Summary
The importance of phosphorus nutrition and the adverse effects of widespread P deficiencies in cattle grazing the rangelands of northern Australia are well known. P deficiencies decrease growth and increase age of turnoff at slaughter. Productivity is also adversely affected in both heifers and mature breeders with decreased fertility and weaning weight and increased mortality. Although there are generally large economic benefits to addressing P deficiency only a low proportion of cattle grazing P-deficient pastures across northern Australia are effectively managed and supplemented to avoid the productivity losses due to P deficiencies.
A research program investigated aspects of P nutrition in breeder cattle in circumstances where improved knowledge of P physiology and nutrition should lead to practical management manipulations for increased cost-effectiveness in northern Australian production systems. The project objectives were to (i) identify the constituents of old bones which are attractive specifically to P-deficient cattle so that these can be used as attractants in P supplements, (ii) determine the magnitude and diet x animal interactions affecting the deposition and mobilisation of body P reserves in breeder cattle in situations typical of northern Australia, and (iii) understand the physiological mechanisms controlling mobilization and deposition of body P reserves in breeder cattle. Also to use this knowledge to better manage P deficiency in breeders through improved estimation of current animal P supply from diet and body reserves and animal responses and by better diagnostic tools of P status.
For objective (i) the attraction of P-deficient cattle to ingest old bones was examined to identify the olfactory constituents causing attraction which might be used to increase intake of P supplements during the wet season. It was shown that the attraction was a learned response, not innate, and thus there are not likely to be any universal attractants. Nevertheless the new knowledge may be used to improve training of cattle to attract them to P supplements.
For objectives (ii) and (iii) five intensive experiments with Droughtmaster mature breeders or first-calf cows (FCC) investigated P mobilization and deposition. The animals were housed in individual pens for 3-8 months and accurate measurements of intake, excretion, P balance, milk production and LW changes in cows and growth of calves during late pregnancy and/or early lactation were measured. Cattle were fed semi-purified or molasses-straw diets to achieve appropriate metabolisable energy (ME) and P intakes while also measuring the effects on voluntary feed intake.
Mature breeder cows calving in high P status (from high P intakes during pregnancy) and fed severely P deficient diets in early lactation decreased VI, extensively mobilized body P (5-10 g P/day) and maintained milk output and calf growth. Calf growth was not affected in one experiment and there was only a small decrease (from 0.92 to 0.80 kg/day) in a second experiment. The mobilised P provided up to about half the P requirements of these lactating cows. However this body P mobilization was associated with large losses in cow LW (e.g. 0.5 kg/day) as well as P in bone. A third experiment with FCC showed that these animals had a lesser capacity to mobilize body P reserves to maintain early lactation. Milk production in FCC and mature cows was comparable when ingesting adequate P diets. However in FCC fed severely P deficient diet during both late pregnancy and early lactation milk output was reduced by up to 44% and calf growth up to 0.57 kg/day. These adverse effects during lactation were reduced by P-adequate diets during pregnancy due to P mobilisation.
Greater adverse effects in FCC were likely due to their need for P for continuing skeletal growth and with less P available for milk secretion.
Another experiment examined the effects diet P deficiency of heifers rapidly losing conceptus-free LW during late pregnancy as occurs routinely in harsh nutritional environments and where P deficiency is common. Regardless of the magnitude of the LW loss feeding a high P diet caused the heifers to store more body P with higher bone P at calving. When heifers were maintaining (or in another experiment gaining) conceptus-free LW during late pregnancy diet P deficiency reduced the voluntary intakes (VI) of DM and ME. Thus P supplementation during the dry season in late-pregnant breeders as well as lactating breeders grazing low P pastures is recommended. Body P mobilized to support lactation must be replenished later in the annual cycle to prepare cows calving annually for the next lactation. An experiment showed that P depleted mature breeders could replenish both bone P and soft tissue P post-weaning when fed diets comparable with late wet season or early dry season pasture, and the replenishment was much greater when a diet high in both P and ME was fed. Thus breeders could respond to P supplementation and stored bone P during the dry season.
The experimental program improved understanding of key physiological mechanisms in beef breeder cows in P deficiency and P replenishment. Severely P deficient diets resulted in a immediate and large decreases in blood P (PIP) concentrations (e.g. < 0.7 mmol/L), reduced VI, rapid loss of LW and often mobilisation of bone minerals. However the bone P mobilisation was insufficient to normalise PIP in breeders but did maintain PIP in weaners. Substantial mobilisation of bone unexpectedly did not involve the key bone mobilising hormone, parathyroid hormone PTH). With low P diets there is also an increase in the active form of Vit D3 (1,25-diOH Vitamin D3) which would promote intestinal absorption of Ca and P. Overall diet P deficiency in cows was characterised by low PIP, high blood Ca, high blood Ca/P ratio, markedly increased concentration of the bone mobilisation marker carboxy-terminal telopeptides of type I collagen (CTX-1) despite low PTH, and increased active Vit D3 and bone alkaline phosphatase (BAP).
The present project advanced understanding in the physiology of P in breeder cattle. It has improved both prediction of P supplementation responses in breeders through the annual cycle and the diagnosis of P status from blood. Also the recent project B.NBP.0719 has improved reliability of estimation of diet P concentration from faecal measurements. The body P reserves in breeders can be mobilised to alleviate diet P deficiency during the wet season, and replenished slowly through the dry season when diet P is adequate. Breeders, particularly if mature, can tolerate intervals of P deficiency while lactating but with severe loss of body condition. The basic recommendation that it is most effective to feed P supplements through the wet season is not changed and should be the most effective and efficient use of P supplements. When feeding P supplements through the entire wet season is not possible then P supplements should be fed for the remainder of the wet season. Feeding some P supplements during the dry season to maintain and/or replenish bone P in some classes of breeders (lactating, late pregnant, depleted bone P) is recommended. The estimation of diet P adequacy should be based on blood and P and F.NIRS of faeces. Because it is now clear that the relationship between concentrations of P in the diet and in faeces is inconsistent the FP:ME ratio should not continue to be recommended as a diagnostic. The recent commercial availability of portable vet clinic analysers (for blood P, Ca, BAP, other metabolites), NIRS spectrometers (for faeces, urine and blood) and X-ray and ultrasound units offer potential for on-farm crush-side diagnostic systems for improved management of P deficiency in grazing cattle.
