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. 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.

Hypohosphataemia is a frequent finding in early lactating and anorectic dairy cows. Sodium phosphate is commonly used for oral phosphorus (P) supplementation, although other phosphate salts may present useful treatment alternatives. Objectives of this study were to compare the efficacy of monopotassium phosphate (KH2PO4) and monocalcium phosphate (Ca(H2PO4)2) to monosodium phosphate (NaH2PO4) in P-depleted cows. Furthermore, the effect of concentrated NaH2PO4 on the reticular groove reflex was studied. Six healthy but P-depleted dairy cows underwent four treatments in randomised order. Treatments consisted of intraruminal administration of NaH2PO4, KH2PO4 and Ca(H2PO4)2 providing the equivalent of 60 g P. A fourth treatment consisting of concentrated NaH2PO4 combined with acetaminophen as a marker substance was administered orally to determine whether the reticular groove reflex could be induced. Intraruminal administration of NaH2PO4 and KH2PO4 resulted in similar increases in plasma Pi concentrations ([Pi]) while intraruminal Ca(H2PO4)2 resulted in lower increases in plasma [Pi]. Oral and intraruminal administration of NaH2PO4 resulted in similar times to peak plasma [Pi] and acetaminophen concentration, indicating that concentrated NaH2PO4 administered orally did not trigger the reticular groove reflex. These results suggest that oral administration of KH2PO4 is equally effective as NaH2PO4. Oral administration of Ca(H2PO4)2 in contrast has a less pronounced effect on the plasma [Pi].