Acute effects of an oral calcium load on markers of bone metabolism during endurance cycling exercise in male athletes.

Although sport and physical activity are generally considered as positive factors for bone metabolism some endurance trainings such as running and bicycling have few or no beneficial or even deleterious effects on bone mineral density. The present study was designed to investigate the acute effect of an intensive endurance cycling exercise on biochemical bone markers. Furthermore, the effect of the oral intake of 1 g calcium load, by drinking high-calcium mineral water, just prior to and during the exercise was checked. Twelve well-trained elite male triathletes aged 23-37 years were explored. The serum concentrations of calcium, phosphate, PTH, bone alkaline phosphatase (BALP) and C-terminal cross-linking telopeptide of type 1 collagen (CTX) were measured before, during and after a 60 min 80% VO2max cycle ergometer exercise. Since cycling exercise was accompanied by a reduction in plasma volume the total amount of biochemical bone markers was calculated. When the exercise was performed without calcium load both serum concentrations and total amount of CTX began to increase progressively 30 min after the start of the exercise and were still significantly elevated, by 45-50%, 2h after the end of the exercise. Ingestion of high-calcium mineral water completely suppressed the CTX response. By contrast serum concentrations and total amount of BALP fluctuated and showed no significant difference with or without calcium load. The present study demonstrates that the burst of osteoclastic activity acutely induced by an endurance cycling exercise can be suppressed by the previous intake of a calcium load afforded by drinking high-calcium mineral water.

Mineral water as a source of dietary calcium: acute effects on parathyroid function and bone resorption in young men.

BACKGROUND: Calcium is a major component of mineralized tissues and is required for normal growth and maintenance of bone. Epidemiologic studies showed that a large percentage of the population fails to meet the currently recommended guidelines for optimal calcium intake. OBJECTIVE: The present study was designed to determine whether high-calcium mineral water is an efficient additional source of dietary calcium. DESIGN: Twelve healthy young men (mean +/- SD age: 21.1 +/- 1.2 y) ingested in a randomized order either 0.5 L of a mineral water containing 344 mg Ca/L or 0.5 L of a mineral water with a very low concentration of calcium (<10 mg/L) as a control. Blood samples were drawn before and 1, 2, 3, and 4 h after intake of the water. Urine was collected for 2 h before and every 2 h for 4 h after ingestion of the water. Serum concentrations of intact parathyroid hormone (iPTH) and serum concentrations and urinary excretion of a recently developed biochemical marker of bone resorption, type 1 collagen cross-linked C-telopeptide (CTx), were measured. RESULTS: Serum iPTH was significantly (P < 0.002) lower after ingestion of high-calcium water than after ingestion of the control. There was a significant (P = 0.01) progressive decrease in urinary CTx after ingestion of the high-calcium water, whereas after ingestion of low-calcium water the changes were modest and not significant. The fall in serum CTx concentrations was 34.7% 3 h after ingestion of high-calcium water, compared with 17.6% with the control. The decreases in serum CTx concentrations were significantly (P < 0.05) lower 1, 2, 3, and 4 h after ingestion of high-calcium water than after ingestion of the control. CONCLUSION: The present study showed that one oral intake of water containing a very moderate dose of calcium (172 mg) acutely inhibited iPTH secretion and bone resorption.

Bone assessment in patients with ileal pouch-anal anastomosis for inflammatory bowel disease.

BACKGROUND: Patients with ulcerative colitis are at risk of low bone mineral density (BMD). Proctocolectomy with ileal pouch-anal anastomosis (IPAA) for ulcerative colitis diminishes the risk of bone disease. The aims of this study were to assess the mechanism of low BMD and to measure bone density changes after IPAA. METHODS: Twenty patients with IPAA for ulcerative colitis, of mean(s.d.) age 38(9) (range 21-58) years, had measurements of lumbar spine and femoral neck BMD by dual energy X-ray absorptiometry, a mean(s.d.) 28(23) (range 3-84) months after proctocolectomy. Serum levels of calcium, phosphate, parathyroid hormone, osteocalcin and 25-hydroxy vitamin D were determined. Fifteen patients were followed for 28(12) (range 8-50) months. RESULTS: At baseline, six patients had spine BMD more than two standard deviations below the normal value, and three had vertebral crush fractures. Mean vitamin D values were normal and no patient had osteomalacia. BMD increased with time elapsed since IPAA (spine: r = 0.71, P = 0.005). During follow-up, mean(s.d.) changes in bone density were +2.3(3.8) and +2.1(5.6) per cent per year at the spine and femoral neck respectively. CONCLUSION: These results suggest that in patients with IPAA for ulcerative colitis, low BMD is not associated with vitamin D malabsorption and may be reversible after surgery.

Bone loss in patients with inflammatory bowel disease: a prospective study.

To assess the rate of bone loss in patients with inflammatory bowel disease, we prospectively studied 35 patients (17 women) aged 36 +/- 13 (range 17-60) years, 14 of whom had Crohn's disease and 21 with ulcerative colitis (including 12 with ileoanal anastomosis). Bone mineral density was measured by dual-energy X-ray absorptiometry at the lumbar spine and femoral neck. The follow-up was 19 +/- 8 months. During this period, 14 patients received oral steroids. Lumbar bone density changes expressed as a percentage per year were -3.1 +/- 4.9%, -6.4 +/- 7.5% and +2.0 +/- 4.0% in Crohn's disease and ulcerative colitis without and with ileoanal anastomosis respectively (p = 0.007). The same pattern was observed at the femoral neck. Mean annual lumbar bone density changes were -6.2 +/- 7.0% and +0.9 +/- 3.9% in patients with and without steroids during follow-up (p = 0.002). We conclude that patients with inflammatory bowel disease are at risk of lumbar and femoral bone loss. However, bone loss is not observed in patients with ileoanal anastomosis.

Metabolic bone assessment in patients with inflammatory bowel disease.

BACKGROUND/AIMS: Patients with inflammatory bowel disease are at risk for osteopenia. To study the metabolic bone status of these patients, a cross-sectional study was conducted. METHODS: Eighty-four patients (49 women, 35 men) with inflammatory bowel disease, 34 of whom had Crohn's disease and 50 ulcerative colitis (including 18 with prior coloproctectomy and ileoanal anastomosis), underwent clinical, dietary, and spine radiological assessments. Bone metabolism was assessed by measuring serum levels of calcium, phosphate, parathyroid hormone (1-84), 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and osteocalcin. Lumbar and femoral neck bone mineral densities were measured by dual energy X-ray absorptiometry. RESULTS: Serum osteocalcin level was decreased in 29 patients (34%), 12 of whom had never undergone steroid therapy. The other biochemical markers of bone metabolism were in the normal range. Thirty-six patients (43%) had osteopenia, and 6 patients (7%) had vertebral crush fractures. Osteopenia was observed in 27 patients (52%) and 9 patients (28%) with and without corticosteroid therapy, respectively. No patient had clinical or biological signs of osteomalacia. Analysis of bone density (lumbar Z score) by a multiple regression analysis showed a statistically significant correlation with age, cumulative corticosteroid doses, sedimentation rate, and osteocalcin level (R2 = 0.76; P = 0.05). CONCLUSIONS: The results suggest that bone turnover in inflammatory bowel disease is characterized by low bone formation in the presence of normal levels of calcium-regulating hormones.

Biologic, histologic and densitometric effects of oral risedronate on bone in patients with multiple myeloma.

Recent studies have shown that treatment with bisphosphonates could be effective against the myelomatous skeletal deterioration. However, the mechanisms of action of these drugs in multiple myeloma (MM) have been poorly studied. In the present study, 11 patients with MM and bone lesions were treated orally with 30 mg/day of risedronate for 6 months, and monitored for 6 additional months. Mean serum calcium decreased from day 4, with a concomitant increase in circulating levels of PTH (1-84) and 1,25-(OH)2D. These parameters reached their nadir on day 7 and returned to baseline value during the treatment period. Markers of bone resorption, pyridinoline and deoxypyridinoline decreased from day 7; they were at 50% and 78% of their basal value at the end of treatment and follow-up periods, respectively. A significant reduction of estimates of bone formation (serum alkaline phosphatase and osteoclacin) appeared at month 3 and persisted for the remainder of the 9-month period. Histomorphometric analysis showed a significant reduction of activation frequency, number of osteoclasts and erosion depth. Bone turnover was high at baseline, and normal after treatment, without mineralisation defects. Mean wall thickness was not different before and after treatment. Spinal bone mineral density measured by dual energy X-ray absorptiometry increased (5.3%) at the end of treatment. We conclude that oral risedronate in multiple myeloma induces a noticeable and rapid inhibition of bone resorption.

Comparison of the suppressive effect of two doses (500 mg vs 1500 mg) of oral calcium on parathyroid hormone secretion and on urinary cyclic AMP.

The respective effects of the ingestion of two different doses of calcium (500 and 1500 mg) on serum ionized calcium, intact parathyroid hormone (PTH 1-84), and the urinary excretion of 3',5'-cyclic adenosine monophosphate (cyclic AMP) were evaluated in 15 young male adults. Ionized serum calcium and PTH 1-84 were measured before and 1 hour, 2 hours and 3 hours (P1, P2, and P3) after the oral intake of calcium. Cyclic AMP was measured in 2-hour urine samples collected before and during 4 hours after the ingestion of calcium. Similar increments in serum ionized calcium (delta Ca2+) were observed except at P3 where the delta Ca2+ was significantly (P < 0.02) higher after 1500 mg (0.088 mmol/liter) than after 500 mg of (0.062 mmol/liter). In the same way, the comparison of the PTH 1-84 concentrations showed no statistical difference except at P3 (P < 0.002). When expressed as a percentage of P0, the P1 and P2 PTH 1-84 values were more suppressed after 1500 mg than after 500 mg of calcium (P1: -69% vs -59%; P < 0.02; P2: -66% vs -50%; P < 0.02). However, the simultaneous cyclic AMP responses (-24% vs -19%) were not significantly different. The results show that the respective maximal effects on PTH secretion and on urinary cyclic AMP of two very different oral doses of calcium are only slightly different.

Modification by phosphate of PTH-dependent renal cyclic AMP response.

The PTH response and the renal cAMP response obtained after oral administration of either tricalcium phosphate or calcium gluconolactate were compared in 12 young adult males. Each subject was studied during a control period of two hours before and during an experimental period of four hours after ingestion of a single oral dose of calcium salt. The respective dosages (1.2 g of calcium plus 0.6 g phosphorus for tricalcium phosphate; 0.5 g of calcium for gluconolactate calcium) were chosen to provide similar significant (p = 0.0001) increases in serum ionized calcium (from 1.23 to 1.29 mmol/l vs from 1.23 to 1.28 mmol/l). After tricalcium phosphate a modest (10%) but significant (p < 0.001) rise in serum phosphate was observed. In both series of experiments similar inhibitory effects on PTH circulating levels were obtained (from 22.6 to 12.4 pg/ml after tricalcium phosphate and from 24.1 to 10.6 pg/ml after calcium gluconolactate). After ingestion of calcium gluconolactate the renal secretion of cAMP fell from 12.68 to 8.64 nmol/l GF (p < 0.001), whereas no significant alterations of the mean values of nephrogenous cAMP were detected after ingestion of tricalcium phosphate. In accordance with the role of cAMP as a second messenger, after calcium gluconolactate we obtained a significant increase in tubular maximal reabsorption of phosphate (p < 0.0001) contrasting with the absence of significant effect after tricalcium phosphate. The present results confirm that suppression of PTH secretion only depends on the rise of serum ionized calcium and suggest that additional phosphate administration could have a decoupling effect between PTH and renal cAMP secretion.

[Laparoscopic surgery versus laparotomy. Comparative analysis of stress markers]. / Coelio-chirurgie comparée à la laparotomie. Analyse comparative des marqueurs du stress.

The place of laparoscopic surgery continues to increase in the field of surgery in our specialty. Although the advantages would seem to be obvious, it seemed to us interesting to quantify, if possible, the parameters of operative stress and compare laparoscopic surgery with conventional surgery. Markers studied are Prolactin, Cortisol, Adrenaline, Nor-Adrenaline, Dopamine and the Beta-Endorphins. The only marker that shows any difference in the two procedures in our study is Beta-Endorphin which is significantly less raised in laparoscopic surgery directly after the operation (p less than 0.01). This was very specific for pain, which is one of the benefits of this technique and shown in this parameter which confirms the clinical impression. The curves of the changes in the different markers have been analysed and discussed.

[Exploration of the parathyroid gland function by intake or oral calcium and phosphate (only oral intake and sequential treatment with calcium-phosphate)]. / Exploration de la fonction parathyroïdienne par prise orale de calcium et de phosphate (prise orale unique et traitement séquentiel calcium-phosphate).

The parathyroid hormone response to the oral intake of either calcium or phosphate was explored in 10 young adults (23-28 years). First, the subjects were investigated during free running diet. They ingested a single oral dose of 500 mg of calcium (as a bag of Sandocal) and 10 days later a single oral dose of phosphate (750 mg of phosphorus as a tablet of Phosphore Sandoz Forte). Samples of blood and urine were collected before and during the 4 hours following the ingestion of either calcium or phosphate. After intake of calcium an acute response was obtained with a 58% decrease in PTH 1-84 at 1 hr (p less than 0.001) and a 33% decrease in nephrogenous cAMP (p less than 0.001). After ingestion of phosphate the response was delayed and less constant with a 25% increase in PTH 1-84 at 3 hr (p less than 0.01) and a 27% increase in nephrogenous cAMP (p less than 0.001). Then, the effects of a calcium therapy (3 daily doses of 500 mg each for 20 days) and of a subsequent phosphate therapy (2 daily doses of 750 mg each for 10 days) on the parathyroid hormone response to the administration of a single dose of phosphate were studied. On days 10, 21 and 31 baseline blood and urine samples were obtained prior to calcium and phosphate administration for measuring PTH 1-84 and nephrogenous cAMP. No significant variation was found. On days 21 (after calcium therapy) and 31 (after phosphate therapy) an oral load of phosphate was administered according to the procedure described above.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects on calcium and phosphate metabolism and on parathyroid function of acute administration of tricalcium phosphate.

The effects of the ingestion of tricalcium phosphate on calcium and phosphate metabolism and on parathyroid function were evaluated in 10 young adults. Each subject was studied during a control period of two hours before and during an experimental period of four hours after ingestion of a single oral dose of tricalcium phosphate containing 1500 mg of calcium and 770 mg of phosphorus. Serum and urinary calcium and phosphate and the nephrogenous cAMP fraction were measured. Significant rises in serum (from 2.32 +/- 0.05 to 2.44 +/- 0.08 mmol/l) and urinary (from 1.08 +/- 0.65 to 3.43 +/- 1.38 mumols/l GF) calcium and in serum phosphate (from 1.05 +/- 0.18 to 1.28 +/- 0.14 mmol/l) occurred. Unexpectedly, the acute supply of calcium in the form of tricalcium phosphate did not provoke significant alteration of nephrogenous cAMP level. In order to assess the respective effects of calcium and of phosphate, similar tests with ingestion of similar amounts either of calcium (as a glucoheptogluconate salt) or of phosphate were subsequently performed in the same subjects. Significant increases in serum total calcium were observed after calcium glucoheptogluconate as after tricalcium phosphate. However, the effects on parathyroid function differed, since a significant (p less than 0.001) decrease in nephrogenous cAMP followed the ingestion of calcium glucoheptogluconate. Otherwise, a stimulating effect of phosphate on parathyroid function was observed. These findings suggest that the respective effects of calcium and of phosphate are counterbalanced when administered as tricalcium phosphate, resulting in the absence of parathyroid suppression.

[Primary hyperparathyroidism: value of "intact parathormone" assay (PTH 1-84)]. / Hyperparathyroïdie primaire: apports du dosage de la parathormone "intacte" (PTH 1-84).

In a prospective study of 20 patients with primary hyperparathyroidism the diagnostic value of the intact parathormone assay was compared with that of intermediate fragment measurement and that of nephrogenic cyclic AMP determination. In the basal state, measuring the intact parathormone is the best way of separating hyperparathyroid patients form normal subjects. During calcium infusion tests, there is good concordance between changes in intact parathormone and in nephrogenic cyclic AMP. In addition, the intact parathormone assay enables a thorough study of the relationship between ionized calcaemia and parathyroid secretion to be performed and confirms the existence, in hyperparathyroid patients, of two types of secretory response to a rise in calcaemia. Being more reliable than the measurement of a C-terminal or intermediate fragment and easier to perform than nephrogenic cyclic AMP determination, the intact parathormone assay seems to be particularly suitable for the study of primary hyperparathyroidism.

Development of adrenocortical cyclic nucleotide (cyclic AMP and cyclic GMP) and corticosterone circadian rhythms in male and female rats.

The daily rhythm of the adrenocortical cyclic nucleotides (cyclic AMP and cyclic GMP) was studied in infant male and female Wistar rats before and after the establishment of an adult-like daily rhythm of plasma corticosterone. As in this strain the rhythm of corticosterone is known to be present on postnatal day 18, pups of 2 and 3 weeks of age were studied. The dams and the pups as well as the young adult animals were kept on a controlled 12L-12D photoperiod. Groups of 8-10 pups were killed at 4-hr intervals throughout the day. Plasma corticosterone levels and adrenal cyclic AMP and cyclic GMP concentrations were simultaneously measured and the daily patterns established. Pups of 2 weeks of age showed neither plasma corticosterone nor adrenal cyclic AMP rhythms whereas pups of 3 weeks of age exhibited a typical adult-like circadian rhythm for both variables. The patterns for adrenal cyclic GMP differed according to sex: In female pups no cyclic GMP circadian rhythm could be detected at either 2 or 3 wk. In male pups of 3 wk a typical mature rhythm for adrenal cyclic GMP was evident whereas in younger male pups (2 wk) a circadian rhythm was detected. This circadian rhythm, however, differed from mature circadian rhythm in that its peak was located at 1300 hr instead of 0700 hr. These results demonstrate that, unlike that of cyclic AMP the adrenal cyclic GMP circadian rhythm does not appear at the same time as the plasma corticosterone circadian rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgen metabolism in hirsute patients treated with cyproterone acetate.

Cyproterone acetate (CPA) in association with percutaneously administered estradiol has been used for the treatment of 150 hirsute patients for periods ranging from 6 months to 3 years. A spectacular clinical improvement ensued. Plasma testosterone (T) and androstenedione (A) fell from 69.0 +/- 24 to 33.0 +/- 8 and 210 +/- 103 to 119 +/- 25 ng/dl (mean +/- SD) respectively after 3 months of treatment and remained low thereafter. In contrast, T glucuronide (TG) and 3 alpha-androstanediol (Adiol) remained high during the whole course of treatment: 37 +/- 9 and 115 +/- 43 micrograms/24 h respectively. In vitro T 5 alpha-reductase activity (5 alpha-R) in pubic skin decreased from 147 +/- 34 to 79 +/- 17 fmol/mg skin after 1 year of treatment. To elucidate the discrepancy between plasma and urinary androgens levels, T production rate (PR) and metabolic clearance rate (MCR) were measured with the constant infusion technique in 7 patients before and after 6 months of treatment. PR decreased from 988 +/- 205 to 380 +/- 140 micrograms/24 h (mean +/- SD). In contrast MCRT increased from 1275 +/- 200 to 1632 +/- 360 1/24 h; this increase in MCRT explains the striking plasma T concentration fall and the high TG and Adiol excretion relative to the decrease in PR. Antipyrine clearance rate (n = 8) increased from 36.3 +/- 5.2 to 51.5 +/- 7.4 ml/min whereas 6 beta hydroxycortisol remained unchanged. In conclusion, CPA acts through several mechanisms: (1) it lowers the androgen input to the target cells by (a) depressing T production through its antigonadotropic effect and (b) accelerating T metabolic inactivation due to a partial enzymatic inducer effect on the liver; (2) at the target cell level it competes with any remaining T for the receptor binding sites; (3) the decrease in the androgen-dependent skin 5 alpha-R is a consequence of both actions of androgen suppression and androgen receptor blockade; it reinforces the antiandrogenic effect of CPA.

Effect of dexamethasone on steroidogenesis and on adrenocortical cyclic AMP and cyclic GMP responses to ACTH.

The inhibitory action of dexamethasone on the adrenal steroidogenic response to ACTH was confirmed by im administration of graded doses (5, 10 and 30 ng) of synthetic beta 1-24 ACTH to young adult male rats which had received dexamethasone (0.1 mg/100 g bw) 4 hr prior to sacrifice. Following this, kinetic studies were performed by measuring plasma corticosterone, adrenocortical cyclic AMP and cyclic GMP before and 4, 12 and 30 min after administration of either 10 or 30 ng of ACTH. These doses were selected because their effects could be either completely or partially inhibited by dexamethasone. In rats without dexamethasone all the doses of ACTH which were checked induced an increase in both corticosterone and cyclic AMP and a decrease in cyclic GMP. With the smallest dose of ACTH the earlier administration of dexamethasone resulted in complete suppression of both the steroidogenic response and the cyclic AMP response. With the largest dose of ACTH both responses were diminished. In dexamethasone-treated rats the decrease in cyclic GMP was significantly less pronounced 4 min after ACTH than it was in non-treated rats. These results support the view that cyclic AMP and cyclic GMP might both be concerned with the mechanism of acute adrenal steroidogenesis.

Protein-bound cyclic AMP and steroidogenesis in the adrenal gland of the rat.

Adrenocortical cyclic AMP (both total and protein-bound), and adrenal and plasma concentrations of corticosterone were measured in male rats killed at selected intervals throughout the day. The animals had previously been synchronized for 3 weeks in natural lighting. Adrenal and plasma levels of corticosterone showed similar circadian fluctuations and the onset of their ascending phases started at 13.00 h, maximum concentrations being reached at 21.00 h. On the other hand, a time-lag between the circadian variations of total cyclic AMP and protein-bound cyclic AMP could be seen in adrenocortical tissue. The onset of an increase in adrenocortical protein-bound cyclic AMP was apparent at 15.00 h and the peak occurred at 21.00 h, while total adrenocortical cyclic AMP did not begin to rise before 19.00 h and was maximal at 04.00 h. No direct link between total cyclic AMP and protein-bound cyclic AMP could be seen during the dark phase, suggesting a functional compartmentalization of cyclic AMP in the adrenal gland of the rat. While the ascending phase of the rhythm in steroidogenesis preceded the rise in total adrenocortical cyclic AMP by about 4 h an excellent synchrony between the respective patterns of corticosterone concentration and protein-bound cyclic AMP was noticed.

Clinical chronopharmacology of ACTH 1-17. II. Effects on plasma testosterone, plasma aldosterone, plasma and urinary electrolytes (K, Na, Ca and Mg).

The aim of the investigation was to study the effects of ACTH 1-17 on plasma testosterone, plasma aldosterone as well as on both plasma and urinary electrolytes (K, Na, Mg and Ca) in healthy young adult males with regard to the time (clock hours) at which this polypeptide was injected. Eight healthy adults (males from 28 to 30 years) volunteered for the study. The were synchronized with a diurnal activity from 0700 to midnight and a nocturnal rest. Each week, during 6 consecutive weeks (January 19 to February 25, 1980) a 3-day test was performed on Saturday, Sunday and Monday. On Sundays 3 control-tests and the 3 ACTH-tests were programmed during which either saline or 100 microgram ACTH 1-17 were injected i.m. at respectively 0700, 1400 and 2100. During each 3 day-test period (72 h) the urinary excretion of K, Na, Mg and Ca was determined every 4 h at fixed clock hours. In addition, on Sundays, venous blood was sampled prior to control or ACTH injections at respectively 0700, 1400 and 2100 and 20, 40, 60, 90, 120, 150 and 180 min thereafter. Plasma testosterone, aldosterone (radioimmunoassays) K, Na (flame photometry), Mg and Ca (photocolorimetric methods) were determined in the collected samples. Both conventional and cosinor methods were used for statistical analyses. The injection of ACTH at 0700 was followed by a clear and statistically significant rise of plasma testosterone. No change with regard to control occurred when ACTH was injected at either 1400 or at 2100. A statistically significant rise of plasma aldosterone was observed after each of the ACTH injections. However, the highest plasma aldosterone level was reached when ACTH was administered at 1400 and the lowest level at 2100. ACTH-induced changes in plasma electrolytes were either nil (for Na and Ca) or small (for K and Mg). A more or less important increase of urinary K occurred after the ACTH injection at each of the 3 considered times. The highest values of excreted K occurred after the injection of ACTH at 0700, without shift of the acrophase. In contrast, injections of ACTH at 1400 and 2100 induced a dramatic alteration of the K rhythms. ACTH induced an important fall in the Na urinary excretion. This fall was the greatest when ACTH was injected at 1400. Na rhythm alterations also occurred, particularly after ACTH injections at 2100. However, this effect was less pronounced after ACTH injection at 0700 than at other considered time points. The urinary amount of excreted Ca did not seem to be affected by ACTH. Rhythm alterations occurred after ACTH injections at 1400 and 2100. Peaks of plasma testosterone, plasma aldosterone as well as plasma cortisol (reported in a previous paper) resulting from ACTH stimulation coincided in time with the acrophase of the physiological circadian rhythm in plasma levels of these hormones...