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Phosphorus (P) deficiency and hypophosphatemia are believed to be associated with muscle function disturbances in dairy cows, particularly around parturition. The objective of this study was to determine the effect of dietary P deprivation during late gestation and early lactation on muscle P homeostasis and muscle function in periparturient dairy cows. Thirty-six multiparous dairy cows in late gestation were randomly assigned either to undergo dietary P depletion or to be offered a diet with adequate P content from 4 wk before to 4 wk after parturition. Phosphorus-deficient rations for dry and lactating cows contained 0.15 and 0.20% P on a dry matter basis, respectively. Blood and muscle tissue for biopsy were obtained and electromyographic examinations were conducted on biceps femoris and intercostal muscles in regular intervals throughout the study. Muscle tissue was analyzed for the total P, adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, creatine phosphate, and tissue water content. Dietary P deprivation resulted in a pronounced and sustained decline of the plasma phosphate concentration, reaching a nadir at calving with mean values below 1.5 mg/dL and remaining below 2.0 mg/ dL during the first 4 wk of lactation. Hypophosphatemia was not associated with signs of clinically apparent muscle weakness or disturbed muscle function and was not associated with a decline in the content of any of the studied P-containing compounds in muscle tissue. Accordingly, no association between plasma phosphate concentration and muscle tissue P content was found. Electromyographic examination identified subclinical effects on motor unit action potentials that are indicative of disturbed neuromuscular functionality. Increasing occurrence of pathologic spontaneous activity possibly resulting from membrane instability of nerve or muscle cells and suggestive of myopathy was also recorded as P deprivation progressed. These effects were predominantly observed in intercostal and to a lesser degree biceps femoris muscles. Electromyographic parameters affected by P deprivation were found to be associated primarily with the plasma phosphate and to a lesser extent with the amounts of energy storing P-containing compounds contained in muscle tissue. These results indicate that prolonged and pronounced dietary P deprivation in transition dairy cows leads to marked sustained hypophosphatemia without altering the muscle tissue P homeostasis or causing clinically apparent muscle function disturbances.

Inflammation appears to be a predisposing factor and key component of hepatic steatosis in a variety of species. Objectives were to evaluate effects of inflammation [induced via intravenous lipopolysaccharide (LPS) infusion] on metabolism and liver lipid content in experimentally induced hyperlipidemic lactating cows. Cows (765 ± 32 kg of body weight; 273 ± 35 d in milk) were enrolled in 2 experimental periods (P); during P1 (5 d), baseline data were obtained. At the start of P2 (2 d), cows were assigned to 1 of 2 treatments: (1) intralipid plus control (IL-CON; 3 mL of saline; n = 5) or (2) intralipid plus LPS (IL-LPS; 0.375 μg of LPS/kg of body weight; n = 5). Directly following intravenous bolus (saline or LPS) administration, intralipid (20% fat emulsion) was intravenously infused continuously (200 mL/h) for 16 h to induce hyperlipidemia during which feed was removed. Blood samples were collected at −0.5, 0, 4, 8, 12, 16, 24, and 48 h relative to bolus administration, and liver biopsies were obtained on d 1 of P1 and at 16 and 48 h after the bolus. By experimental design (feed was removed during the first 16 h of d 1), dry matter intake decreased in both treatments on d 1 of P2, but the magnitude of reduction was greater in LPS cows. Dry matter intake of IL-LPS remained decreased on d 2 of P2, whereas IL-CON cows returned to baseline. Milk yield decreased in both treatments during P2, but the extent and duration was longer in LPS-infused cows. Administering LPS increased circulating LPS-binding protein (2-fold) at 8 h after bolus, after which it markedly decreased (84%) below baseline for the remainder of P2. Serum amyloid A concentrations progressively increased throughout P2 in IL-LPS cows (3-fold, relative to controls). Lipid infusion gradually increased nonesterified fatty acids and triglycerides in both treatments relative to baseline (3-and 2.5-fold, respectively). Interestingly, LPS infusion blunted the peak in nonesterified fatty acids, such that concentrations peaked (43%) higher in IL-CON compared with IL-LPS cows and heightened the increase in serum triglycerides (1.5-fold greater relative to controls). Liver fat content remained similar in IL-LPS relative to P1 at 16 h; however, hyperlipidemia alone (IL-CON) increased liver fat (36% relative to P1). No treatment differences in liver fat were observed at 48 h. In IL-LPS cows, circulating insulin increased markedly at 4 h after bolus (2-fold relative to IL-CON), and then gradually decreased during the 16 h of lipid infusion. Inducing inflammation with simultaneous hyperlipidemia altered the characteristic patterns of insulin and LPS-binding protein but did not cause fatty liver.

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