The effect of transient, moderate dietary phosphorus deprivation on phosphorus metabolism, muscle content of different phosphorus-containing compounds, and muscle function in dairy cows

Hypophosphatemia is a common finding in periparturient and anorectic cattle. Although the clinical relevance of hypophosphatemia in cattle is uncertain, it has been empirically associated with persistent recumbency, specifically in periparturient dairy cows. The objective of the present study was to...

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Veröffentlicht in:Journal of dairy science 2015-08, Vol.98 (8), p.5385-5400
Hauptverfasser: Grünberg, W., Scherpenisse, P., Dobbelaar, P., Idink, M.J., Wijnberg, I.D.
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container_issue 8
container_start_page 5385
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creator Grünberg, W.
Scherpenisse, P.
Dobbelaar, P.
Idink, M.J.
Wijnberg, I.D.
description Hypophosphatemia is a common finding in periparturient and anorectic cattle. Although the clinical relevance of hypophosphatemia in cattle is uncertain, it has been empirically associated with persistent recumbency, specifically in periparturient dairy cows. The objective of the present study was to determine if transient dietary phosphorus (P) deprivation over a course of 5 wk, by feeding an approximately 40% P-deficient ration to lactating dairy cows, would result in altered muscle function or muscle P metabolism severe enough to present a risk for animal health and well-being. In addition, we wanted to determine the association between the plasma phosphate concentration ([Pi]) and muscle tissue P content to assess to what extent intracellular P deprivation of muscle cells could be extrapolated from subnormal plasma [Pi]. Ten healthy multiparous, mid-lactating dairy cows received a ration with a P content of 0.18% over a period of 5 wk. Following the P-deprivation phase, the same ration supplemented with P to obtain a dietary P content of 0.43% was fed for 2 wk. Blood and urine samples were collected regularly and muscle biopsies were obtained repeatedly to determine the P content in muscle tissue. Function of skeletal and heart muscles was evaluated by electrocardiography and electromyography conducted repeatedly throughout the study. Feeding the P-deficient ration resulted in the rapid development of marked hypophosphatemia. The lowest plasma [Pi] were measured after 9 d of P depletion and were, on average, 60% below predepletion values. Plasma [Pi] increased thereafter, despite ongoing dietary P depletion. None of the animals developed clinical signs commonly associated with hypophosphatemia or any other health issues. Urine analysis revealed increasing renal calcium, pyridinoline, and hydroxypyridinoline excretion with ongoing P deprivation. Biochemical muscle tissue analysis showed that dietary P depletion and hypophosphatemia were not associated with a decline in muscle tissue P content. Electromyographic examination revealed increased occurrence of pathological spontaneous activity in striated muscles after 2 wk of dietary P depletion in several cows, which could be suggestive of neuromuscular membrane instability. No effect on heart muscle activity was identified electrocardiographically. These results suggest that counter-regulatory mechanisms were sufficient to maintain normal muscle tissue P content during transient and moderate P deprivation.
doi_str_mv 10.3168/jds.2015-9357
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Although the clinical relevance of hypophosphatemia in cattle is uncertain, it has been empirically associated with persistent recumbency, specifically in periparturient dairy cows. The objective of the present study was to determine if transient dietary phosphorus (P) deprivation over a course of 5 wk, by feeding an approximately 40% P-deficient ration to lactating dairy cows, would result in altered muscle function or muscle P metabolism severe enough to present a risk for animal health and well-being. In addition, we wanted to determine the association between the plasma phosphate concentration ([Pi]) and muscle tissue P content to assess to what extent intracellular P deprivation of muscle cells could be extrapolated from subnormal plasma [Pi]. Ten healthy multiparous, mid-lactating dairy cows received a ration with a P content of 0.18% over a period of 5 wk. Following the P-deprivation phase, the same ration supplemented with P to obtain a dietary P content of 0.43% was fed for 2 wk. Blood and urine samples were collected regularly and muscle biopsies were obtained repeatedly to determine the P content in muscle tissue. Function of skeletal and heart muscles was evaluated by electrocardiography and electromyography conducted repeatedly throughout the study. Feeding the P-deficient ration resulted in the rapid development of marked hypophosphatemia. The lowest plasma [Pi] were measured after 9 d of P depletion and were, on average, 60% below predepletion values. Plasma [Pi] increased thereafter, despite ongoing dietary P depletion. None of the animals developed clinical signs commonly associated with hypophosphatemia or any other health issues. Urine analysis revealed increasing renal calcium, pyridinoline, and hydroxypyridinoline excretion with ongoing P deprivation. Biochemical muscle tissue analysis showed that dietary P depletion and hypophosphatemia were not associated with a decline in muscle tissue P content. Electromyographic examination revealed increased occurrence of pathological spontaneous activity in striated muscles after 2 wk of dietary P depletion in several cows, which could be suggestive of neuromuscular membrane instability. No effect on heart muscle activity was identified electrocardiographically. These results suggest that counter-regulatory mechanisms were sufficient to maintain normal muscle tissue P content during transient and moderate P deprivation. Muscle function was not grossly affected, although the increased occurrence of pathological spontaneous activity suggests that subclinical neuropathy or myopathy, or both, may have occurred with ongoing P deprivation. 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Although the clinical relevance of hypophosphatemia in cattle is uncertain, it has been empirically associated with persistent recumbency, specifically in periparturient dairy cows. The objective of the present study was to determine if transient dietary phosphorus (P) deprivation over a course of 5 wk, by feeding an approximately 40% P-deficient ration to lactating dairy cows, would result in altered muscle function or muscle P metabolism severe enough to present a risk for animal health and well-being. In addition, we wanted to determine the association between the plasma phosphate concentration ([Pi]) and muscle tissue P content to assess to what extent intracellular P deprivation of muscle cells could be extrapolated from subnormal plasma [Pi]. Ten healthy multiparous, mid-lactating dairy cows received a ration with a P content of 0.18% over a period of 5 wk. Following the P-deprivation phase, the same ration supplemented with P to obtain a dietary P content of 0.43% was fed for 2 wk. Blood and urine samples were collected regularly and muscle biopsies were obtained repeatedly to determine the P content in muscle tissue. Function of skeletal and heart muscles was evaluated by electrocardiography and electromyography conducted repeatedly throughout the study. Feeding the P-deficient ration resulted in the rapid development of marked hypophosphatemia. The lowest plasma [Pi] were measured after 9 d of P depletion and were, on average, 60% below predepletion values. Plasma [Pi] increased thereafter, despite ongoing dietary P depletion. None of the animals developed clinical signs commonly associated with hypophosphatemia or any other health issues. Urine analysis revealed increasing renal calcium, pyridinoline, and hydroxypyridinoline excretion with ongoing P deprivation. Biochemical muscle tissue analysis showed that dietary P depletion and hypophosphatemia were not associated with a decline in muscle tissue P content. Electromyographic examination revealed increased occurrence of pathological spontaneous activity in striated muscles after 2 wk of dietary P depletion in several cows, which could be suggestive of neuromuscular membrane instability. No effect on heart muscle activity was identified electrocardiographically. These results suggest that counter-regulatory mechanisms were sufficient to maintain normal muscle tissue P content during transient and moderate P deprivation. Muscle function was not grossly affected, although the increased occurrence of pathological spontaneous activity suggests that subclinical neuropathy or myopathy, or both, may have occurred with ongoing P deprivation. The results presented here indicate that plasma [Pi] is unsuitable for assessing muscle tissue P content in cattle.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26026765</pmid><doi>10.3168/jds.2015-9357</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Elsevier ScienceDirect Journals Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects Amino Acids - urine
Animal Feed - analysis
Animals
Calcium - urine
Cattle
dairy cattle
Diet - veterinary
Dietary Supplements
electromyography
Female
hypophosphatemia
Hypophosphatemia - blood
Lactation
muscle
Muscle, Skeletal - drug effects
Muscle, Skeletal - physiology
Phosphates - blood
phosphorus
Phosphorus - blood
Phosphorus - deficiency
Phosphorus, Dietary - administration & dosage
Phosphorus, Dietary - pharmacokinetics
Tissue Distribution
title The effect of transient, moderate dietary phosphorus deprivation on phosphorus metabolism, muscle content of different phosphorus-containing compounds, and muscle function in dairy cows
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