Lipopolysaccharide challenge following intravenous amino acid infusion in postpartum dairy cows: I. Production, metabolic, and hormonal responses.

Postpartum cows experience a nadir in energy and AA deficit early postpartum. At the same time, cows are challenged with inflammatory stimuli and often show heightened immune responsiveness, further increasing their metabolic needs during this critical time. This study investigated the response to a systemic inflammatory stimulus after a 4-d intravenous (IV) AA infusion designed to ameliorate the estimated metabolizable protein (MP) deficit in postpartum cows. Our objectives were to (1) describe the production and metabolic responses to early postpartum IV AA infusion, (2) determine the metabolic and hormonal responses to an acute IV lipopolysaccharide (LPS) challenge in early postpartum cows, and (3) compare these metabolic and hormonal responses between IV AA treated and control cows. Cows (n = 14, 4 ± 1 d in milk) were continuously IV infused for 4 d in a matched-pair randomized controlled design and received IV AA (IVAA) or 0.9% NaCl (CTRL). Treatment with IV AA consisted of 1 g/kg of BW per day of combined essential AA (EAA) and nonessential AA (NEAA). After infusion ended, cows were challenged IV with LPS (0.0625 µg/kg of BW over 1 h), and serial blood samples were collected to quantify AA, metabolite, and hormone concentrations. Amino acid infusion increased plasma EAA and NEAA concentrations and ameliorated the estimated MP deficit but not the metabolizable energy deficit in IVAA cows. Patterns of dry matter intake during infusion were different between groups. Milk yield and milk protein content and yield were unaffected, but IV AA was associated with increased milk fat content and yield of both de novo and preformed fatty acids. Before LPS infusion, plasma EAA and NEAA concentrations were greater in IVAA compared with CTRL. During LPS challenge, plasma AA concentrations decreased to a greater degree in IVAA than CTRL. Glucagon concentrations were greater and glucose concentrations lower in IVAA during challenge; however, previous AA infusion did not affect the time-dependent changes in concentrations of energy metabolites or glucoregulatory hormones. Plasma urea nitrogen concentration increased in both treatments following challenge, although the temporal pattern depended on treatment. Effects of AA infusion on milk fat response were pronounced and likely due to a combination of increased lipolysis and de novo milk fat synthesis. Despite differences in circulating concentrations of nutrients and hormones before challenge, metabolic responses to systemic inflammation did not differ between the 2 treatments. We conclude that AA infusion changed metabolic status and milk fat but did not appear to alter the metabolic response to subsequent systemic inflammation.