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.

目的是确定产酸饮食中干物质（DM）摄入量的减少是否由产酸产物，含Cl的盐含量或酸碱状态的改变所介导。假设是摄入的减少是由代谢性酸中毒介导的。在重复的5×5拉丁方形设计中，使用了十头148±8 d的荷氏初乳母牛。日粮的日粮阳离子负离子差异（DCAD）和奶牛的酸碱状态是通过掺入产酸产品或在日粮中添加含Cl，Na和K的盐来控制的。治疗是基础饮食（T1； 1.42％K，0.04％Na，0.26％Cl； DCAD = 196 mEq / kg）；基本饮食中添加了1％NaCl和1％KCl（T2; 1.83％K，0.42％Na，1.23％Cl; DCAD = 194 mEq / kg）; 基本饮食中添加了7.5％产酸产品，1.5％NaHCO ₃；和1％K ₂ CO ₃（T3； 1.71％K，0.54％Na，0.89％Cl； DCAD = 192 mEq / kg）；基本饮食中添加了7.5％的产酸产品（T4; 1.29％的K，0.13％的Na，0.91％的Cl; DCAD = -114 mEq / kg）; 基础饮食含7.5％产酸产物，1％NaCl和1％KCl（T5； 1.78％K，0.53％Na，2.03％Cl； DCAD = -113 mEq / kg）。持续时间为14天，最后7天用于数据收集。在每个周期的最后2天，对12h的进食行为进行评估。通过饲喂产酸产品降低DCAD会降低血液pH（T1 = 7.450对T2 = 7.436对T3 = 7.435对T4 = 7.420对T5 = 7.416），并导致代偿性代谢性酸中毒，碳酸氢根，碱过量减少，CO _2的分压血液中的pH值降低，尿液中的离子差异变大。降低DCAD可以减少DM摄入量0.6 kg / d（T1 = 10.3 vs. T4 = 9.7 kg / d），这是由于酸碱状态的变化（T2 + T3 = 10.2 vs. T4 + T5 = 9.6 kg / d）引起的d）因为通过向饮食中添加具有强阳离子的盐来抵消产酸产品的酸化作用，从而阻止了摄入量的下降。调整体重后，还可以观察到由代谢性酸中毒引起的摄入量下降（T2 + T3 = 1.75对T4 + T5 = 1.66％BW）。用产酸饮食改变酸碱状态可减少进食（T2 + T3 = 6.7 vs. T4 + T5 = 5.9发作/ 12 h）和咀嚼（T2 + T3 = 14.6 vs. T4 + T5 = 13.5发作/ 12 h）发作，以及进餐时间延长（T2 + T3 = 19.8 vs. T4 + T5 = 22.0分钟/餐）和进餐间隔（T2 + T3 = 92.0 vs. T4 + T5 = 107.7分钟）。结果表明，降低DCAD可引起代偿性代谢性酸中毒并减少DM摄入量，但纠正代谢性酸中毒可防止干奶牛的DM摄入量下降。DCAD阴性的日粮中DM摄入量的减少是由代谢性酸中毒引起的，而不是由产酸产物或含Cl的盐引起的。