Hypokinetic Subjects Research Articles

Chronic head-down-tilt sleeping as physiological regulator of bone remodelling during diminished muscular activity in humans.

Head-down-tilt (HDT) sleeping with periodic fluid redistribution (PFR) assumes a significant importance by the possibility of regulating bone remodelling. We hypothesized that HDT sleeping with chronic PFR which expands fluid volume would contribute to and/or increase bone formation. Therefore, we studied the potential benefits of osteogenesis with HDT sleeping of chronic PFR during diminished muscular activity (hypokinesia; HK). Studies were conducted on 40 male healthy volunteers. They were divided into four groups: head-down-tilt sleeping control subjects (HDTSCS), head-down-tilt sleeping hypokinetic subjects (HDTSHS), active control subjects (ACS) and hypokinetic subjects (HKS). The iliac crest cancellous bone and trabecular bone volume and cortical thickness were measured during pre-experimental period of 390days and experimental period of 360days. Iliac crest cancellous bone and trabecular bone volume and cortical thickness were increased (P<0·05) in the HDTSHS group compared to the HKS group. Iliac crest cancellous bone volume, cortical thickness and trabecular bone volume were reduced (P<0·05) in the HKS group compared to their pre-experimental values and the level in the other groups. In the HDTSCS group, iliac crest cancellous bone volume, cortical thickness and trabecular bone volume were increased much less than in the HDTSHS group. Bone mineral density was not affected in the ACS group compared to their pre-experimental values. The current study shows the impact of chronic HDT sleeping with PFR on increases formation of bone demonstrating osteogenesis of bone during diminished muscular activity.

Increased muscle potassium from head down tilt sleeping of healthy subjects during diminished muscular activity

Background and Aim: Periodic fluid redistribution (PFR) with head down tilt (HDT) sleeping produces less fluid loss and more fluid volume. We hypothesized that chronic PFR with HDT sleeping would contribute to and improve electrolyte regulation. Therefore, we studied the potential of regulation of muscle potassium (K + ) and K + losses with chronic PFR of HDT sleeping during diminished muscular activity (hypokinesia). Methods: Studies were conducted on 40 male healthy volunteers. They were equally divided into four groups: Active control subjects (ACS), hypokinetic subjects (HKS), HDT sleeping control subjects (HDTSCS), and HDT sleeping hypokinetic subjects (HDTSHS). Results: Muscle K + increased ( P + and K + losses decreased ( P + reduced ( P + and K + losses increased ( P + , plasma K + , and K + losses were affected much less than in the HDTSHS group. Muscle K + , plasma K + , and K + losses did not change in the ACS group compared to their preexperimental values. Conclusion: The current study shows that muscle K + muscular increases and K + losses decrease with chronic PFR of HDT sleeping suggesting regulation of K + deposition during diminished activity.

Sodium regulation with periodic fluid redistribution during diminished muscular activity in healthy subjects

Background and Aim: Mineral loss is an established reaction to diminished muscular activity (Hypokinesia; HK). It has been assumed that periodic fluid redistribution (PFR) contributes to vascular volume. Fluid volume expansion could affect electrolyte metabolism. We hypothesized that chronic PFR may contribute to or improve electrolyte regulation during diminished activity. Therefore, we studied the potential benefits of sodium (Na + ) regulation with chronic PFR during HK. Methods: The study was conducted on 40 male subjects for the duration of 390-days preexperimental period and a 364-days experimental period. They were equally divided into four-groups: Active control subjects (ACS), hypokinetic subjects (HKS), periodic fluid redistribution control subjects (PFRCS), and periodic fluid redistribution hypokinetic subjects (PFRHS). Results: Muscle Na + increased ( P + and Na + losses decreased ( P + decreased ( P + and Na + losses increased ( P + , plasma Na + and Na + losses were benefited much less in the PFRCS group than in the PFRHS group. Muscle Na + , plasma Na + and Na + losses were not affected in the ACS group compared with their preexperimental values. Conclusion: The current study shows that muscle Na + increases and Na + losses decreases with chronic PFR suggesting the potential benefits of Na + regulation during diminished activity.

Age-related androgen deficiency and erectile dysfunction in men of the reproductive age presenting with type 2 diabetes mellitus

Aim of the study. To detect hypogonadism and elucidate its relationship with erectile dysfunction (ED) and the main risk factors of cardiovascular diseases (CVD) among the patients with type 2 diabetes mellitus (DM2). Materials and methods. This clinical epidemiological study included 261 men with DM2 at the age varying from 30 to 59 years. The following exclusion criteria were used: type 1 diabetes mellitus, primary hypogonadism, drug-induced and congenital diseases accompanied by hypogonadism, oncological and cardiovascular diseases. All the patients underwent routine clinical examination, questionnaire and instrumental studies, laboratory analysis including assays for sex hormones. Results. Hypogonadism was diagnosed based on the results of all above studies in 114 (43.7%) men presenting with type 2 diabetes mellitus whereas the AMS questionnaire revealed a 10% higher incidence of age-related hypogonadism (in 141 or 54% subjects). It means that the incidence of hypogonadism increases with age both among the patients with DM2 and in the general male population. For example, only 17.5% of the men at the age of 30-39 years suffered hypogonadism compared with thrice this frequency in the groups of 40-49 and 50-59 year-old subjects. The summarized international erectile function index (IEFI) in the patients with hypogonadism and DM2 was 14.2±0.5 compared with 19.0±0.9 in the group without hypogonadism (p&lt;0.001). Erectile dysfunction was diagnosed in 42 (28.6%) of the 147 patients with DM2 in the absence of hypogonadism whereas all the patients with hypogonadism suffered ED. The groups of the patients presenting with DM2 and hypogonadism and with DM2 without hypogonadism were not significantly different in terms of the number of smokers and hypokinetic subjects (roughly 70%). A similar tendency was documented in the occurrence of such parameters as waist circumference and serum triglycerides levels whereas the total and LDLP cholesterol levels, arterial pressure and body mass index were significantly higher in the patients with hypogonadism. Conclusion. Almost each second man with type 2 diabetes mellitus suffers hypogonadism and the number of such patients increases with age. The presence of DM2 increases the risk of development of ED. Also, the probability of ED and its severity increase under effect of androgen deficiency. The combination of DM2 and hypogonadism promotes manifestation of the main risk factors of cardiovascular diseases.

Chronic periodic fluid redistribution effect on muscle calcium in healthy subjects during prolonged hypokinesia

Studies have shown that chronic periodic fluid shifting upwards is not sensed as excessive fluid volume and excretion mechanisms are not activated. To determine if chronic periodic fluid and volume shifting upwards can affect muscle calcium (Ca(2+)) during hypokinesia (HK) we measured muscle Ca(2+) content, plasma Ca(2+) concentration, and Ca(2+) losses in urine and feces. Studies were conducted on 40 healthy male volunteers. They were divided into four equal groups: active control subjects (ACS), hypokinetic subjects (HKS), periodic fluid redistribution control subjects (PFRCS), and periodic fluid redistribution hypokinetic subjects (PFRHS). Plasma Ca(2+) level decreased (p < 0.05) in Ca(2+) repleted muscle, muscle Ca(2+) level increased (p < 0.05), and Ca(2+) losses in urine and feces decreased (p < 0.05) in the PFRHS group compared with the HKS group. Plasma Ca(2+) level increased (p < 0.05) in Ca(2+) deficient muscle, muscle Ca(2+) level decreased (p < 0.05), and Ca(2+) losses in urine and feces increased (p < 0.05) in the HKS group compared with their pre-experimental levels and the values in their respective control groups (ACS and PFRCS). This study shows that the muscle Ca(2+) content increases and Ca(2+) excretion decreases, suggesting the clinical potential of chronic periodic fluid and volume redistribution in treatment of muscle Ca(2+) deficiency.

The impact of physical exercise on calcium balance in healthy subjects during prolonged hypokinesia

Objective To determine whether during hypokinesia (diminished movement) periodic physical exercise affects calcium (Ca 2+) balance and Ca 2+ loss. Methods Studies were conducted on 30 physically healthy male volunteers during the preexperimental period of 30 days and the experimental period of 364 days. They were equally divided into three groups: active control subjects (ACS), hypokinetic subjects (HKS), and periodic training subjects (PTS). The ACS group ran an average distance of 9.3 ± 1.2 km/d; the HKS group walked an average distance of 1.3 ± 0.2 km/d; and PTS group walked and ran average distances of 1.3 ± 0.2 km/d and 9.2 ± 1.2 km/d for 5 and 2 days per week, respectively. Results Serum Ca 2+ level, fecal and urine Ca 2+ loss, and Ca 2+ imbalance increased ( P < 0.05) in the PTS and HKS groups compared with their preexperimental levels and the values in their respective ACS group. The serum Ca 2+ concentration, urine and fecal Ca 2+ loss, and Ca 2+ imbalance increased more ( P < 0.05) in the PTS group than in the HKS group. Conclusion During hypokinesia, Ca 2+ imbalance is more evident with than without physical exercise and Ca 2+ loss is exacerbated more with higher than lower Ca 2+ imbalance.

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.

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

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. 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. 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. 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.

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

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. 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 +/- 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. 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. 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.

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.

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.

Copper absorption during and after hypokinesia in copper supplemented and unsupplemented healthy subjects

Measuring copper (Cu) absorption, and serum, urinary and fecal Cu levels during and after hypokinesia (HK) and Cu supplementation, the aim of this study was to determine whether Cu deposition could be depressed significantly more with or without Cu supplementation. Studies were conducted during 30 days pre-HK, 364 days HK and 30-days post-HK. A total of 40 male healthy volunteers 24.7 ± 4.8 years of age were chosen as subjects. They were divided into four groups: unsupplemented active control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented active control subjects (SACS), and supplemented hypokinetic subjects (SHKS). Hypokinetic subjects were limited to an average walking distances of 0.5 ± 0.1 km · day −1for 364 days. Active control subjects were running average distances of 5.3 ± 1.2 km · day −1 for 364 days. All SHKS and SACS consume daily 54.02 μmol copper sulfate (CuSO 4). Copper absorption, serum Cu level, and urinary and fecal Cu excretion did not change in SACS and UACS compared with their pre-HK values. During HK, Cu absorption decreased significantly ( P < 0.05) with time, whereas serum Cu level, urinary and fecal Cu excretion increased significantly ( P < 0.05) with time in UHKS and SHKS compared with their pre-HK values and their respective active controls (SACS and UACS). During the post-HK period, Cu absorption increased significantly ( P < 0.05), whereas serum Cu level and urinary and fecal Cu losses decreased significantly ( P < 0.05) in hypokinetic subjects compared with their pre-HK and control values, and by day 30 approached the control values. However, during HK and post-HK respectively, Cu absorption decreased significantly ( P < 0.05) and serum Cu level as well as urinary and fecal Cu losses increased significantly ( P < 0.05) and Cu absorption increased significantly ( P < 0.05) and serum Cu level and Cu excretion decreased significantly ( P < 0.05) more in SHKS than UHKS. Decreased Cu absorption with Cu depletion during HK showed decreased Cu deposition. Increased Cu absorption during the post-HK period demonstrated Cu depletion. The greater Cu changes in SHKS than UHKS, during HK and post-HK, showed that Cu deposition decreased more with than without Cu supplementation. We conclude that dissociation between Cu absorption and Cu depletion showed decreased Cu deposition as the main reason for Cu depletion during 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.

Calcium absorption measurements in normal subjects in determining calcium deposition during prolonged hypokinesia and with and without calcium loading

Measuring calcium (Ca) absorption, Ca balance and Ca level in serum,feces and urine during HK (hypokinesia) with and without Ca loading, the aim of this study was to disclose if prolonged HK could reduce Ca deposition more with or without Ca load contributing to greater Ca imbalance. Studies were conducted during 30-days pre-HK and 364-days HK. Forty male normal volunteers 23.7+/-6.0 years of age were chosen as subjects. They were divided into four groups: unloaded active control subjects (UACS), unloaded hypokinetic subjects (UHKS), loaded active control subjects (LACS), loaded hypokinetic subjects (LHKS). All hypokinetic subjects were walking average distances of 0.5+/-0.2 km day(-1), and active control subjects were running average distances of 6.6+/-1.2 km day(-1). LACS and LHKS were loaded with 1.3 mmol calcium lactate/kg body wt. Before Ca load, fecal Ca loss, urinary Ca and phosphate (P) losses, Ca imbalance, serum ionized calcium (CaI), P and total Ca (Ca(t)) levels increased significantly. (P < 0.05) with time, and serum intact parathyroid hormone (iPTH), 1.25 dihydroxyvitamin D (1.25(OH)2D3) levels and Ca absorption, decreased significantly (P < 0.05) with time in LHKS and UHKS compared with their pre-HK values and their respective active controls (LACS and UACS). After Ca load, however, Ca absorption, serum iPTH and 1.25 (OH)2D3 levels decreased significantly (P < 0.05) more with time, while fecal Ca loss, urinary Ca and P excretion and Ca imbalance increased significantly (P < 0.05) more with time in LHKS than UHKS. Conversely, before and after Ca load, fecal Ca excretion, urinary P and Ca loss, serum CaI, P, Ca, iPTH and 1.25 (OH)2D3 levels, Ca absorption and Ca balance did not change in LACS and UACS compared with their pre-HK values. The greater Ca losses with than without Ca load have shown that the more Ca is consumed the more Ca is eliminated during HK and Ca imbalance. The significant increase of Ca loss with Ca imbalance demonstrated reduced Ca deposition. Dissociation between Ca loss and Ca imbalance demonstrated reduced Ca deposition as the mechanism of Ca imbalance development during HK.

Zinc measurements during hypokinesia and zinc supplementation in determining zinc retention during hypokinesia in normal subjects

Measuring zinc (Zn) retention, Zn balance, serum, fecal and urinary Zn levels with and without Zn supplementation, the aim of this study was to show if hypokinesia (HK) could contribute to the smaller Zn retention and consequently to the development of Zn imbalance. Studies were conducted during 30 days pre-HK and 364 days HK. Forty male normal individuals 23. 8 ± 5.0 years of age were chosen as subjects. They 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). All SHKS and UHKS were walking average distances of 0.5 km.day-l, while SACS and UACS were running average distances of 9.1 km.day-l. All SHKS and SACS consume daily 30 mg Zn. Zinc retention decreased significantly (p < 0.05) with time, while Zn imbalance, serum Zn level, fecal and urinary Zn excretion increased significantly (p < 0.05) with time in SHKS and UHKS compared with their pre-HK values and the levels in their respective active controls (SACS and UACS). However, Zn retention decreased significantly (p < 0.05) more with time, while Zn imbalance, and Zn levels in serum, feces and urine increased significantly (p < 0.05) more with time in SHKS than UHKS. Conversely, Zn retention, Zn balance, serum Zn level, urinary and fecal Zn excretion did not change in SACS and UACS compared with their pre-HK control values. Significant increase of Zn losses with Zn imbalance and Zn supplementation may demonstrate decreased Zn retention. Significantly higher Zn loss in SHKS than UHKS may demonstrate that Zn is wasted more with than without Zn supplementation. It was concluded that dissociation between Zn loss from the body and Zn imbalance may demonstrate the presence of decreased Zn retention as the mechanism of development of Zn depletion during prolonged HK.

Fluid balance measurements in disclosing fluid deposition during prolonged hypokinesia in healthy subjects.

Measuring fluid absorption and fluid homeostasis, the aim of this study was to establish if hypokinesia (HK) could depress fluid deposition and thus contribute to the development of fluid depletion. Studies were performed during 30 days pre-HK period and during 364 days HK period. Twenty healthy male individuals 24.0 +/- 6.6 years of age were chosen as subjects. They were equally divided into two groups: active control subjects (ACS) and hypokinetic subjects (HKS). All HKS were walking average distances of 0.7 +/- 0.2 km x day(-1) for 364 days, while all ACS were running average distances of 8.5 +/- 1.2 km x day(-1) for 364 days. Water imbalance, whole blood hemoglobin (Hb) and hematocrit (Hct), plasma protein, plasma osmolality, urinary and plasma sodium (Na+) and potassium (K+) levels and fluid loss increased significantly (p < 0.05), while fluid absorption, fluid consumption, glomerular filtration rate (GFR), and renal blood flow (RBF) reduced significantly (p < 0.05) in HKS compared with their pre-HK values and their respective active controls (ACS). Conversely, water balance, whole blood Hb and Hct, plasma protein, plasma osmolality, fluid absorption, GFR, RBF, urinary and plasma Na+ and K+ levels, fluid consumption and fluid loss did not change in ACS compared with their pre-HK control values. Significant increase of fluid loss with fluid imbalance may demonstrate decreased fluid deposition. Dissociation between fluid loss and fluid imbalance may demonstrate decreased fluid deposition as the mechanism of development of fluid depletion. It was concluded that fluid imbalance and the significant increase of Hb, Hct, plasma protein, plasma osmolality, urinary and plasma Na+ and K+ levels may demonstrate the presence of fluid depletion during prolonged HK in humans.

Phosphate Deposition Capacity of Athletes During Hypokinesia, Phosphate Loading, and Ambulation

Hypokinesia (diminished movement) induces significant phosphate (P) excretion; however, little is known about the P deposition ability of the body during hypokinesia (HK). Using P loads, the aim of this study was to establish the deposition ability of the body to retain P during prolonged HK. Studies were done during a 30-d period of pre-HK and a 364-d period of HK. Forty male trained athletes aged 24.7 +/- 8.0 yr were chosen as subjects. They were equally divided into four groups: unloaded ambulatory control subjects (UACS), unloaded hypokinetic subjects (UHKS), loaded ambulatory control subjects (LACS), and loaded hypokinetic subjects (LHKS). All hypokinetic subjects were limited to an average walking distance of 0.7 km/d. Loading tests with 85.0 mg of calcium phosphate/kg body weight were performed on the LACS and LHKS. Fecal P loss, urinary calcium (Ca) and P loss, serum P, Ca, and the ionized calcium (CaI) levels increased significantly (p < or = 0.05) in the LHKS and UHKS groups when compared with the LACS and UACS groups, respectively. Serum intact parathyroid hormone (iPTH) and the 1,25-dihydroxyvitamin D3 [1,25-(OH)2 D3] levels decreased significantly (p < or = 0.05) in the LHKS and UHKS groups when compared with the LACS and UACS groups, respectively. After the P load, significant (p < or = 0.05) differences were observed between LHKS and UHKS groups regarding serum, urinary, and fecal P changes. Thus, the deposition capacity of P decreased significantly (p < or = 0.05) more in the LHKS group than in the UHKS group. The deposition of P, fecal P, urinary P and Ca, serum CaI, P, Ca, 1,25-(OH)2 D3, and iPTH changed insignificantly (p > 0.05) in control groups when compared with their baseline values. It was shown that after the P load, significant differences were observed between the loaded and unloaded hypokinetic subjects regarding serum, urinary, and fecal P values and P retention. The oral P load intensified P loss from the body. It was concluded that the higher the P intake increased the greater P loss and the lower P deposition and thus the less likely it is for the P load to benefit hypokinetic subjects.

Effect of fluid and salt supplementation on body hydration of athletes during prolonged hypokinesia

Body hydration decreases significantly during hypokinesia (HK) (diminished movement), but little is known about the effect of fluid and salt supplements (FSS) on body hydration during HK. The aim of this study was to measure the effect of FSS on body hydration during HK. Studies were done during 30 days pre HK period and 364 days HK period. Thirty male athletes aged 24.5±6.6 yr were chosen as subjects. They were equally divided into three groups: unsupplemented ambulatory control subjects (UACS), unsupplemented hypokinetic subjects (UHKS) and supplemented hypokinetic subjects (SHKS). Hypokinetic subjects were limited to an average walking distance of 0.7 km day −1 . The SHKS group took daily 30 ml of water/kg body weight and 0.1 g of sodium chloride (NaCl)/kg body weight. Control subjects experienced no changes in their professional training and routine daily activities. Plasma volume (PV), urinary and plasma sodium (Na) and potassium (K), plasma osmolality, plasma protein, whole blood hemoglobin (Hb) and hematocrit (Hct), plasma renin activity (PRA) plasma aldosterone (PA) levels, physical characteristics, food and fluid intakes were measured. Plasma osmolality, plasma protein, urinary and plasma Na and K, whole blood Hct and Hb, PRA and PA levels decreased significantly ( p⩽0.01), while PV and body weight increased significantly ( p⩽0.01) in the SHKS group when compared with the UHKS group and did not change when compared with the UACS group. Plasma osmolality, plasma protein, urinary and plasma Na and K, PRA and PA, whole blood Hb and Hct levels increased significantly ( p⩽0.01), while PV body weight, food and fluid intakes decreased significantly ( p⩽0.01) in UHKS group when compared with the SHKS and UACS groups. The measured parameters did not change in the UACS group when compared with their baseline control values. It was shown that during HK body hydration decreased significantly, while during HK and FSS body hydration increased significantly. It was concluded that daily intake of FSS prevents the decrease of PV and blunts the increase of activity of the PRA and PA during prolonged HK.

Measurements in Potassium-Supplemented Athletes During and After Hypokinetic and Ambulatory Conditions

Hypokinesia (diminished movement) induces significant potassium (K) changes; however, little is known about K deposition and deficiency during hypokinesia (HK). Using K supplements during and after HK, the aim was to establish body K deposition and K deficiency during HK. Studies were done during the pre-HK period of 30 d, HK period of 364 d, and post-HK period of 30 d. Forty male trained athletes aged 24.9 +/- 8.0 y were chosen as subjects. They 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). Hypokinetic subjects were limited to an average walking distance of 0.7 km/d. Control subjects ran an average distance of 11.6 km/d. The SHKS and SACS groups took 95.0 mg elemental K/kg body weight daily. Fecal K excretion, urinary sodium (Na) and K excretion, plasma K and Na levels, plasma renin activity (PRA), plasma aldosterone (PA), food and fluid intake, and physical characteristics were measured. During HK, fecal K loss, urinary K and Na loss, and plasma K, Na, PRA, and PA levels increased significantly (p < or = 0.05), whereas during the initial days of post-HK, the levels of the measured parameters decreased significantly (p < or = 0.05) in the SHKS and UHKS groups as compared with the SACS and UACS groups, respectively. During HK, body weight, body fat, peak oxygen uptake, food and fluid intake decreased significantly (p < or = 0.05), whereas during the initial days of post-HK period remained significantly (p < or = 0.05) depressed and fluid intake increased in SHKS and UHKS groups when compared with the SACS and UACS groups, respectively. However, during HK and post-HK plasma, urinary, and fecal K changed significantly (p < or = 0.05) more in the SHKS group than in the UHKS group. The deposition of K was significantly (p < or = 0.05) lower and K deficiency much higher in the SHKS group than in the UHKS group. Fecal K loss, urinary K and Na loss, plasma K, Na, PRA, and PA levels, body weight, body fat, peak oxygen uptake, and food and fluid intake did not change significantly in the SACS and UACS when compared with their baseline control values. It was shown that plasma K concentration and urinary and fecal K excretion increased during HK and decreased significantly (p < or = 0.05) during post-HK. Oral K supplements did not influence plasma or fecal and urinary K either during HK or post-HK. It was concluded that the low plasma K level and fecal and urinary K loss during post-HK may indicate the presence of K deficiency, and increased K in plasma, urine, and feces during HK and in the presence of K deficiency may suggest the body's inability to retain K during HK.

Phosphate Determination During Hypokinesia and Ambulation in Establishing Phosphate Changes in Trained and Untrained Subjects

Hypokinesia (diminished movement) induces phosphate (P) changes; however, it is not known if P change is greater in trained than untrained subjects. Measuring P balance and P retention during hypokinesia (HK) and P load, we studied if changes in P retention and P depletion were significantly (p<0.05) greater in trained than untrained subjects. Studies were done during a 30-d pre-HK period and a 364-d HK period. Forty male trained and untrained healthy individuals aged 24.5+/-5.4 yr were chosen as subjects. All volunteers were equally divided into four groups: trained ambulatory control subjects (TACS), trained hypokinetic subjects (THKS), untrained ambulatory control subjects (UACS), and untrained hypokinetic subjects (UHKS). All THKS and UHKS were limited to an average walking distance of 0.3 km/d, and TACS and UACS were on an average running distance of 9.8 and 1.8 km/d, respectively. Subjects took daily 12.7-mmol dicalcium-phosphate/kg body weight in the form of supplementation. Negative P balance, fecal P loss, urinary P and calcium (Ca) excretion, serum P, and total Ca (Cat) levels increased significantly (p<0.05), whereas P retention, serum 1,25-dihydroxyvitamin D [1,25 (OH)2D3] and intact parathyroid hormone (iPTH) level decreased significantly (p<0.05) in THKS and UHKS when compared with their pre-HK values and their respective ambulatory controls (TACS and UACS). However, P retention, P balance, serum, urinary, and fecal P, and serum hormone level changed significantly (p<0.05) more in THKS than UHKS. Retention of P, fecal P, urinary P and Ca loss, serum P and Cat level, P balance, 1,25(OH)2D3, and iPTH level change insignificantly (p>0.05) in TACS and UACS when compared with their pre-HK control values. It was concluded that significant negative P balance may indicate P depletion, whereas significant P loss in spite of negative P balance and P load may suggest P retention incapacity; however, P depletion was greater in THKS than UHKS. Clearly, P is wasted much more in THKS than UHKS.