| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
,1
* Agriculture Victoria Ellinbank, Victoria 3820, Australia
Department of Animal Science and Production, University College Dublin, Ireland
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
Key Words: dietary cation-anion difference • hypocalcaemia • pasture
Abbreviation key: Creat = creatinine, DCAD = dietary cation-anion difference, DMD = dry matter digestibility, HC = high postcalving dietary Ca, HD = high precalving DCAD, Hy = hydroxyproline, ICP-ES = inductively coupled plasma emission spectrometry, LC = low postcalving dietary Ca, LD = low precalving DCAD, ME = metabolizable energy, [SID] = strong ion difference, [SIDB] = strong ion difference in blood, [SIDU] = strong ion difference in urine
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
More recently, supplementation of cows, precalving, with Cl and S (while maintaining or reducing the dietary concentration of Na and K) to reduce blood pH has been effectively used to prevent hypocalcemia. Stewart (1983) proposed that the ratio of strong ions (strong ion difference; [SID]) in the diet (ions created when a strong electrolyte is added to a solution) had the potential to change acid-base balance. In mammalian extracellular solutions, the most concentrated inorganic strong ions are Na+, K+, Cl-, and S2-. Therefore, a reduction in [SID] should result in a reduction in blood pH, and there is general agreement that such a change increases Ca absorption and excretion (Block, 1984; Joyce et al., 1997; Roche et al., 2003).
A prepartum diet, with a relative predominance of dietary macromineral anions to cations (i.e., a negative dietary cation-anion difference; DCAD), has reduced the [SID] in blood and hence reduced blood pH (Stewart, 1981; 1983; Roche et al., 2003). Results from many countries have shown a reduction in the incidence of hypocalcemia and an increase in milk production when a negative DCAD is fed to dairy cows in the final weeks before parturition (Block, 1984; Joyce et al., 1997). The dairying industry of southeastern Australia is largely based on perennial ryegrass (Lolium perenne L.) and supplemented with crushed barley, hay, and pasture silage (Doyle et al., 1996). This is different from diets previously investigated in other countries, as it is very high in K and the DCAD can be as high as +76 mEq/100 g (Roche et al., 2000). An increased incidence of milk fever was reported by Roche et al. (2003) when this diet was supplemented with the macromineral anions Cl and S, even though Ca absorption, as indicated by urine Ca concentration, had been increased. This apparent increase in the incidence of hypocalcaemia was attributed to a greater demand for dietary Ca postcalving following a reduction in the pH of systemic fluids precalving and the fact that pasture-based diets, as opposed to TMR diets, are generally low in Ca. In Australia and New Zealand, cows are not traditionally supplemented with Ca after calving.
The experiment described here tested the hypothesis that a reduction in the DCAD offered to dairy cows precalving, on a predominantly perennial ryegrass pasture and pasture-hay diet, would reduce the incidence of hypocalcemia and increase subsequent milk production when additional dietary Ca was fed postcalving.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
Experimental Design and Treatments
Forty multiparous Holstein cows, 17 ± 7 d precalving, were randomly allocated to four dietary treatments in a 2 x 2 factorial design (10 cows/treatment). Cows were allocated randomly to treatment on the basis of total production for the previous lactation, and age. The cows were (mean ± SD) 5 ± 3 yr old and had produced 4910 ± 843 kg of milk the previous lactation with 4.4 ± 0.5% fat and 3.2 ± 0.2% protein.
Feeds
All cows were offered a daily diet of 5 kg DM of perennial ryegrass dominant pasture-hay in the morning and ad libitum freshly cut pasture in the afternoon for 21 ± 10 d before calving. After calving, the cows were switched to a ration of 6 kg DM of barley and ad libitum pasture-hay for 2 wk. Ad libitum was defined as 110% of the pasture that had been eaten the previous day. The nutritive characteristics and mineral concentrations of the feeds offered are given in Table 1
.
|
Before calving, the cows received their appropriate salt mixture twice daily at 0600 and 1500 h. If DCAD is to be accurately manipulated in pasture-based systems it will be through supplementation of cows with appropriate salt mixtures once or twice daily, as the consistent and predictable manipulation of DCAD is very difficult (Roche et al., 2002). Furthermore the pasture-based system, where cows are generally a considerable distance from supplementation facilities precludes a more frequent supplementation strategy. In support of this method of supplementation, Roche (1999) showed increased Ca absorption and urinary Ca excretion, and little or no diurnal variation in urine pH when anionic salts were supplemented twice daily to reduce the DCAD to -20 mEq/100 g, thereby suggesting that twice daily supplementation of anionic salts in pasture-based systems had similar effects to continuous supplementation in a TMR.
As the precalving DCAD was high and the resultant amount of salts required to reduce it to the predetermined levels was great, the salts used were administered orally in a bolus form. The ‘bolus’ was created by mixing the salts with 15 g of whole milk powder (as a binder) and pressing the mixture in a preformed die. Each bolus was cylindrical in shape and approximately 130 mm in length and 40 mm in diameter. One bolus was administered morning and evening.
Animal Management
Cows were individually fed for the duration of the experimental period. Feeds were offered daily for two 5-h periods, in a manner similar to that described by Roche et al. (2003). At 1200 to 1445 h and 2100 to 0545 h the cows were held as a single group on a bare paddock where water was available ad libitum.
After receiving their salt supplement, precalving, the cows received their morning and afternoon feed. They calved indoors. After calving the cows were milked at 0600 and 1500 h each day. For 14 d postcalving, cows received their barley grain supplement, with or without Ca supplementation, before being given access to ad libitum pasture-hay.
Fresh pasture was offered to the dry cows to best represent the precalving diets used on dairy farms in Victoria. The pastures used in this experiment had not been grazed for 6 to 7 wk and had a mass of approximately 2500 kg DM/ha. Pasture was cut to about 40 mm, twice daily, and collected using a loader wagon. The cut pasture was not chopped further so as to best represent grazed pasture. The pasture and pasture-hay were composed of predominantly perennial ryegrass (Lolium perenne L.). The hay was not chopped. The crushed barley grain was fed as a pellet containing 5% molasses. The nutritive characteristics and mineral concentrations of the feeds offered are in Table 1
.
Following the 14-d indoor feeding period postcalving, the cows were managed as one herd in a manner similar to that described by Roche et al. (2000) for farmlets B and C. Cows were stocked at approximately 2.5 cows/ha and rotationally grazed. Nitrogen fertilizer was applied in the form of urea (46% N) at a rate of 100 kg urea/ha after each grazing when soil moisture was not limiting pasture growth. Crushed barley was fed whenever it was deemed necessary (a lack of either quantity or quality of pasture). Fodder turnips were grown on approximately 10% of the farm in summer and were strip-grazed during February and March.
Measurements
Cows were manually stimulated to urinate 5 d each week at approximately 0700 h for the duration of the indoor feeding period, and a sample of urine, from midstream, was collected in a 30-ml container. Within 30 min of collection, pH was measured and 30 ml of sample was frozen for subsequent mineral, hydroxyproline (Hy) and creatinine (Creat) analysis. Urine samples were bulked weekly, and urine minerals were determined by inductively coupled plasma emission spectrometry (ICP-ES) having been diluted with 1% nitric acid. Urine Hy was determined by a method developed by Parekh and Jung (1970) using a microplate reader (Biorad 550, Philadelphia). Urine Creat was determined using a procedure modified from Bartels et al. (1972) using an autoanalyzer (Boehringer Mannheim Hitachi 911, Germany).
Blood from the jugular vein was collected from each cow on 2 d each week for the duration of the experiment, using 2 x 10 ml heparinized evacuated tubes. A sample of blood was also collected from each cow on the day of calving approximately 2 h after the HC treatment received their Ca supplementation. All plasma samples were centrifuged immediately post-sampling for 10 min at 1120 x g, and the plasma pipetted off and frozen awaiting mineral analysis. Plasma minerals were determined by ICP-ES after digestion using nitric acid assisted microwave digestion (Milestone Application Laboratory, 1995).
Individual milk yields were recorded daily (Alfa Laval Alpro milk meter system, Tumba, Sweden) for the entire lactation. Individual p.m. and a.m. milk samples were collected on 2 d each week for 14 d postcalving and on 1 d each month for the remainder of lactation to determine milk composition. Fat, protein, and lactose concentrations of milk were determined using Milkoscan (Foss Electric, Hillorød, Denmark).
During the indoor feeding period (precalving until 2 wk postcalving), individual cow DMI was measured, and representative samples of each feed offered and refused were dried at 105°C to constant weight to determine their DM content. Samples of all feeds were bulked on a weekly basis and dried at 65°C for 72 h, ground to pass through a 0.5-mm sieve (Christy Lab Mill, Ipswich, UK) and analyzed for in vitro DM digestibility (DMD), N, and macrominerals. The DMD was determined by the method of Clarke et al. (1982). Metabolizable energy (ME; Mcal/kg DM) was calculated from DMD; ME = ((DMD*0.17)-2)/4.186; (Standing Committee on Agriculture, 1990).
Nitrogen was determined by a Kjeldahl method using Buchi Kjeldahl nitrogen apparatus, with CP being calculated from N (CP = N * 6.25). Macrominerals were determined using X-ray spectroscopy (Hutton and Norrish, 1977; Norrish and Hutton, 1977).
Calculations and Statistical Analysis
Urinary minerals (Ca, Mg, Na, Cl, and S) and Hy are expressed as ratios to Creat concentration to overcome variations in urine volume among animals (Roche et al., 2002).
The [SID] is the difference, in milliequivalents, between certain cations (Na and K) and anions (Cl and S) in body fluids and is calculated by subtracting the milliequivalents of anions from the milliequivalents of cations, in either plasma (mg/L) or urine ([SIDB] and [SIDU], respectively).
All data were analyzed by ANOVA procedures for a factorial design using the statistical procedures of Genstat V (1997) with cows as the experimental unit.
Milk yields were summed within each month to give monthly yields, which were then multiplied by monthly fat, protein, and lactose concentrations (g/kg) to calculate monthly component yields. These values were used to calculate average fat, protein, and lactose concentrations for the lactation. Milk yield and composition for the 14-d postcalving period and total lactation milk yields and average fat, protein, and lactose concentrations were then analyzed by analysis of variance using the statistical procedures of Genstat V (1997). Main effects (precalving DCAD level and postcalving dietary Ca concentration) and interactions were examined.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
lists the concentrations of minerals in the diet consumed by the cows on all treatments before and after calving.
|
and Table 4). Postcalving dietary Ca concentration did not affect urine pH or [SIDU], although there was a significant interaction between anionic salt supplementation precalving and dietary Ca concentration postcalving on postcalving urine pH (Table 4). The cows on treatment LDHC had a lower pH (P < 0.05), postcalving, than the cows fed the low Ca treatment (LDLC).
|
|
). The Na/Creat was lower (P < 0.01) postcalving in cows fed a low DCAD precalving (Table 4), while Cl/Creat was higher (P < 0.01). The supplementation of Ca, postcalving, did not significantly affect the concentration of minerals or hydroxyproline in urine.
Precalving DCAD did not affect the strong ion difference of blood ([SIDB]) or plasma mineral concentrations in the cows precalving (Table 5) although there was a trend (P = 0.06) towards reduced blood Ca concentration in cows receiving the low DCAD diet precalving. As a main effect, precalving DCAD did not significantly affect plasma mineral concentration, either on the day of parturition or in the following 2 wk (Table 6). However, although the interaction was not significant at the 5% level (P < 0.08), cows in HDLC had lower (P < 0.05) plasma Ca concentrations on the day of calving than either their low precalving DCAD comparison or their high postcalving Ca comparison. Furthermore, 78% of cows in HDLC had plasma Ca concentrations less than 1.4 mmol/L on the day of calving compared with 15, 8, and 8% for LDHC, LDLC, and HDHC, respectively. HDLC also had a 30% incidence of parturient paresis (three cows) compared with 10% (one cow) in LDLC and zero in the other two treatments. The Ca supplementation postcalving also increased (P < 0.05) plasma Ca concentration. [SIDB] was not affected by treatment either on the day of calving or in the subsequent 2 wk. Plasma Mg concentrations were low in cows on all treatments.
|
|
). Precalving, cows on the LD and HD treatments ate 4.0 and 4.9 kg of pasture, respectively, and 5.0 kg of pasture-hay. The trend towards a reduced DMI (P = 0.11) in cows supplemented with anionic salts precalving was not statistically significant. There was no effect of treatment on DMI postcalving.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
It was hypothesized that a reduction in the DCAD before calving, combined with an increase in the dietary Ca concentration after calving, would reduce the incidence of periparturient hypocalcemia and increase the subsequent milk production of dairy cows on a pasture-based diet. The reduced precalving DCAD significantly increased plasma Ca concentration on the day of calving. This increase is supported by the results of Oetzel et al. (1988), who reduced the incidence clinical paresis from 17 to 4% and hypocalcemia (i.e., plasma ionized Ca < 1 mmol/L) from 66 to 30% when precalving DCAD level was reduced. In the present experiment, clinical paresis was reduced from 30 to 0% and the incidence of clinical hypocalcaemia (i.e., total blood Ca < 1.4 mmol/L) was reduced from 78 to 15% by feeding a low DCAD diet precalving or alternatively through Ca supplementation postcalving. The availability of Ca in the urine of cows offered a low DCAD diet (Schonewille et al., 1999), when a demand is placed on plasma Ca, as would be expected at calving (Roche et al., 2001), supports the improvement in Ca homeostasis observed in LD cows in this trial.
However, this increase in plasma Ca in LD cows was short-lived without dietary Ca supplementation. On the other hand, elevated dietary Ca concentrations postcalving, corrected the negative Ca balance created by the onset of lactation, with HC cows exhibiting higher plasma Ca concentrations postcalving, irrespective of the precalving DCAD. Roche et al. (2001) reported that the nadir in periparturient plasma Ca concentration occurred the day following calving, and that plasma Ca concentration was significantly lower in cows fed a TMR compared with those fed fresh pasture and pasture silage. The increased concentration of plasma Ca following dietary Ca supplementation postcalving in this study suggests that supplementation of dietary Ca may reduce the normal decline in plasma Ca concentration postcalving and aid in preventing clinical hypocalcemia in pasture-based systems. Considering the difficulties in consistently and accurately manipulating the DCAD of grazing animals (Roche et al., 2002), postcalving Ca supplementation may prove a more practical solution to the problem of periparturient hypocalcemia in grazing systems. The results of Roche et al. (2002) suggest that the first 4 d postcalving is the critical period for Ca supplementation.
The plasma Mg concentration of cows on all treatments was very low. Dietary K reduces the absorption of Mg (Underwood and Suttle, 1999). However, grazing dairy cows often consume diets with greater K concentrations than presented in this study (Roche et al., 2000), and the dietary Mg concentration is higher than normal. Genotype may be a factor. Roche et al. (2001) did show very low plasma Mg concentrations in Holstein-Friesian cows of US origin when compared with Holstein-Friesian cows of New Zealand origin, under grazing systems. The high dietary Ca concentration may also be a factor. Roche et al. (2002) reported an inverse relationship between plasma Mg and plasma Ca concentration, when dietary Ca concentration was high. Further research is required to more fully understand the reason for the low periparturient Mg concentration in blood.
The decrease in urine pH and [SIDU] observed when the precalving DCAD was reduced (LD) is consistent with the nonrespiratory systemic acidosis discussed by other investigators (Stewart, 1981, 1983; Tucker et al., 1988; West et al. 1992; Roche et al., 2003). The precalving reduction in systemic pH in the current experiment was associated with an increased urinary output of Ca. In other research this increase has been attributed to either increased gastro-intestinal absorption of dietary Ca, an increased resorption of Ca from bone stores or both (Chu et al., 1975; Kim and Linkswiler, 1979; Block, 1984; Schonewille et al., 1994). The theory that acidification of the medium surrounding bone will cause the release of bone Ca (Bushinsky et al., 1993) is supported by research indicating increased bone resorption, through indicators of collagen degradation, precalving when DCAD was reduced (Block, 1984; Goff et al., 1991). However, this does not appear to be the case in our experiment, as Hy/Creat was not affected by precalving DCAD. In fact, the concomitant tendency (P = 0.06) for plasma Ca concentration to decrease suggests that the increased urinary Ca was not being replenished from bone stores.
Decreased urine pH postcalving in treatment LDHC cows is not consistent with earlier findings that indicated an immediate rise in urine pH when supplementation of anionic salts ceased (Tucker et al., 1992a; Roche et al., 2003) and does not correspond with a decrease in [SIDU]. The postcalving supplementation of Ca in the present study increased the cow’s supply of dietary Ca, potentially reducing the cow’s requirement for bone Ca. Because bone is one of the main sources of the buffers required to resist systemic pH change, with the ability to release both Na and Ca when needed (Bushinsky et al., 1993), less bone resorption would result in less buffering. While, the Hy/Creat results do not seem to support this view, Hy/Creat may not be a reliable indicator of bone resorption immediately postcalving, since the cow would be undergoing significant uterine involution, a biological process for which Hy/Creat is also considered to be a good indicator (Kaidi et al., 1991). More research is required to define these relationships.
There was no significant effect of precalving DCAD on the production of milk or milk components. This differs from the findings of Beede et al. (1992), where the incidence of subclinical hypocalcemia was reduced by addition of anionic salts, and total lactation milk production was increased by 327 kg of milk/cow. Similarly, Block (1984) reported a 14 and 7% increase in milk production through a low-DCAD induced reduction in the incidence of clinical and subclinical hypocalcemia, respectively. However, many authors have also reduced the incidence of hypocalcemia through reducing precalving DCAD and have either not reported effects on milk production (Oetzel et al., 1988; Goff et al., 1991) or have not found an effect of precalving DCAD on milk production (Joyce et al., 1997; Roche et al., 2003).
The negative effect of DCAD on precalving DMI, although not significant in this study, is supported by the literature (Joyce et al., 1997). Bertics et al. (1992) highlighted the importance of maintaining a high DMI precalving. It is not possible from the present study to determine whether the positive effects of a reduced hypocalcemia are more important than the negative effects of reducing DMI. However, one would suspect that the improved plasma Ca concentration achieved through postcalving dietary Ca supplementation, while avoiding the negative DMI effects of precalving anionic salt administration, suggests that postcalving Ca supplementation is a more appropriate hypocalcemia preventative than precalving DCAD manipulation in grazing dairy cows, especially when Roche et al. (2001) reported that the nadir in plasma Ca concentration occurs 24 h postcalving, thereby allowing time for Ca to be supplemented.
Although Ca supplementation postcalving increased plasma Ca concentration, it did not affect DMI or milk production. This is possibly because the Ca concentration of the postcalving diet (0.68% without Ca supplementation) was approximately double that normally found in the diet of pasture-based dairy cows in early lactation in southeastern Victoria (Jacobs and Rigby, 1999; Roche et al., 2000).
|
CONCLUSIONS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
|
ACKNOWLEDGEMENTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
|
FOOTNOTES |
|---|
2 Present address: University of Pennsylvania, School of Veterinary Medicine, Biostatistics Section, Clinical Science, New Bolton Center, Kennett Square, PA 19348, USA.
Corresponding author:
J. R. Roche; e-mail:
john.roche{at}dexcel.co.nz.
Received for publication December 12, 2002. Accepted for publication January 31, 2003.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  G. B. Penner, G. F. Tremblay, T. Dow, and M. Oba Timothy Hay with a Low Dietary Cation-Anion Difference Improves Calcium Homeostasis in Periparturient Holstein Cows J Dairy Sci, May 1, 2008; 91(5): 1959 - 1968. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Charbonneau, D. Pellerin, and G. R. Oetzel Impact of Lowering Dietary Cation-Anion Difference in Nonlactating Dairy Cows: A Meta-Analysis J Dairy Sci, February 1, 2006; 89(2): 537 - 548. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. Roche, S. Petch, and J. K. Kay Manipulating the Dietary Cation-Anion Difference via Drenching to Early-Lactation Dairy Cows Grazing Pasture J Dairy Sci, January 1, 2005; 88(1): 264 - 276. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
