ABSTRACT
The objective of this study was to show that prolonged restriction of motor activity (hypokinesia) could reduce phosphate (P) deposition and contribute to P loss with tissue P depletion. To this end, measurements were made of tissue P content, P absorption, plasma P levels, urinary and fecal P excretion of rats during and after hypokinesia (HK) and daily phosphate supplementation. Studies were conducted on male Wistar rats during a pre-hypokinetic period, a hypokinetic period and a post-hypokinetic period. All rats were equally divided into four groups: unsupplemented vivarium control rats (UVCR), unsupplemented hypokinetic rats (UHKR), supplemented vivarium control rats (SVCR) and supplemented hypokinetic rats (SHKR). Bone and muscle P content, plasma intact parathyroid hormone (iPTH) levels, P absorption, plasma P levels and urinary and fecal P excretion did not change in SVCR and UVCR compared with their pre-HK values. During HK, plasma P levels, urinary and fecal P excretion increased significantly (p<0.05) while muscle and bone P content, P absorption and plasma iPTH levels decreased significantly (p<0.05) in SHKR and UHKR compared with their pre-HK values and the values in their respective vivarium controls (SVCR and UVCR). During the initial 9-days of post-HK, plasma, urinary and fecal P levels decreased significantly (p<0.05), and plasma iPTH levels, muscle and bone P levels remained significantly (p<0.05) depressed in hypokinetic rats compared with their pre-HK values and the values in their respective vivarium control rats. By the 15th day, these values approached the control values. During HK and post-HK, changes in P absorption, plasma iPTH levels, and P levels in muscle, bone, plasma, urine and feces were significantly (p<0.05) greater in SHKR than in UHKR. Decreased tissue P content with increased P loss in animals receiving and not receiving P supplementation demonstrates decreased P deposition during HK. Higher P excretion with lower tissue content in SHKR and UHKR demonstrates that P deposition is decreased more with P supplementation than without. Because SHKR with a lower tissue P content showed higher P excretion than UHKR it was concluded that the risk of decreased P deposition with greater tissue P depletion is inversely related to P intake, that is, the higher the P intake the greater the risk for decreased P deposition and the greater tissue P depletion. It was shown that P (regardless of the intensity of its tissue depletion) is lost during HK unless factors contributing to the decreased P deposition are partially or totally reversed. It was concluded that dissociation between (decreased) tissue P content and (increased) P uptake indicates decreased P (absorption and) deposition as the main mechanisms of tissue P depletion during prolonged HK.
