J. Dairy Sci. 90:1842-1850. doi:10.3168/jds.2006-546
© American Dairy Science Association, 2007.
Effect of Dietary Cation-Anion Difference and Dietary Crude Protein on Performance of Lactating Dairy Cows During Hot Weather
C. D. Wildman,
J. W. West1 and
J. K. Bernard
Department of Animal and Dairy Science, The University of Georgia, Tifton 31793-0748
1 Corresponding author: joewest{at}uga.edu
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ABSTRACT
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Thirty-two lactating Holstein cows (225 ± 63 d in milk) were used in a 6-wk trial to determine the effect of dietary cation-anion difference (DCAD) and dietary crude protein (CP) concentration on milk and component yield, acid-base status, and serum AA concentrations during hot weather. Treatments were arranged as a 2 x 2 factorial within a randomized complete block design to provide 15 or 17% CP and a DCAD of 25 or 50 mEq (Na + K – Cl)/100 g of dry matter (DM). A DCAD x CP interaction was detected for milk yield; milk yield was less for high DCAD than for low DCAD for the high-CP diets. No differences were noted at low dietary CP. Milk fat percentage was greater for high DCAD than for low DCAD, and high-CP diets supported greater milk fat percentage than low-CP diets. No differences were observed among treatments for dry matter intake or milk protein percentage. Serum total AA and essential AA concentrations and ratio of essential AA:total AA were greater for high DCAD. These results suggest that increasing DCAD improves AA availability for protein synthesis by taking the place of AA that would otherwise be used for maintenance of acid-base balance. A better understanding of the mechanisms behind this AA-sparing effect will improve management of protein nutrition in the lactating dairy cow.
Key Words: dietary cation-anion difference • heat stress • electrolytes • crude protein
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INTRODUCTION
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The role of AA in maintenance of blood buffering has long been established. Van Slyke et al. (1943) reported that Gln influenced acid-base chemistry via its use for ammoniagenesis. Method of N excretion is dependent on acid-base chemistry. Cai and Zimmerman (1995) reported increased plasma urea N concentration when pigs were fed cationic diets, and increased urinary ammonia concentration when fed anionic diets. Although the method of N excretion may be dependent upon acid-base chemistry, the effect on overall N excretion is unclear. Cai and Zimmerman (1995) reported that although the method of N excretion was altered with changes in acid-base chemistry, total N excretion did not change. However, Welbourne et al. (1986) reported greater total urea and ammonia N excretion during acidosis. May et al. (1986) also noted increased protein degradation and decreased N retention during metabolic acidosis. The primary interaction between AA and acid-base chemistry is the role of Gln in ammoniagenesis. The body can supply increasing quantities of Gln or Gln precursor AA as required for ammonia excretion (Vinay et al., 1978). Under conditions of normal acid-base chemistry, sufficient Gln is present in the diet or can be generated from other AA to meet ammoniagenesis needs. However, Heitmann and Bergman (1978) reported that skeletal tissue in sheep was killed to release Gln when dietary supply was inadequate.
Another facet of the interaction between acid-base chemistry and AA metabolism is the contribution of sulfur-containing AA to the acid load of the animal. Sulfur-containing AA are metabolized for energy when fed in excess of that needed for protein synthesis. Patience (1990) calculated the contribution of sulfur-containing AA to total acid production in swine and reported that growing swine consuming 2 kg/d of a 16% CP corn-soybean meal diet produce approximately 26 mEq of acid per day from the catabolism of sulfur-containing AA. The author estimated that net acid excretion in swine ranges from 100 to 200 mEq/d. Although not the predominant source of acid production, metabolism of these AA contributes a considerable amount of acidogenic strong ions.
Higher DCAD results in increased blood bicarbonate concentration, greater blood alkalinity, and greater acid-buffering capability (Tucker et al., 1988; West et al., 1991). Because DCAD alters acid-base chemistry, it may also affect AA metabolism. O’Dell and Savage (1966) reported that the growth-inhibiting antagonism between Lys and Arg was reduced by feeding potassium acetate. In a review, Patience (1990) reported inconsistent results from previous research to determine if a Lys-sparing effect occurred with high DCAD diets. The author reported greater improvements in BW gain in swine when larger quantities of alkaline salts were fed, and that the positive effect of alkaline salts on BW gain increased as dietary Lys deficiency became more severe. Sulfur-containing AA, although fed at recommended levels, were actually in excess due to the Lys deficiency. Excess acid produced from the metabolism of the sulfur-containing AA increased acid load, which was buffered by the cationic salts. Patience (1990) suggested that improved performance might have resulted from the alleviation of the excess acid load by the cationic salts instead of a Lys-sparing effect.
Although much research has been conducted to determine the relationship between acid-base chemistry and protein metabolism in other species, limited data exist for the lactating dairy cow. Metabolic challenges faced by the lactating dairy cow are unique, especially under heat stress conditions. Because heat stress in dairy cows reduces DMI and MY (West et al., 2003), more efficient nutrient utilization is important to maintain production. The objective of this study was to determine the effects of low or high DCAD on N utilization by lactating dairy cows fed low or high concentrations of dietary CP. Results of this research will lead to further understanding of the mechanism by which Na and K affect N utilization in the lactating dairy cow.
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MATERIALS AND METHODS
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Thirty-two multiparous lactating Holstein cows averaging 255 ± 63 DIM were used. Cows more advanced in stage of lactation were used in the study to reflect a common management practice in the southeastern United States in which the number of fresh cows is reduced during the summer months when heat stress is greatest. Experimental design was a randomized complete block with a 2 x 2 factorial treatment arrangement. The trial was conducted from July 8 to August 27 and consisted of a 9-d standardization period (SP) followed by a 6-wk treatment period (TP). During the SP cows were offered the standard herd diet, and baseline DMI, milk yield (MY), BW, milk composition, and serum and urinary electrolyte concentrations were determined. Data collected during the SP were used for covariate analysis of the treatment period data. Cows were ranked by DMI per BW (kg/100 kg) during the SP and were blocked into groups of 4 by rank for random assignment to treatment within block.
Dietary treatments were formulated to represent the low and high end of the optimal DCAD range reported by Sanchez and Beede (1996). They contained DCAD of 25 (DCAD25) or 50 (DCAD50) mEq Na + K –Cl/100 g of DM and CP concentration of 15 (CP15) or 17% (CP17) within each DCAD treatment (Table 1
). The SP diet contained a DCAD of 25 mEq Na + K –Cl/100 g of DM and 18% CP. Low-protein treatment diets contained 48.3% forage and 51.7% concentrate; high-protein diets contained 46.1% forage and 53.9% concentrate on a dry basis (Table 2). Low- and high-DCAD diets contained 58.0% DM. All diets were formulated to meet or exceed all other NRC (2001) requirements. Sodium bicarbonate and potassium carbonate were used to alter DCAD and were carried in experimental premixes using ground corn as a carrier (Table 2). Blood meal, fish meal, urea, and soybean meal were used in an experimental premix for adjustment of CP (Table 2).
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Table 1. Chemical composition of standardization period diets and treatment period diets1 formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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Table 2. Ingredient composition of diets formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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Before beginning the trial, all cows were trained to eat at individual bunks using electronic gates (American Calan, Inc., Northwood, NH). Cows were fed once daily (0800 h), the amount of feed offered and refused was recorded, and feed offered was adjusted daily based on the previous day’s consumption to maintain approximately 10% orts. The TMR was pushed up to cows at least 4 times daily. Ingredient DM content for adjustment of ration components was determined weekly by drying in a forced air oven at 60 ° C for 72 h. Cows were housed in a freestall barn with fans activated by thermostat when the ambient temperature exceeded 24 ° C and high-pressure misters activated by a humidistat when relative humidity (RH) dropped below 88% and fans were active. Cows were milked twice daily at approximately 0400 and 1500 h.
Sampling
Forage, concentrate, treatment mixes, and experimental TMR were sampled 3 times weekly, dried at 60 ° C for 72 h, and composited by week for later analysis. Samples were ground to pass through a 1-mm screen using a Wiley mill (Arthur H. Thomas Co., Philadelphia, PA) and analyzed for DM, CP, Ca, P, Na, K, Mg (AOAC, 1990), ADF, and NDF (Van Soest et al., 1991).
Milk yield was measured using the Alpro electronic weight system (DeLaval, Kansas City, MO). Milk samples were collected from consecutive p.m. and a.m. milkings during each week of the trial. Samples were shipped to Southeast Milk Inc. (Belleview, FL) for analyses of fat and protein using infrared analysis (B2000; Bentley Instruments Inc., Chaska, MN).
Whole blood samples were collected by coccygeal venipuncture into evacuated tubes at the end of the SP and 3 times during the TP at 1300 h. Blood was centrifuged at 2,500 x g for 20 min for separation of serum. Serum was harvested and analyzed immediately for Ca, P, Mg, Na, K, Cl, bicarbonate, urea N, creatinine, and glucose using a Boehringer Mannheim/Hitachi 912 automated chemistry analyzer (Roche Laboratory Systems, India-napolis, IN) at the University of Georgia Veterinary Diagnostic Laboratory in Tifton. Plasma was analyzed for pH, partial pressure of CO2 (pCO2), and ionized Na, K, and Ca using an AVL OPTI Critical Care Analyzer (Osmetech, Inc., Roswell, GA) at the University of Georgia Veterinary Diagnostic Laboratory. Serum samples from the SP collection and final TP collection were analyzed for free AA using a Beckman 6300 Amino Acid Analyzer (Beckman Coulter, Inc., Fullerton, CA; Slocum and Lee, 1983) at the University of Missouri Experiment Station Chemical Laboratories (Columbia, MO). Urine samples were collected via manual stimulation at the same time as blood collection for analysis of Ca, Mg, Na, K, Cl, bicarbonate, urea N, and creatinine concentration. Respiratory rates were counted at 1300 h once during the SP and 3 times during the TP. Two individuals counted the respiration rate of each cow for 1 min; counts differing by more than 10% were recounted until a difference of less than 10% was obtained. Body weights were recorded once weekly immediately following the 1500-h milking.
Milk temperature, an indicator of body temperature, was measured for individual cows at each milking using a thermocouple in one short milk tube of each milker (Temp-Sense, Udder Health Systems, Bellingham, WA). Ambient temperature and RH were recorded hourly within the free stall barn using a HOBO Pro RH/Temp Data Logger (Onset Computer Corp., Bourne, MA). Temperature-humidity index (THI) was calculated using the equation, THI = db – (0.55 –0.55 RH) x (db –58), where db was the dry bulb temperature in degrees Fahrenheit and RH was expressed in decimals (NOAA, 1976).
Statistical Analysis
Data were analyzed as a randomized complete block design with a factorial arrangement of treatments using PROC MIXED of SAS (SAS Institute, 1999). Cow within treatment was included in the model as a random variable and week as the repeated measure. The model was
where µ= the mean intercept; I = the covariate; Bi = the effect due to the ith block; Dj = the effect due to the jth DCAD; Pk = the effect due to the kth CP concentration; Wl = the effect due to the lth week; Cm(ijk) = the effect due to cow m being in the ith block with the jth DCAD and kth CP concentration (error a); and eijklm = residual error associated with each Yijklm (error b).
Least squares means were compared using PDIFF in the presence of a significant F-test (P < 0.10). Main effects were tested using error a, and interactions were tested using the residual error (error b) from the model. Three-way interactions were tested and not found to be significant and were therefore pooled in the residual error.
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RESULTS AND DISCUSSION
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Chemical Composition of Diets
The difference between low and high CP (approximately 2%) was near the original desired range of 15 and 17% CP for treatments (Table 1
). The DCAD was as formulated, representing the high and low ends of the optimal range reported by Sanchez and Beede (1996). Low- and high-DCAD diets also met or exceeded the DCAD (27 mEq/100 g of DM) that results from a calculated DCAD using current NRC (2001) guidelines for Na, K, and Cl (0.19, 1.02, and 0.25%, respectively).
Environmental Conditions
The environmental conditions during the study are presented in Table 3. Mean maximum and minimum temperatures were similar across the SP and TP and averaged 31.7 and 22.3 ° C, respectively. Mean maximum and minimum THI (81.3 and 71.7, respectively), as well as mean daily THI (76.7) were similar across SP and TP. Johnson (1987) reported that Holstein cows become less productive due to heat stress when daily mean THI exceeds 72. Mean daily THI exceeded 72 across all periods, causing heat stress conditions for the duration of the trial.
DMI
No differences in DMI or DMI/100 kg of BW were observed among treatments (Table 4). Tucker et al. (1988) reported an 11% increase in DMI when DCAD was increased from –10 to +20 mEq (Na + K –Cl)/100 g of DM. The DCAD values in that research were lower than those used in the present study. West et al. (1991) reported a quadratic response for DMI when DCAD ranged from –12 to 31 mEq/100 g of DM during hot weather. These researchers reported a plateau for DMI at approximately 20 mEq/100 g of DM, which is consistent with the results of the present study. In later work West et al. (1992) observed a linear improvement in DMI as DCAD increased from 12 to 46 mEq/100 g of DM. The lack of a DCAD effect in the present study may be explained by stage of lactation. Delaquis and Block (1995) reported improved DMI and milk yield for cows in early and mid lactation when DCAD was increased, but no difference for cows in late lactation, perhaps due to an increase in blood pH and bicarbonate concentration as lactation progresses (Erdman et al., 1982). The absence of a DCAD or CP effect for DMI also indicates that late-lactation cows have a wider tolerance of both DCAD and dietary CP.
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Table 4. Dry matter intake, milk and component yield, and milk composition for cows fed diets formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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MY
A DCAD x CP interaction was observed for MY (P < 0.10; Table 4) due to lower yield for the DCAD50-CP17 treatments. No differences for DCAD were observed for CP15 diets. These results contrast with earlier DCAD work (Tucker et al., 1988; West et al., 1991) in which DCAD improved MY. As with DMI, much of the previous work was conducted with early- and mid-lactation cows. Meta-analyses established optimal DCAD ranges for MY and DMI (Sanchez and Beede, 1996; Hu and Murphy, 2004). In each of these studies, a quadratic response was observed for MY, and MY declined when DCAD exceeded 50 mEq (Na + K –Cl)/100 g of DM. Much of the data included in this work was for early-and mid-lactation cows, with little data available on late-lactation cows. Because the need for additional dietary buffer decreases as stage of lactation increases (Erdman et al., 1982), the optimal DCAD levels would decline. The high-DCAD treatment in the present study was at the high end of the optimal range established using early- and mid-lactation cows (Sanchez and Beede, 1996) and may have been too high to elicit a response in late-lactation cows. The absence of a DCAD response suggests that additional buffering provided by a DCAD at the high end of the optimal range for late-lactation cows is not beneficial. Additional blood bicarbonate that results from DCAD above the low end of the optimal range is excreted via the urine. In high-CP diets, dietary CP may provide sufficient buffering for late-lactation cows. Consequently, providing additional buffering via DCAD may reduce MY, similar to the quadratic DCAD response observed for DCAD outside of the optimal range in early- and mid-lactation cows (Sanchez and Beede, 1996; Hu and Murphy, 2004).
Milk fat percentage was improved for DCAD50 (Table 4), in agreement with previous reports (Tucker et al., 1991; West et al., 1991). Higher milk fat percentage in the present study may result from additional ruminal buffering provided by DCAD50 diets. Higher rumen pH has been reported to decrease the concentration of trans fatty acids in the rumen (Kalscheur et al., 1997). Trans fatty acids are produced as intermediates of fatty acid biohydrogenation in the rumen and are linked to milk fat depression in dairy cattle (Griinari et al., 1998). Increased milk fat percentage (P < 0.10) was observed for CP17 diets. No treatment differences were observed among treatments for fat or ECM yield or milk protein percentage. Protein yield was lower (P < 0.10) for DCAD50, which may have been due to lower MY for DCAD50, especially within CP17 treatments.
BW, Temperature, and Respiration Rate
Similar initial BW and BW gains were observed among treatments and averaged 670 and 10 kg, respectively (Table 5). Morning and evening milk temperature and change in milk temperature were not affected by treatment and averaged 38.3, 38.4, and 0.1 ° C, respectively. Respiration rates, although elevated, were similar across treatments with a mean respiration rate of 68 breaths/min.
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Table 5. Mean BW, respiration rate, and milk temperature for cows fed diets formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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Blood and Urinary Minerals and Metabolites
An interaction between DCAD and CP was observed for serum Na and Cl (Table 6), and for fractional excretion of Na (Table 7). Within CP15 treatments, serum Na concentration decreased for DCAD50 compared with DCAD25. Serum Na was higher for DCAD50 than for DCAD25 within the CP17 treatments. Because the numerical differences between treatments for serum Na were relatively small, the physiological differences associated with these statistical differences may be negligible. Serum Cl concentration decreased for DCAD50 compared with DCAD25 within CP15 treatments. No differences were noted within CP17 diets. Fractional excretion of Na and Cl was higher for DCAD50 diets across CP treatments (Table 7). This increase in urinary Na excretion is consistent with greater Na intake from the DCAD50 diets. In earlier work, greater urinary Cl was associated with increased blood bicarbonate (Yen et al., 1981). Serum bicarbonate concentrations were higher (P < 0.01) for DCAD50 in the current study, and may have contributed to the increase in urinary Cl excretion.
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Table 6. Blood serum mineral and metabolite concentrations for cows fed diets formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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Table 7. Fractional and urinary excretion of mineral and metabolites for cows fed diets formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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Serum bicarbonate concentration (Table 6) and urinary bicarbonate excretion (Table 7) were higher for DCAD50 diets, which is consistent with previous research (Tucker et al., 1988; West et al., 1991). Greater bicarbonate excretion at high DCAD is reflective of the increased buffering capacity associated with higher DCAD diets. High pCO2 (P < 0.10), which is indicative of greater blood carbonic acid concentration, was observed for DCAD50 treatments. Although not statistically different, respiration rates for DCAD50 were numerically lower than those observed for DCAD25 within CP17 treatments. Lower respiration rates could contribute to elevated pCO2. To maintain the optimal 20:1 blood bicarbonate:carbonic acid ratio (Houpt, 1977), greater pCO2 would also contribute to elevated serum bicarbonate concentration. A higher serum bicarbonate concentration for DCAD50 is consistent with these findings. Serum DCAD, calculated as mEq (Na + K –Cl)/L, was also greater (P < 0.01) for DCAD50 diets across CP treatments (Table 6). A more positive serum DCAD results in increased serum bicarbonate, as was observed in the current research, and is indicative of improved buffering capacity. Greater serum DCAD in the current trial is caused primarily by the decrease in serum Cl concentration.
Reductions in both serum Mg concentration (P < 0.01) and Mg fractional excretion (P < 0.01) were observed for DCAD50 (Tables 6 and 7). Increased dietary K concentrations reduce Mg absorption (Ram et al., 1998; Jittakhot et al., 2004), which is consistent with the results of the present study. Lower absorption reduces Mg available for excretion, resulting in a decline in urinary Mg excretion.
No differences in BUN or urine urea N were observed for DCAD treatments. Earlier work (Cai and Zimmerman, 1995) reported increased plasma urea N, urea-cycle AA, and urinary urea N as a percentage of total N excretion in swine when DCAD was elevated. No difference in total N excretion was observed by the authors. This suggests that in swine, DCAD has a greater effect on method than amount of N excretion. Escobosa et al. (1984) reported increased BUN in lactating dairy cows when DCAD was increased from –19 to 17 mEq (Na + K –Cl)/100 g of DM. No change was observed when DCAD was increased to 32 mEq/100 g of DM. The results of the current research are consistent with these findings. Blood urea N and urinary urea N were greater for CP17 compared with CP15 treatments as a result of the greater dietary CP concentrations in CP17 treatments. Fractional excretion of Ca decreased for DCAD50 treatments. This agrees with earlier work in which greater urinary Ca excretion occurred in acidogenic vs. alkalinogenic diets (West et al., 1991; Wang and Beede, 1992). Greater fractional excretion of K and P was also observed for DCAD50 compared with DCAD25. Increased excretion of K resulted from greater dietary K concentrations associated with DCAD50 treatments. Greater P excretion is inconsistent with earlier work in which acidogenic diets resulted in greater urinary P excretion (Roby et al., 1987). West et al. (1991) reported a cubic DCAD effect on urinary P excretion as DCAD was increased from –8 to 31 mEq (Na + K –Cl)/100 g of DM. In these studies, maximum DCAD values were lower than those used in the current research.
Blood AA
Concentrations of total serum AA, essential AA, and essential:total AA ratio were greater for DCAD50 treatments (Table 8). Increased Lys, Arg, Val, Ile, and Leu concentrations were also observed for DCAD50 treatments. These differences may be attributed to a decreased role of these AA in acid-base chemistry in high-DCAD diets. Van Slyke et al. (1943) and May et al. (1986) demonstrated greater Gln metabolism and protein degradation during acidosis. May et al. (1987) also reported that administration of NaHCO3 reduced proteolysis in acidotic rats. Based on blood pH, the cows in the present study were not acidotic as were the rats in these previous studies. However, because some enzymes are sensitive to changes in pH, differences in the acid-base status of the animal may alter AA metabolism. Because AA are absorbed via a Na cotransport mechanism (Guyton, 1981), greater AA absorption may lead to higher serum AA concentrations in high DCAD diets, which contain greater dietary Na concentrations. Arnauld and Lachance (1980) reported that feeding excess Lys to rats resulted in a decreased concentration of muscle potassium, suggesting that Lys and Arg play a charge replacement role in muscle tissue. Greater dietary K concentration associated with higher DCAD may alleviate the need for Lys and Arg as intracellular and extracellular buffers. Robbins et al. (1982) reported decreased muscle Lys and Arg in chicks when dietary K concentration was greater than 0.18%. The authors proposed that the mechanism affecting intracellular AA concentration is related to intracellular K+:Na+ ratio. Greater dietary K concentration may increase cellular AA efflux by decreasing the role of AA in intracellular buffering. Greater efflux of AA could result in increased serum AA concentrations. Greater Met (P < 0.01) for CP17 is consistent with increased milk fat percentage observed for CP17 diets (Table 4). Misciattelli et al. (2003) reported a positive response on milk fat percentage with increased postruminal availability of Met. Although greater serum AA concentrations in the present study did not result in greater milk protein percentage, results may be greater for early- or mid-lactation cows in which the metabolic challenges faced are greater than those for cows later in lactation.
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Table 8. Serum, essential, and total AA concentrations for cows fed diets formulated to contain a DCAD of 25 or 50 mEq (Na + K –Cl)/100 g of DM and 15 or 17% CP
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CONCLUSIONS
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The absence of a MY and DCAD response to DCAD in late-lactation cows suggests that adequate blood buffering is supplied in diets with DCAD concentrations near NRC (2001) recommendations for Na, K, and Cl. No change in serum Na or K concentrations coupled with greater Na and K urinary excretion suggest that adequate buffering is supplied when DCAD is 25 mEq (Na + K –Cl)/100 mg of feed DM in late-lactation cows. Although respiratory rates were elevated due to environmental conditions, cow body temperatures did not reflect heat stress. Whereas positive DCAD effects were observed in earlier work for heat-stressed cows, the combination of adequate buffering for DCAD25 and management such as fans and misters masked any DCAD and heat stress interactions. Increased blood concentration of essential AA suggests that the higher DCAD reduced the need for AA degradation to maintain acid-base balance, sparing AA for other uses. Whether the mechanisms behind these changes in AA metabolism are a result of changes in ruminal protein metabolism or postruminal utilization is unclear. A better understanding of these mechanisms, however, offers the opportunity to improve the efficiency of protein use by the lactating dairy cow.
Received for publication August 21, 2006.
Accepted for publication December 4, 2006.
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