifers induced into lactation to that of heifers reared using traditional methods. Holstein heifers (n = 32) were induced into lactation by administration of estradiol-17β (0.075 mg/kg of body weight per d) and progesterone (0.25 mg/kg of body weight per d) for 7 d. Milking began on experimental d 18. Heifers were paired based on milk production, and one in each pair was assigned randomly to bST or control treatment groups; treatments began on 25 ± 7 d of lactation, and milk production was compared for 70 d. Heifers treated with bST produced 14.7% more milk than did controls. After the 70-d comparison period, all heifers received bST for the remainder of their lactations. Throughout the induced lactation, heifers gained 0.69 kg/d, averaged 1.8 services/pregnancy, and 27 heifers calved for a second lactation. For the herd life and economic analyses, heifers induced into lactation were compared with similarly aged heifers in the same herd reared by traditional management methods. The animals induced into lactation had a 62.7% chance of remaining in the herd as long as the peer cohorts, but both groups had similar productive lifespans. Net present value for an induced animal ($2,459) was not different from that of a traditionally raised peer ($3,137). In summary, heifers hormonally induced into lactation with estrogen and progesterone were healthy, grew normally, had a mean daily milk production of 18 kg with normal composition, and had good reproductive performance. Based upon the assumptions and prevailing financial environment of this experiment, hormonally induced lactation of 15-mo-old heifers, as a routine management tool, was not more profitable than traditional management practices.
Milk production in heifers induced into lactation is lower than that of postpartum primiparous cows. A method to improve milk production in induced lactations may provide opportunities for increased profitability as well as increase our understanding of the mechanisms that regulate mammary gland development and colostrum composition. The present study was conducted to determine if dexamethasone administration at the onset of milking or age at lactation induction would affect milk production in heifers induced into lactation. Holstein heifers at 14 [n=20; 354 ± 38 kg of body weight (BW)] and 18 mo of age (n=20; 456 ± 30 kg of BW) were assigned randomly to dexamethasone (DEX) or control (CON) treatment groups in a 2 × 2 factorial arrangement with age and dexamethasone treatment as the 2 factors. Heifers were induced into lactation with daily subcutaneous injections of estradiol-17β and progesterone (0.075 and 0.25 mg/kg of BW per d, respectively) on experimental d 1 to 7. They also received bovine somatotropin (bST) every 14 d beginning on experimental d 1. Milking began on experiment d 18 (lactation d 1). Dexamethasone (10mg) was administered on lactation d 1 and 2 following the morning milking; CON heifers did not receive dexamethasone. Milk yield from d2 to 15 of lactation of heifers receiving DEX (7.8 kg/d) was greater than that of CON heifers (6.0 kg/d) but was similar thereafter through 305 d of lactation (18.2 kg/d). Milk production to d 11 was similar for 14- and 18-mo-old heifers but was greater for 18- (18.9 kg/d) than for 14-mo-old animals (17.4 kg/d) through 305 d in milk. Milk fat percentage increased initially and was greater in DEX (4.51%) compared with CON (3.53%) heifers until 21 d in milk. Milk protein and lactose concentrations were not affected by DEX treatment. Age at induction did not affect milk fat, protein, or lactose percentages. Mean milk IgG concentration declined from 107.4 mg/mL on d 1 to 5.0mg/mL on d 7 of lactation, tended to be greater for 18- compared with 14-mo-old heifers, and was not different due to DEX treatment. Administration of DEX to heifers induced into lactation increased initial milk production during the first 2 wk of lactation but this effect did not persist through 305 DIM. Treatment with DEX appeared to stimulate mammary cell differentiation but did not change the rate of decline of milk IgG concentrations. Higher milk yield in 18-mo-old heifers may be due to greater mammary epithelium, higher body mass, or both.
Colostrum formation is thought to occur slowly over an extended period (4wk) prepartum. Furthermore, colostrum formation is highly variable among cows in total volume, IgG concentration, and mass obtained at first postpartum milking. Recent work has suggested that a rapid transfer of IgG to secretions may occur if animals are milked prepartum. Our objective was to establish the concentration, mass, and mass transfer rates of IgG in multiparous Holstein cows (n=11, parity=3.6±1.1) milked prepartum (-74 to -1h) and again around 4h postpartum. Blood concentrations of IgG were very low (<1mg/mL) in 7 cows at prepartum milking and did not decline following prepartum milking. Cows showed variability in the capacity to recover total volume, IgG concentration, and IgG mass. Three groupings of cows were considered based on the time between the 2 milkings (prepartum + 4h postpartum): long-time (-74 to -54h, n=3), medium-time (-25 to -17h, n=4), and short-time (< -13h, n=4) groups. The average rates of transfer of these groups were 1.4±0.8, 3.0±1.3, and 25.1±15.8g/h, respectively. The data indicate that a longer time between prepartum and postpartum milking is not a main factor in IgG secretion transfer. Furthermore, because blood concentrations did not change after prepartum milking and the mass of blood plasma IgG was not sufficient to account for the mass occurring in postpartum colostrum, a source of IgG other than blood circulation appears to be present during colostrogenesis.
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