Short communication: Short-term intravenous amino acid infusions as a method to detect limiting amino acids in dairy cattle diets.

We hypothesized that the addition of limiting AA increases dry matter intake (DMI) by reducing anaplerosis and hepatic oxidation. Accordingly, the objective of this work was to examine the effects of short-term intravenous infusions of Met, Lys, and His (which are considered the most limiting AA) on DMI as a method to detect whether specific AA are limiting in dairy cow diets. We conducted 4 experiments using Holstein cows in the immediate postpartum period to address this objective. The first experiment used 4 cows 6 to 10 d postpartum (PP) in a 4 × 4 Latin square design with 1-d periods including 12 h for infusions and 12 h for recovery. Treatments were continuous infusions of 5 (low), 10 (medium), or 15% (high) of the calculated requirement of metabolizable Met, Lys, and His or 0.9% saline (control, CONT). In the second and third experiments, 8 cows (4-12 d PP) were divided into 2 groups of 4 cows, and each group received a different diet formulated to either be low in Lys (experiment 2) or Met (experiment 3). Each experiment was a crossover design with two 1-d periods with 12-h infusions (continuous) and 12 h for recovery. Treatments were 15% of the calculated requirement of metabolizable Met, Lys, and His (high), or 0.9% saline (CONT). In the fourth experiment, 5 cows (4-14 d PP) were used in a 5 × 5 Latin square design. Periods were 2 d in which treatments were continuously infused for the first 46 h. Treatments were 0.9% saline (CONT), all (Lys, Met, and His), LM (Lys and Met), LH (Lys and His), and MH (Met and His); dosages were equal to the estimated shortage in each specific AA. In each experiment, feed intake was recorded by a computerized data acquisition system, milk yield was recorded, and milk composition was analyzed for fat, protein, lactose, and milk urea nitrogen (MUN) concentrations. Treatments did not affect DMI or yield of milk or milk components in the first experiment. In the second experiment, AA treatment increased protein percentage and reduced lactose percentage but had no effect on protein and lactose yields or DMI. In the third experiment, the AA treatment tended to increase yields of milk, lactose, and protein as well as MUN concentration but did not affect DMI. In the fourth experiment, no effects were detected for DMI and milk yield, whereas the all, LH, and LM treatments reduced milk lactose concentration compared with CONT, and MH increased MUN concentration compared with CONT and other treatments. These results failed to provide support for our hypothesis that short-term addition of these potentially limiting AA will increase DMI. This may be due to our hypothesis being inaccurate or to other factors; other limiting AA could have prevented the effects of Lys, Met, and His infusions or the infusion periods could have been too short to induce a response in DMI. Accordingly, short-term infusion of AA is probably not a sensitive method to detect limiting AA in dairy cow diets.

The effects of fructose and phosphate infusions on dry matter intake of lactating cows.

The objective of this study was to examine the effects of fructose and phosphate (Pi) infusions on dry matter intake by dairy cows to further understand the mechanisms controlling feed intake related to hepatic energy status. We performed 3 experiments in which we infused fructose and Pi intravenously or abomasally to Holstein cows. The first experiment used 8 cows (4-8 d postpartum) in a duplicated 4 × 4 Latin square experiment with 1 square of multiparous and 1 square of primiparous cows. A 2 × 2 factorial arrangement of treatments was used including jugular infusions of solutions (1 L/h) containing fructose or glucose (0.6 mol/h) and Pi (NaH2PO4) or NaCl (0.3 mol/h). Periods were 24 h, including 2 h for infusions and 22 h for recovery. The second experiment used 4 multiparous cows (74-81 d postpartum) in a 4 × 4 Latin square design and infused fructose or glucose and either Pi or no Pi at the same rates as experiment 1. Periods were 24 h, including 1 h for infusions and 23 h for recovery. The third experiment used 4 ruminally cannulated multiparous cows (15-26 d postpartum) in a 4 × 4 Latin square design and infused fructose or glucose and either Pi or NaCl at the same rates as experiment 1 but to the abomasum. Periods were 24 h, including 1 h for infusions and 23 h for recovery. In each experiment, feed intake was recorded by a computerized data acquisition system; blood was analyzed for the concentrations of glucose, nonesterified fatty acids, and Pi; and the liver was analyzed for the concentration of Pi (experiments 2 and 3 only). Overall, fructose infusion increased DMI by fresh cows when infused intravenously and abomasally, but it did not affect DMI by mid-lactation cows. Fructose infusion also reduced hepatic Pi, and Pi infusion increased hepatic Pi when infused abomasally but not intravenously. These results suggest that fructose increases feed intake, likely by sequestering Pi and preventing ATP production. When infused intravenously to multiparous cows, Pi increased DMI and did not affect hepatic Pi content. However, when infused abomasally, Pi reduced DMI and increased hepatic Pi content. These results suggest that although Pi infusion prevents the effect of fructose loading and reduces DMI, it also increases intake through a competing mechanism. Examining long-term effect of Pi infusion on DMI could determine if competing mechanisms complicate the determination of P requirement for dairy cows. These results are consistent with the control of feed intake by hepatic energy status in dairy cows.