Muscle potassium and potassium losses during hypokinesia in healthy subjects.

Hypokinesia (HK) induces electrolyte losses in electrolyte-deficient tissue, yet the mechanisms of electrolyte losses in electrolyte-deficient tissue remain unknown. Mechanisms of electrolyte deposition could be involved. To determine the effect of prolonged HK on potassium (K+) deposition were measured muscle K+ content and K+ losses. Studies were conducted on 20 physically healthy male volunteers during 30 days pre-experimental period and 364 days experimental period. Subjects were equally divided into two groups: control subjects (CS) and experimental subjects (ES). The CS group was run average distances of 9.8±1.7 km day(-1) and the ES group was walked average distances of 2.7±0.6 km day(-1). Muscle K+ content decreased (p<0.05) and plasma K+ concentration, and K+ losses in urine and feces increased (p<0.05) in the ES group compared to their pre-experimental level and the values in their respective CS group. Muscle K+ content, plasma K+ level, and urine and fecal K+ losses did not show any changes in the CS group compared to their pre-experimental values. The conclusion was that K+ losses in K+-deficient muscle of healthy subjects could have been attributable to the less efficient K+ deposition inherently to prolonged HK.

Utilization of magnesium during hypokinesia and magnesium supplementation in healthy subjects.

OBJECTIVE: The incompleteness of electrolyte utilization during hypokinesia and electrolyte supplementation is the defining factor of electrolyte metabolic changes, yet the effect of electrolyte supplementation and HK upon electrolyte utilization is poorly understood. To determine the influence of magnesium (Mg(2+)) supplementation and hypokinesia (diminished movement) on magnesium utilization, we investigated the use of Mg(2+) supplementation to establish its effect upon muscle Mg(2+) content and Mg2(2+) losses. METHODS: This study was conducted in 40 physically healthy male volunteers during a pre-experimental period of 30 d and an experimental period of 364 d. Subjects were equally divided into four groups: unsupplemented control subjects (UCSs), unsupplemented experimental subjects (UESs), supplemented control subjects (SCSs), and supplemented experimental subjects (SESs). A daily supplementation of 3.0 mmol of magnesium-chloride per kilogram of body weight was given to subjects in the SCS and SES groups. RESULTS: Muscle Mg(2+) content decreased (P < 0.05) and plasma Mg(2+) concentration and Mg(2+) loss in urine and feces increased (P < 0.05) in the SES and UES groups compared with their pre-experimental levels and values in their respective control groups (SCS and UCS). Muscle Mg(2+) content decreased more (P < 0.05) and plasma Mg(2+) concentration and Mg(2+) loss in urine and feces increased more (P < 0.05) in the SES group than in the UES group.The muscle Mg(2+) content and plasma Mg(2+) level and Mg(2+) losses did not change in the control groups. CONCLUSION: Daily Mg(2+) supplementation during prolonged hypokinesia decreases more muscle Mg(2+) content and Mg(2+)-deficient muscle increases more Mg(2+) loss in healthy subjects indicating lower Mg(2+) utilization with than without Mg(2+) supplementation.

Muscle calcium metabolic effects of hypokinesia in physically healthy subjects.

The incompleteness of electrolyte deposition during hypokinesia (HK; diminished movement) is the defining factor of electrolyte metabolic changes, yet the effect of prolonged HK upon electrolyte deposition is poorly understood. The objective of this investigation was to determine the effect of muscle calcium (Ca(++)) changes upon Ca(++) losses during prolonged HK. Studies were conducted on 20 physically healthy male volunteers during a pre-experimental period of 30 days and an experimental period of 364 days. Subjects were equally divided in two groups: control subjects (CS) and experimental subjects (ES). The CS group ran average distances of 9.2 ± 1.2 km day(-l), and the ES group walked average distances of 2.3 ± 0.2 km day(-l). Muscle Ca(++) contents, plasma Ca(++) concentrations, and Ca(++) losses in urine and feces were measured in the experimental and control groups of subjects. The muscle Ca(++) contents decreased (p < 0.05), and plasma Ca(++) levels and Ca(++) losses in the urine and feces increased (p < 0.05) in the ES group compared with their pre-experimental levels and the values in their respective CS group. Muscle Ca(++) contents and plasma Ca(++) levels and urinary and fecal Ca(++) losses did not change in the CS group compared to their pre-experimental levels. It is concluded that prolonged HK increase plasma Ca(++) concentrations and Ca(++) losses in Ca(++) deficient muscle indicating decreased Ca(++) deposition.

Vanadium supplementation effect on vanadium metabolism during hypokinesia in rats.

OBJECTIVES: Microelement supplementation during Hypokinesia (HK; diminished movement) affects differently microelement metabolism from that of normal muscular activity. In view of the effect of trace element supplementation and HK upon microelement metabolism we investigated the effect of vanadium (V) supplements on tissue V content and V loss during HK. METHODS: Studies were performed on 240 male Wistar rats during a pre-experimental period of 9 days and an experimental period of 98 days. Rats were equally divided into four groups: unsupplemented control rats (UCR), unsupplemented experimental rats (UER), supplemented control rats (SCR) and supplemented experimental rats (SER). A daily supplementation of 0.8 µmol vanadium sulfate was given to the rats in the SCR and SER groups. Muscle V content, plasma V level and V loss was measured in the experimental and control groups of rats. RESULTS: The gastrocnemius muscle and right femur bone V content decreased (p < 0.05), and plasma V level and urinary and fecal V loss increased (p < 0.05) in the SER and UER groups compared to their pre-experimental values and their respective control groups (SCR) and UCR). However, the tissue V content decreased more (p < 0.05) and plasma V level and V loss increased more (p < 0.05) in the SER group than in the UER group. The tissue V content and plasma V level and V loss did not change in the control groups of rats compared to the pre-experimental values. CONCLUSIONS: It is concluded that during HK V supplementation decreases more tissue V content and increases more V loss and plasma V level in V deficient tissue indicating lower V utilization.

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.

Effect of hypokinesia on calcium loss in calcium-supplemented and -unsupplemented rats.

BACKGROUND: We undertook this study to determine total calcium (Ca(2+)) loss in Ca(2+)-deficient tissue and tissue Ca(2+) loss with and without Ca(2+) supplementation during hypokinesia (HK; diminished movement). METHODS: Studies were conducted on 240 male Wistar rats during a pre-experimental period of 9 days and an experimental period of 98 days. 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). Calcium supplementation of 2.6 mmol was given to animals in the SVCR and SHKR groups. RESULTS: Gastrocnemius muscle and right femur bone Ca(2+) level reduced (p <0.05) and plasma Ca(2+) level, and urine and fecal Ca(2+) loss increased (p <0.05) in the SHKR and UHKR groups compared to their pre-experimental values and the values in their respective vivarium control groups (SVCR and UVCR). Muscle and bone Ca(2+) content decreased more (p <0.05), while plasma Ca(2+) level, and urine and fecal Ca(2+) loss increased more (p <0.05) in the SHKR group than in the UHKR group. CONCLUSIONS: Tissue Ca(2+) deficiency during HK is more evident with than without Ca(2+) supplementation and Ca(2+) loss was exacerbated with higher than lower tissue Ca(2+) deficiency. This shows that tissue Ca(2+) deficiency does not result from the lower Ca(2+) content in the food consumed and the total bodily Ca(2+) loss is not caused by the higher tissue Ca(2+) content but due to the impossibility of the body to use Ca(2+) during prolonged HK.

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: Gastrocnemius 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.

Inadequacy of calcium supplements to normalize muscle calcium deficiency in healthy subjects during prolonged hypokinesia.

OBJECTIVE: We investigated the effect of hypokinesia (diminished movement) on muscle calcium (Ca(2+)) content with and without Ca(2+) supplementation and Ca(2+) loss with different muscle Ca(2+) deficiency; muscle Ca(2+) content, plasma Ca(2+) level, and Ca(2+) loss were measured. METHODS: Studies were performed in 40 physically healthy male volunteers during a pre-experimental period of 30 d and an experimental period of 364 d. Subjects in equal numbers were assigned to one of four groups: unsupplemented active control subjects (UACSs), unsupplemented hypokinetic subjects (UHKSs), supplemented active control subjects (SACSs), and supplemented hypokinetic subjects (SHKSs). A daily supplementation of 0.7 mmol of calcium lactate per kilogram of body weight was given to SACSs and SHKSs. RESULTS: Muscle Ca(2+) content decreased, and plasma Ca(2+) concentration and Ca(2+) loss in urine and feces increased (P < 0.05) in the SHKS and UHKS groups compared with their pre-experimental values and the values in their respective active control groups (SACS and UACS). However, muscle Ca(2+) content decreased more, and plasma Ca(2+) concentration and Ca(2+) loss increased more (P < 0.05) in the SHKS group than in the UHKS group. CONCLUSION: Muscle Ca(2+) deficiency is more evident when Ca(2+) intake is higher and Ca(2+) loss is more exacerbated with higher than with lower muscle Ca(2+) deficiency, indicating that muscle Ca(2+) deficiency during prolonged hypokinesia is due to an inability of the body to use Ca(2+) but not to a Ca(2+) shortage in the diet.

Mechanism of sodium loss with muscle sodium deficiency in sodium supplemented and unsupplemented subjects during hypokinesia.

BACKGROUND: This study aims at showing the effect of hypokinesia (HK) on sodium (Na+) loss with different muscle Na+ deficiency and different Na+ intake. Muscle Na+ content, plasma Na+ level and Na+ loss with and without Na+ supplementation were measured. METHODS: This study was conducted on 40 healthy male volunteers during a pre-experimental and an experimental period. Subjects were equally divided into four groups: unsupplemented active control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented active control subjects (SACS) and supplemented hypokinetic subjects (SHKS). A daily supplementation of 3.21 mmol of sodium chloride (NaCl) per kg body weight was given to subjects in the SACS and SHKS groups. RESULTS: Muscle Na+ content levels decreased and plasma Na+ levels, and levels of Na+ loss in urine and feces increased (p<0.05) in the SHKS and UHKS groups compared to their pre-experimental values and the values in the respective active control groups (SACS and UACS). However, muscle Na+ content levels decreased more (p<0.05), and plasma Na+ levels and levels of Na+ loss in urine and feces increased more (p<0.05) in the SHKS group than in the UHKS group. CONCLUSIONS: The greater muscle Na+ deficiency with higher than lower Na+ consumption shows that the risk of greater muscle Na+ deficiency is directly related to Na+ consumption. The higher Na+ loss with higher than lower muscle Na+ deficiency shows that the risk of greater muscle Na+ loss is directly related to muscle Na+ deficiency. It is concluded that muscle Na+ deficiency is more evident when Na+ consumption is higher and that muscle Na+ loss was more exacerbated with higher than lower muscle Na+ deficiency indicating that during prolonged HK the muscle Na+ deficiency is due to the inability of the body to use Na+, but not to Na+ shortage in diet.

Phosphate homeotasis in healthy subjects during prolonged periodic and continuous hypokinesia.

OBJECTIVE: This study aimed to show that during hypokinesia (HK), phosphate (P(i)) imbalance increases more with higher than lower physical activity and that P(i) absorption reduces more with higher than lower P(i) imbalance in subjects with higher than lower muscular activity. METHODS: Studies were conducted on 30 healthy male subjects during 364 days of HK. They were equally divided in three groups: unrestricted active control subjects (UACS), continuously hypokinetic subjects (CHKS) and periodically hypokinetic subjects (PHKS). CHKS were kept under average walking distances of 0.5+/-0.2 km day(-1) PHKS were kept under average walking distances of 0.5+/-0.1 and running average distances of 8.7+/-1.2 km day(-l) for 5 days and 2 days per week, respectively. UACS were placed under average running distances of 8.7+/-1.2 km day(-l). RESULTS: P(i) imbalance, serum, urine and fecal P(i) levels, and urine and serum calcium (Ca(2+)) levels increased significantly (p<0.05) and P(i) absorption, and serum intact parathyroid hormone (iPTH) and 1,25-dehydroxyvitamin D (1,25 (OH)(2) D(3)) levels decreased significantly (p<0.05) in CHKS and PHKS compared with their pre-HK values and their respective active control (UACS). However, the P(i) imbalance, serum, urine and fecal P(i) levels, and serum and urine Ca(2+) levels increased more significantly (p<0.05), and P(i) absorption and serum iPTH and 1,25 (OH)(2) D(3) levels decreased more significantly in PHKS than in CHKS. CONCLUSIONS: Higher P(i) imbalance with higher than lower physical activity shows that the risk of higher P(i) imbalance is inversely related to the intensity of physical activity. Lower P(i) absorption with higher than lower P(i) imbalance shows that the risk of lower P(i) absorption is inversely related to magnitude of P(i) imbalance. In conclusion P(i) imbalance increases more with higher than lower physical activity and that P(i) absorption decreases more with higher than lower P(i) imbalance indicating that during HK the use of P(i) decreases more with higher than lower physical activity.

Electrolyte homeostasis in trained and untrained healthy subjects during prolonged hypokinesia.

OBJECTIVE: This study aimed to show that during hypokinesia (HK) electrolyte imbalance increases more in trained than untrained subjects and that electrolyte loss increases more with higher than lower electrolyte imbalance in trained than untrained subjects. METHODS: Studies were conducted during 364-day HK. Subjects were equally divided in four groups: trained ambulatory control subjects (TACS), trained hypokinetic subjects (THKS), untrained ambulatory control subjects (UACS) and untrained hypokinetic subjects (UHKS). THKS and UHKS were limited to average walking distances of 0.5+/-0.1 km day(-1). TACS were running average distances of 9.8+/-1.3 and UACS were walking average distances of 1.8+/-0.2 km day(-1). RESULTS: Plasma potassium (K(+)), calcium (Ca(+2)) and magnesium (Mg(+2)) levels, urine and fecal electrolyte excretion, electrolyte imbalance, plasma aldosterone (PA) and plasma rennin activity (PRA) increased significantly (p<0.05), while electrolyte absorption, plasma intact parathyroid hormone (iPTH) and dihydroxyvitamin D (1,25 (OH)(2) D(3)) levels decreased significantly (p<0.05) in THKS and UHKS compared with their pre-HK values and their respective controls (TACS and UACS). Electrolyte imbalance, plasma electrolyte levels, urine and fecal electrolyte excretion, PA and PRA levels increased more significantly (p<0.05), while electrolyte absorption, plasma iPTH and 1, 25 (OH)(2) D(3) levels decreased more significantly (p<0.05) in THKS than in UHKS. CONCLUSION: The higher electrolyte imbalance in trained as compared to untrained subjects shows that the risk of higher electrolyte imbalance is inversely related to the magnitude of physical conditioning. The higher electrolyte loss with higher than lower electrolyte imbalance shows that the risk of higher electrolyte loss is inversely related to the magnitude of electrolyte imbalance. In conclusion electrolyte imbalance increases more in trained than untrained subjects and that electrolyte loss increase more with higher than lower electrolyte imbalance indicating that during prolonged HK the use of electrolytes decreases more with higher than lower physical conditioning.

Sodium loss with tissue sodium deficiency in sodium supplemented and unsupplemented rats during prolonged hypokinesia.

To demonstrate the effect of sodium supplementation and hypokinesia (HK; diminished movement) on the total bodily sodium (Na+) loss and tissue Na+ deficiency, tissue Na+ content, plasma Na+ level and Na+ loss were measured. Studies were conducted on male Wistar rats during a pre-experimental and 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). A daily supplementation of 3.50 mEq sodium chloride (NaCl) was given to animals in the SVCR and SHKR groups. Gastrocnemius muscle and right femur bone Na+ level decreased (p<0.05), and plasma Na+ level and urine and fecal Na+ loss increased (p<0.05) in the SHKR and UHKR groups compared to their pre-experimental values and the values in their respective vivarium control groups (SVCR and UVCR). Muscle and bone Na+ content decreased more (p<0.05), and plasma Na+ level and urine and fecal Na+ loss increased more (p<0.05) in the SHKR group than in the UHKR group. It is concluded that tissue Na+ deficiency during HK is more evident when Na+ intake is higher and that the total bodily Na+ loss exacerbated more with higher than lower tissue Na+ deficiency. This shows that tissue Na+ deficiency is not the result of the lower Na+ content in the food consumed and that the total bodily Na+ loss is not caused by the higher tissue Na+ content but due to the impossibility of the body to use Na+ when animals are submitted to prolonged HK.

Measurement of potassium absorption during hypokinesia in potassium supplemented and unsupplemented healthy subjects.

Measuring potassium (K+) absorption, and K+ levels in plasma, urine and feces during and after hypokinesia (HK) and K+ supplementation, the aim of this study was to determine if prolonged HK could depress K+ deposition significantly more with or without K+ supplementation. Studies were conducted during 30-days pre-HK, 364-days HK and 30-days post-HK. Forty male healthy volunteers 24.2+/-5.5 years of age were chosen as subjects. They were equally divided in four groups: unsupplemented active control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented active control subjects (SACS), and supplemented hypokinetic subjects (SHKS). Hypokinetic subjects were walking average distances of 0.5+/-0.2 km day(-1). Active control subjects were running average distances of 5.8+/-1.2 km day(-1). Both SHKS and SACS consumed daily 2.17 mEq elemental potassium per kg body weight. Potassium absorption, fecal and urinary K+ excretion, sodium (Na+) loss, plasma K+ and Na+ level and plasma aldosterone (PA) level did not change in SACS and UACS compared with their pre-HK values. During HK, K+ absorption decreased significantly (P < 0.05) with time, and fecal and urinary K+ loss, urinary Na+ loss, plasma K+ and Na+ levels and PA level increased significantly (P < 0.05) with time in SHKS and UHKS compared with their pre-HK values and their respective active controls (SACS and UACS). During initial 15-days of post-HK, K+ absorption increased significantly (P < 0.05), fecal and urinary K+ excretion, urinary Na+ excretion and plasma K+ and Na+ levels and PA level decreased significantly (P < 0.05) in hypokinetic compared with active control subjects; by the 30th day they approached the control levels. During HK and post-HK, K+ absorption, fecal and urinary K+ losses, urinary Na+ excretion, plasma K+ and Na+ levels and PA level, changed significantly (P < 0.05) more in SHKS than UHKS. Decreased K+ losses during post-HK showed K+ depletion during HK. Decreased K+ absorption with K+ depletion during HK showed decreased K+ deposition. The greater K+ changes in SHKS than UHKS, during HK and post-HK, demonstrated that K+ deposition decreased more with than without K+ supplementation. It was concluded that dissociation between K+ absorption and K+ depletion showed decreased K+ deposition as the main mechanism for K+ depletion during HK.

Fluid volume measurements in normal subjects to disclose body hydration during acute bed rest.

Measuring intercompartmental, blood and urinary biochemical parameters during acute bed rest (ABR) and rigorous bed rest (RBR) the aim of this work was to disclose if ABR or RBR could influence significantly more and significantly faster the body hydration level in normal subjects. Studies conducted during pre-bed rest (BR) period of 3-days and during 7-days period of ABR and RBR. Thirty normal male individuals 24.6 +/- 5.7 years of age were chosen as subjects. They were divided into three groups: unrestricted active control subjects (UACS), acute bed rested subjects (ABRS) and rigorous bed rested subjects (RBRS). Acute bed rested subjects confined abruptly to RBR, while they did not have any prior knowledge of the exact date and time when they would be subjected to RBR. RBRS were submitted to RBR in a predetermined date and time known to them right from the start of the study. UACS were not subjected to any form of BR. Fluid loss, urinary and plasma sodium (Na+) and potassium (K+), plasma osmolality, whole blood hematocrit (Hct) and hemoglobin (Hb), and total plasma protein level increased significantly (p < 0.05), while urinary osmolality, extracellular volume (ECV), plasma volume (PV), red cell volume (RCV), blood volume (BV), interstitial volume (IV) and fluid consumption decreased significantly (p < 0.05) in ABRS and RBRS compared with their pre-BR values and their control (UACS). However, the measured variables changed significantly (p < 0.05) more and significantly faster in ABRS than RBRS. Conversely, whole blood Hct and Hb levels, fluid consumption and fluid loss, urinary and plasma osmolality, urinary and plasma electrolytes, plasma protein, ECV, PV, RCV, BV and IV levels were not change in UACS compared with their pre-BR values. Significantly greater and significantly faster intercompartmental, blood and urinary biochemical changes were observed in ABRS than RBRS. Body hydration was affected significantly more and significantly faster in ABR than RBR. It was concluded, the more abruptly normal activity is restricted the smaller the body hydration in bed rested subject is, and probably in patients who are abruptly confined to RBR.