Effects of dietary cation-anion difference on ruminal metabolism and blood acid-base regulation in dairy cows receiving 2 contrasting levels of concentrate in diets.

Dietary cation-anion difference [DCAD=Na+K-Cl in mEq/kg of dry matter (DM)] increases DM intake (DMI) in cows fed diets containing rapidly degraded starch. Increased DMI of diets containing rapidly degraded starch could potentially exacerbate subacute acidosis. The objective of this study was to determine metabolic effects of increasing DCAD in low and high starch diets. Six cannulated Holstein cows were blocked into 2 groups of 3 cows and assigned to two 3 x 3 Latin squares in a split-plot design. Each group received a level of concentrate at either 20 or 40% on a DM basis. The diet containing 20% concentrate supplied 4% rapidly degraded starch, whereas the diet containing 40% concentrate supplied 22% rapidly degraded starch. Diets in each square were formulated to provide a DCAD of 0, 150, or 300 mEq/kg of DM. The 3 values were obtained by manipulating Na and Cl contents. Increasing the proportion of rapidly degraded starch decreased rumen pH and the acetate to propionate ratio but did not affect digestibility, blood acid-base status, pH of urine, and strong ion excretion. Increasing DCAD increased DMI, the effect being higher when the cows were fed the 40% concentrate diet. Increasing DCAD did not affect mean ruminal pH, molar proportion of VFA, and fiber digestibility; reduced the range of rumen pH decrease during the meal in cows fed the 40% concentrate diet; and strongly increased blood pH and blood HCO3 concentration. Increasing DCAD increased urine pH and modified the urinary excretion of minerals. With low DCAD, 70% of Cl and only 16% of Na were excreted in urine whereas with high DCAD, 33% of Cl and 53% of Na were excreted. These results suggest that DMI of cows fed diets rich in rapidly degraded starch and low DCAD was limited to maintain the blood pH in a physiological range. Increasing DCAD allowed the cows to increase DMI because of the ability of positive DCAD to maintain blood acid-base status. A localized rumen buffering effect could not be excluded and could be linked with a higher amount of HCO3 recycled into the rumen. Main mechanisms involved in regulating blood pH might be renal excretion of protons and strong ions and renal HCO3 reabsorption.

Apper-Bossard E ，Faverdin P ，Meschy F ，Peyraud JL ... -  《-》

Changing dietary cation-anion difference for dairy cows fed with two contrasting levels of concentrate in diets.

Apper-Bossard E ，Peyraud JL ，Faverdin P ，Meschy F ... -  《-》

Effect of dietary cation-anion difference on acid-base status and dry matter intake in dry pregnant cows.

The objective was to determine if the reduction in dry matter (DM) intake of acidogenic diets is mediated by inclusion of acidogenic products, content of salts containing Cl, or changes in acid-base status. The hypothesis was that a decrease in intake is mediated by metabolic acidosis. Ten primigravid Holstein cows at 148 ± 8 d of gestation were used in a duplicated 5 × 5 Latin square design. The dietary cation-anion difference (DCAD) of diets and acid-base status of cows were manipulated by incorporating an acidogenic product or by adding salts containing Cl, Na, and K to the diets. Treatments were a base diet (T1; 1.42% K, 0.04% Na, 0.26% Cl; DCAD = 196 mEq/kg); the base diet with added 1% NaCl and 1% KCl (T2; 1.83% K, 0.42% Na, 1.23% Cl; DCAD = 194 mEq/kg); the base diet with added 7.5% acidogenic product, 1.5% NaHCO3, and 1% K2CO3 (T3; 1.71% K, 0.54% Na, 0.89% Cl; DCAD = 192 mEq/kg); the base diet with added 7.5% acidogenic product (T4; 1.29% K, 0.13% Na, 0.91% Cl; DCAD = -114 mEq/kg); and the base diet with 7.5% acidogenic product, 1% NaCl, and 1% KCl (T5; 1.78% K, 0.53% Na, 2.03% Cl; DCAD = -113 mEq/kg). Periods lasted 14 d with the last 7 d used for data collection. Feeding behavior was evaluated for 12 h in the last 2 d of each period. Reducing the DCAD by feeding an acidogenic product reduced blood pH (T1 = 7.450 vs. T2 = 7.436 vs. T3 = 7.435 vs. T4 = 7.420 vs. T5 = 7.416) and induced a compensated metabolic acidosis with a reduction in bicarbonate, base excess, and partial pressure of CO2 in blood, and reduced pH and strong ion difference in urine. Reducing the DCAD reduced DM intake 0.6 kg/d (T1 = 10.3 vs. T4 = 9.7 kg/d), which was caused by the change in acid-base status (T2 + T3 = 10.2 vs. T4 + T5 = 9.6 kg/d) because counteracting the acidifying action of the acidogenic product by adding salts with strong cations to the diet prevented the decline in intake. The decline in intake caused by metabolic acidosis also was observed when adjusted for body weight (T2 + T3 = 1.75 vs. T4 + T5 = 1.66% BW). Altering the acid-base status with acidogenic diets reduced eating (T2 + T3 = 6.7 vs. T4 + T5 = 5.9 bouts/12 h) and chewing (T2 + T3 = 14.6 vs. T4 + T5 = 13.5 bouts/12 h) bouts, and extended meal duration (T2 + T3 = 19.8 vs. T4 + T5 = 22.0 min/meal) and intermeal interval (T2 + T3 = 92.0 vs. T4 + T5 = 107.7 min). Results indicate that reducing the DCAD induced a compensated metabolic acidosis and reduced DM intake, but correcting the metabolic acidosis prevented the decline in DM intake in dry cows. The decrease in DM intake in diets with negative DCAD was mediated by metabolic acidosis and not by addition of acidogenic product or salts containing Cl.

Zimpel R ，Poindexter MB ，Vieira-Neto A ，Block E ，Nelson CD ，Staples CR ，Thatcher WW ，Santos JEP ... -  《-》

Dietary cation-anion difference effects on performance and acid-base status of dairy cows postpartum.

Hu W ，Murphy MR ，Constable PD ，Block E ... -  《-》

Dietary cation-anion difference and dietary protein effects on performance and acid-base status of dairy cows in early lactation.

Hu W ，Murphy MR ，Constable PD ，Block E ... -  《-》