The steady-state concept of Na(+) homeostasis, based on short-term investigations of responses to high salt intake, maintains that dietary Na(+) is rapidly eliminated into urine, thereby achieving constant total-body Na(+) and water content. We introduced the reverse experimental approach by fixing salt intake of men participating in space flight simulations at 12 g, 9 g, and 6 g/day for months and tested for the predicted constancy in urinary excretion and total-body Na(+) content. At constant salt intake, daily Na(+) excretion exhibited aldosterone-dependent, weekly (circaseptan) rhythms, resulting in periodic Na(+) storage. Changes in total-body Na(+) (±200-400 mmol) exhibited longer infradian rhythm periods (about monthly and longer period lengths) without parallel changes in body weight and extracellular water and were directly related to urinary aldosterone excretion and inversely to urinary cortisol, suggesting rhythmic hormonal control. Our findings define rhythmic Na(+) excretory and retention patterns independent of blood pressure or body water, which occur independent of salt intake.
Compared with age-matched men, women are resistant to the hypertensive effects of dietary NaCl; however, after menopause, the incidence of salt-sensitive hypertension is similar in women and men. We recently suggested that osmotically inactive Na+ storage contributes to the development of salt-sensitive hypertension. The connective tissues, including those immediately below the skin that may serve as a reservoir for osmotically inactive Na+ storage, are affected by menopause. We tested the hypothesis that ovariectomy (OVX) might reduce osmotically inactive Na+ storage capacity in the body, particularly in the skin. Male, female-fertile, and female OVX Sprague-Dawley (SD) rats were fed a high (8%)- or low (0.1%)-NaCl diet. The groups received the diet for 4 or 8 wk. At the end of the experiment, subgroups received 0.9% saline infusion and urinary Na+ and K+ excretion was measured. Wet and dry weight (DW), water content in the body and skin, total body Na+ (rTBNa+) and skin Na+ (rSKNa+) content were measured relative to DW by desiccation and dry ashing. There were no gender differences in osmotically inactive Na+ storage in SD rats. All SD rats accumulated Na+ if fed 8% NaCl, but rTBNa+ was lower in OVX rats than in fertile rats on a low (P < 0.001)- and a high (P < 0.05)-salt diet. OVX decreased rSKNa+ (P < 0.01) in the rats. A high-salt diet led to Na+ accumulation (DeltaSKNa+) in the skin in all SD rats. Osmotically inactive skin Na+ accumulation was approximately 66% of DeltaSKNa+ in female and 82% in male-fertile rats, but there was no osmotically inactive Na+ accumulation in OVX rats fed 8% NaCl. We conclude that skin is an osmotically inactive Na+ reservoir that accumulates Na+ when dietary NaCl is excessive. OVX leads to an acquired reduction of osmotically inactive Na+ storage in SD rats that predisposes the rats to volume excess despite a reduced Na+ content relative to body weight.
Accurately collected 24-hour urine collections are presumed to be valid for estimating salt intake in individuals. We performed two independent ultra-long-term salt balance studies lasting 105 (4 men) and 205 (6 men) days in 10 men simulating a flight to Mars. We controlled dietary intake of all constituents for months at salt intakes of 12, 9, and 6 grams per day and collected all urine. The subjects’ daily menus consisted of 27,279 individual servings, out of which 83.0% were completely consumed, 16.5% completely rejected, and 0.5% incompletely consumed. Urinary recovery of dietary salt was 92% of recorded intake, indicating long-term steady state sodium balance in both studies. Even at fixed salt intake, 24-hour sodium excretion (UNaV) showed infradian rhythmicity. We defined a ±25 mmol deviation from the average difference between recorded sodium intake and UNaV as the prediction interval to accurately classify a 3-gram difference in salt intake. Due to the biological variability in UNaV, only every-other daily urine sample correctly classified a 3-gram difference in salt intake (49%). By increasing the observations to three consecutive 24-hour collections and sodium intakes, classification accuracy improved to 75%. Collecting seven 24-hour urines and sodium intake samples improved classification accuracy to 92%. We conclude that single 24-hour urine collections at intakes ranging from 6–12 grams salt per day were not suitable to detect a 3-gram difference in individual salt intake. Repeated measurements of 24-hour UNaV improve precision. This knowledge could be relevant to patient care and the conduct of intervention trials.
Vibration exercise (VbX) is a new type of physical training to increase muscle power. The present study was designed to assess the influence of whole-body VbX on metabolic power. Specific oxygen uptake (sVO(2)) was assessed, testing the hypotheses that sVO(2) increases with the frequency of vibration (tested in 10 males) and with the amplitude (tested in 8 males), and that the VbX-related increase in sVO(2) is enhanced by increased muscle force (tested in 8 males). With a vibration amplitude of 5 mm, a linear increase in sVO(2) was found from frequencies 18 to 34 Hz (p < 0.01). Each vibration cycle evoked an oxygen consumption of approximately 2.5 micro l x kg(-1). At a vibration frequency of 26 Hz, sVO(2) increased more than proportionally with amplitudes from 2.5 to 7.5 mm. With an additional load of 40 % of the lean body mass attached to the waist, sVO(2) likewise increased significantly. A further increase was observed when the load was applied to the shoulders. The present findings indicate that metabolic power in whole-body VbX can be parametrically controlled by frequency and amplitude, and by application of additional loads. These results further substantiate the view that VbX enhances muscular metabolic power, and thus muscle activity.
Adaptive changes of major body systems in astronauts during spaceflight can be simulated by strict anti-orthostatic head-down tilt (HDT) bed rest (BR), a ground-based microgravity (microG) model that provides a meaningful opportunity to study atrophy mechanisms and possible countermeasures under controlled experimental conditions. As nitric oxide (NO) signaling is linked to muscle activity, we investigated altered expression of the three major isoforms of nitric oxide synthase (NOS 1-3) at cellular compartments during prolonged HDT BR without (control group) and with resistance exercise interventions (exercise group) using a flywheel ergometer (FWE). Atrophy detected in mixed (fast-slow) m. vastus lateralis (VL) and slow-type m. soleus (SOL) myofiber Types I and II (minus 35-40% of myofiber cross-sectional area) was prevented by FWE training. Concomitant to muscle atrophy, reduced NOS 1 protein and immunostaining was found in VL not in SOL biopsies. In trained VL, NOS 1 protein and immunostaining at myofibers II were significantly increased at the end of BR. Exercise altered NOS 2/caveolin 3 co-immunostaining patterns of subsarcolemmal focal accumulations in VL or SOL myofibers, which suggests reorganization of sarcolemmal microdomains. In trained VL, increased capillary-to-fiber (C/F) ratio and NOS 3 protein content were documented. Activity-linked NO signaling may be widespread in skeletal muscle cellular compartments that may be directly or indirectly impacted by adequate exercise countermeasure protocols to offset the negative effects induced by disuse, immobilization, or extended exposure to microgravity.
Recent evidence suggested that Na can be stored in an osmotically inactive form. We investigated whether osmotically inactive Na storage is reduced in a rat model of salt-sensitive (SS) hypertension. SS and salt-resistant (SR) Dahl-Rapp rats as well as Sprague-Dawley (SD) rats were fed a high (8%)-or low (0.1%)-NaCl diet for 4 wk (n ϭ 10/group). Mean arterial pressure (MAP) was measured at the end of the experiment. Wet and dry weights, water content, total body Na (TBS), and bone Na content were measured by dessication and dry ashing. MAP was higher in both Dahl strains than in SD rats. In SS rats, 8% NaCl led to Na accumulation, water retention, and hypertension due to impaired renal Na excretion. There was no dietary-induced Na retention in SR and SD rats. TBS was variable; nevertheless, TBS was significantly correlated with body water and MAP in all strains. However, the extent of Na-associated volume and MAP increases was strain specific. Osmotically inactive Na in SD rats was threefold higher than in SS and SR rats. Both SS and SR Dahl rat strains displayed reduced osmotically inactive Na storage capacity compared with SD controls. A predisposition to fluid accumulation and high blood pressure results from this alteration. Additional factors, including impaired renal Na excretion, probably contribute to hypertension in SS rats. Our results draw attention to the role of osmotically inactive Na storage. salt sensitive; bone sodium; Dahl rats THE RELATIONSHIP BETWEEN SALT intake and blood pressure has been extensively studied in humans and provides evidence that subpopulations of humans are sensitive to alterations in salt intake. A well-established animal model for salt-sensitive (SS) hypertension is the Dahl rat. SS rats develop hypertension when fed a high-NaCl diet (6). Salt-resistant (SR) Dahl rats developed increased blood pressure after they received a transplanted kidney from an SS donor animal. Conversely, transplantation of SR donor kidneys into SS rats lowers blood pressure (5, 10). Despite the fact that the glomerular filtration rate is not different between both strains (2, 14), SS rats have an impaired ability to excrete Na (1, 2). However, this feature does not fully explain the development of SS hypertension (11). Thus the role of Na retention in the development of hypertension is unclear.Recent studies on long-term Na balance in humans showed that high dietary Na consumption with Na retention does not necessarily lead to expansion of the extracellular volume (8). This finding suggests that Na might be stored in an osmotically inactive form. We studied the relationship between osmotically inactive Na storage, total body Na (TBS), total body water (TBW), and hypertension in Dahl SS rats and control animals. Our initial primary hypothesis was that Dahl SS rats exhibit a reduced capacity for osmotically inactive Na storage that would predispose these animals to volume retention and thus lead to SS hypertension. The secondary hypothesis was that osmotically inactive Na storage is also deficient in...
We investigated the changes in the cardiovascular system [resting blood pressure (BP) and heart rate (HR), measured by means of a 24-h ambulatory BP and a holter-electrocardiogram (ECG)], glycemic parameters, and lipid metabolism of subjects suffering from metabolic syndrome during a 3-week sojourn at 1,700 m in the Austrian Alps. A total of 22 male subjects with metabolic syndrome were selected. Baseline investigations were performed at Innsbruck (500 m above sea level). During the 3-week altitude stay the participants simulated a holiday with moderate sports activities. Examinations were performed on days 1, 4, 9, and 19. After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days and 6-7 weeks, respectively. The 24-h ambulatory BP and holter ECG revealed a decrease in average HR, BP, and rate pressure product (RPP: systolic blood pressure x HR) after 3 weeks of altitude exposure. In some patients, an increase in premature ventricular beats was observed at the end compared to the beginning of the exposure to moderate altitude. The ECG revealed no ischemic ST-segment changes. Maximal physical capacity as measured by symptom-limited maximal cycle ergometry tests remained unchanged during the study. Six weeks after the altitude exposure the blood pressure increased again and returned to pretest levels. The Homeostasis Model Assessment index, which is a measure of insulin resistance, decreased significantly and glucose concentrations obtained after an oral glucose tolerance test were significantly lower after the stay at altitude compared to the basal values. We conclude that after a 3-week exposure to moderate altitude, patients with metabolic syndrome (1) tolerated their sojourn without any physical problems, (2) exhibited short-term favorable effects on the cardiovascular system, and (3) had significant improvements in glycemic parameters that were paralleled by a significant increase in high-density-lipoprotein-cholesterol.
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