Phosphate balance in phosphate supplemented and unsupplemented health subjects during and after hypokinesia

Objective: To demonstrate the effect of hypokinesia (HK) and post-HK on phosphate (Pi) imbalance and use of Pi with different Pi imbalance and different Pi consumption: were measured Pi balance, plasma Pi level and Pi loss during HK. Methods: Experiments were conducted during the pre-experimental period of 30 days, and the HK period of 364-days and post-HK period of 30-days. Forty healthy male volunteers 24.2 &#177; 2.0 yr, were divided into four groups: unsupplemented active control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented active control subjects (SACS), and supplemented hypokinetic subjects (SHKS). All SACS and SHKS were supplemented with 0.6 mmol dicalcium-phosphate per kg body weight daily. Results: During HK, Pi imbalance, serum Pi and calcium (Ca2+) levels, fecal Pi loss, and urine Ca2+ and Pi loss increased (P < 0.05) in SHKS and UHKS compared with pre-experimental values and the values in their respective active controls (SACS and UACS). The measured parameters were changed (P < 0.05) more in SHKS than in UHKS. During the initial 20-days of post-HK, serum Pi and Ca2+ levels, fecal P loss, and urine Pi and Ca2+ losses decreased (P < 0.05), while Pi imbalance remained (P < 0.05) depressed in SHKS and UHKS compared with UACS and SACS. The measured parameters were changed (P < 0.05) more in SHKS than in UHKS. Conclusion: The greater Pi imbalance with than without Pi supplementation shows that the risk of higher Pi imbalance is directly related to the magnitude of Pi intake. The higher Pi loss with higher than lower Pi imbalance shows that the risk of greater Pi loss is directly related to the magnitude of Pi imbalance. It is concluded that Pi imbalance increases more when the Pi consumption is higher and that Pi loss increases more with higher than lower Pi imbalance indicating that during HK Pi imbalance is due to the inability of the body to use Pi but not to the Pi shortage in the diet

Inability of healthy subjects to deposit potassium during hypokinesia and potassium supplementation

Objective: To determine the effect of potassium (K+) supplementation and hypokinesia (HK; diminished movement) on muscle K+ content and K+ loss. Methods: Studies were conducted on 40 healthy male volunteers during a pre-experimental period of 30 days and an experimental-period of 364 days. Volunteers were equally divided into four groups: unsupplemented control subjects (UCS), unsupplemented experimental subjects (UES), supplemented control subjects (SCS), and supplemented experimental subjects (SES). A daily supplement of 1.17 mmol potassium-chloride (KCl) per kg body weight was given to the subjects in the SCS and SES groups. Results: Muscle K+ content decreased (P < 0.05), and plasma K+ concentration, and K+ loss in urine and feces increased (P < 0.05) in the SES and UES groups compared with their pre-experimental levels and the values in their respective control groups (SCS and UCS). Muscle K+ content decreased more (P < 0.05), and plasma K+ concentration and K+ loss in urine and feces increased more (P < 0.05) in the SES group than in the UES group. Conclusion: Muscle K+ content is not decreased by the K+ deficient diet and K+ loss is not increased by the higher muscle K+ content in the body. Rather it is caused by the inability of the body to use K+ during HK and K+ supplementation

Magnesium loss in magnesium deficient subjects with and without physical exercise during prolonged hypokinesia

Objective: To show the effect of hypokinesia (HK; diminished movement) on magnesium (Mg2+) loss in Mg2+ deficient subjects and the effect of physical exercise and on Mg2+ deficiency with and without physical exercise: Mg2+ balance, serum Mg2+ concentration and Mg2+ loss were measured. Methods: Studies were conducted on 30 healthy male volunteers during a pre-experimental period of 30 days and an experimental period of 364 days. They were divided equally into three-groups: unrestricted active control subjects (UACS), continuous hypokinetic subjects (CHKS) and periodic hypokinetic subjects (PHKS). The UACS group ran average distances of 9.3 ± 1.2 km.day-l; the CHKS group walked average distances of 0.9 ± 0.2 km.day-l; and the PHKS group walked and ran average distances of 0.9 ± 0.2 km and 9.3 ± 1.2 km.day-l for 5-and 2-days per week, respectively. Results: Mg2+ deficiency, serum Mg2+ level, fecal and urine Mg2+ loss increased (P < 0.05), in the PHKS and CHKS groups compared with their pre-experimental values and the values in the UACS group. However, serum Mg2+ concentration, urine and fecal Mg2+ loss and Mg2+ deficiency increased more (P < 0.05) in the PHKS group than in the CHKS group. Conclusions: Mg2+ deficiency is more evident with than without physical exercise and Mg2+ loss is exacerbated more with higher than lower Mg2+ deficiency. This indicates that Mg2+ deficiency with and without physical exercise and Mg2+ loss with higher and lower Mg2+ deficiency is due to inability of the body to use Mg2+ and more so when physically healthy subjects are submitted to prolonged periodic than continuous hypokinesia

Potassium loss with tissue potassium deficiency in rats during hypokinesia

Background. This study aims at showing the effect of hypokinesia (HK) on tissue potassium (K+) loss with different tissue K+ depletion and tissue K+ deficiency with different K+ intake. To this end, tissue K+ content, plasma K+ level, and K+ loss with and without K+ supplements during HK were measured. Methods. Studies were conducted on male Wistar rats during a pre-experimental and an experimental period. Animals 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). SVCR and SHKR were supplemented daily with 2.50 mEq potassium chloride (KCl). Results. Gastrocnernius muscle and right femur bone K+ content reduced significantly, whereas plasma K+ level and urine and fecal K+ loss increased significantly in SHKR and UHKR compared with their pre-experimental values and the values in their respective vivarium controls (SVCR and UVCR). Bone and muscle K+ content decreased more significantly, and plasma K+ level and urine and fecal K+ loss increased more significantly in SHKR than in UHKR. Conclusions. The greater tissue K+ deficiency with higher than lower K+ intake shows that the risk of higher tissue K+ deficiency is directly related to K+ intake. The higher K+ loss with higher tissue K+ deficiency and the lower K+ loss with lower K+ tissue deficiency shows that the risk of greater K+ loss is directly related to tissue K+ deficiency. Tissue K+ deficiency increases more when the K+ intake is higher and K+ loss increases more with higher than lower tissue K+ deficiency indicating that, during HK, tissue K+ deficiency is due to the inability of the body to use K+ but not to K+ shortage in the diet. (c) 2008 IMSS. Published by Elsevier Inc