Effect of 6-month high-impact step aerobics and resistance training on BMD and tibial bending strength in sedentary premenopausal women.

The rationale of this study was to examine the effectiveness of 6-month high-impact step aerobics (SA) or moderate-intensity resistance training exercise (RT) on bone mineral density (BMD) and bone bending strength in sedentary women. Results show that SA enhanced BMD in the heel, lower leg, and lumbar spine 2. INTRODUCTION: To determine the effectiveness of 6 months of high-impact step aerobics (SA) or moderate-intensity resistance training (RT) on areal bone mineral density (aBMD) and tibial bending strength in sedentary premenopausal women. METHODS: Sixty-nine women (20-35 years old) who were randomly assigned to RT (n = 22), SA (n = 26), or non-treatment control (CON, n = 21) groups completed the study. SA had a minimum of 50 high-impact landings each training session. RT had a periodized lower body resistance training program incorporating eight exercises (65-85% of 1 repetition maximum: 1-RM). Both RT and SA met 3 times weekly. aBMD was assessed using dual X-ray absorptiometry (DXA). Tibial bending strength was assessed using mechanical response tissue analysis (MRTA). Measurements at 6 months were compared to baseline using ANCOVA, adjusted for baseline measures and covariates with α = 0.05. RESULTS: Calcaneus aBMD (0.0176 vs -0.0019 or -0.0009 g/cm2 relative to RT, p < 0.004, and CON, p < 0.006, respectively), lower leg aBMD (0.0105 vs -0.0036 g/cm2, relative to RT, p = 0.02), and lumbar spine 2 (L2) aBMD (0.0082 vs -0.0157 g/cm2 relative to CON, p < 0.02) were significantly greater in the SA group after 6 months. Tibial bending strength and bone resorption biomarkers were unchanged in all three groups after 6 months. CONCLUSION: Sedentary premenopausal women engaging in 6 months of high-impact aerobic exercise improved aBMD in the calcaneus, lower leg, and L2.

Association between body mass index, bone bending strength, and BMD in young sedentary women.

The rationale was to determine whether body mass index (BMI) is a predictor of bone bending strength and bone mineral density (BMD) in young sedentary women. Results show that BMI is not a predictor of bone bending strength and that young women with low BMI also have low BMD. INTRODUCTION: The purpose of this study was to determine whether body mass index (BMI) is a predictor of tibial or ulnar bending strength and bone mineral density (BMD) in sedentary women. METHODS: Sedentary women (n = 34), age 19-27 years, with low BMI (LBMI < 18.5 kg/m2, n = 16), and normal or high BMI (NHBMI between 18.5 and 29.9 kg/m2, n = 18) participated as study subjects. Study outcomes included tibial and ulnar bending strength (EI in Nm2) using a non-invasive mechanical response tissue analyzer (MRTA); BMD and bone mineral content (BMC) of the whole body (WB), femoral neck (FN), total hip (TH), lumbar spine 1-4 (LS1-4), and ulna; and bone turnover biomarkers. RESULTS: The LBMI group have lower (p < 0.01) body weight [group difference (Δ) = 32.0%], lean mass (LM) (Δ = 23.1%), fat mass (FM) (Δ = 77.2%), and tibial bending strength (Δ = 22.0%), compared to the NHBMI. The LBMI group also have lower (all p < 0.025) BMC in WB (Δ = 19.9%), FN (Δ = 20.1%) and TH (Δ = 19.0%), compared to the NHMBI, not in BMD results. Multivariate regression analysis shows that significant predictors of tibial bending strength are tibia length (adjusted R2 = .341), age (adjusted R2 = .489), ulna BMD (adjusted R2 = .536), and LM (adjusted R2 = .580). BMI was positively correlated with tibial EI (p < 0.05), height, weight, FM, LM, body fat% (all p < 0.01), and BMD of WB, FN, TH, and LS 1-4 (p < 0.05 or < 0.01). CONCLUSIONS: Our results show that BMI is not a significant predictor of tibial or ulnar bending strength in young sedentary women.

Effect of high-impact aerobics and strength training on BMD in young women aged 20-35 years.

To evaluate the effects of a 12-month exercise intervention using either high-impact step aerobic exercise or moderate-intensity strength training on areal bone mineral density (aBMD) we studied 51 untrained women, aged 20-35 years, for this study. Whole body and heel and wrist aBMD were measured by dual-energy X-ray absorptiometry (DXA, Hologic or PIXI Lunar). Subjects were randomly assigned to: impact-loaded step aerobic exercise (SA, n=15), moderate-intensity lower body strength training (ST, n=16) or non-exercise control (CON, n=20). Data analysis only included those who completed 95% of each training routine and attended at least 80% of all sessions. Group differences in aBMD, leg press strength and urinary cross-link deoxypridinoline (µDPD) were analysed using analysis of variance. After a 12-month intervention, the SA elicited an increase in aBMD of the heel (4.4%, p<0.05) and leg press strength (15%, p<0.05), relative to baseline. Meanwhile, the ST showed an increase in leg press strength (48%, p<0.05) with no significant increase in aBMD at any measured site. Similar and unchanged µDPD was observed in all 3 groups at baseline, 6 and 12 months. In conclusion, a 12-month high-impact step aerobic exercise resulted in a significant increase in the heel aBMD in untrained young women, who complied with the exercise regimen. A moderate intensity strength training intervention of similar duration had no effect on aBMD although leg strength increased significantly.

Intestinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients: effect of age and dietary calcium.

Intestinal calcium absorption assessed by a double-isotope method, decreased significantly with aging in 94 normal subjects (r = -0.22, P < 0.025). In 52 untreated patients with postmenopausal osteoporosis, calcium absorption was significantly lower than normal when either age or habitual calcium intake was used as a covariable (P < 0.001). Serum 25-hydroxyvitamin D (25-OH-D) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) were measured in 44 normal subjects and 27 osteoporotic patients. For all normals, calcium absorption and serum 1,25(OH)(2)D were positively correlated (r = 0.50, P < 0.001). In nonelderly normal subjects (ages 30-65 yr), dietary calcium intake correlated inversely with both calcium absorption (r = -0.39, P < 0.01) and with serum 1,25(OH)(2)D (r = -0.50, P < 0.01). Both osteoporotic patients and elderly normal subjects (ages 65-90 yr) differed from nonelderly normals in that these correlations were not present. In addition although serum 25-OH-D was normal, serum 1,25(OH)(2)D was significantly decreased in both osteoporotic patients and elderly normals (P < 0.001). In osteoporotic patients, calcium absorption increased significantly (P < 0.001) after 7 d administration of a small dose (0.4 mug/d) of synthetic 1,25(OH)(2)D(3). In osteoporotics mean serum immunoreactive parathyroid hormone was either normal (COOH-terminal assay) or low (NH(2)-terminal assay) relative to age-matched controls, and mean serum phosphate was increased. The data suggest that inadequate metabolism of 25-OH-D to 1,25(OH)(2)D contributes significantly to decreased calcium absorption and adaptation in both osteoporotics and elderly normal subjects. In patients with osteoporosis this abnormality could result from a decrease in factors that normally stimulate 1,25(OH)(2)D production, such as the decreased parathyroid hormone secretion and increased serum phosphate demonstrated in this group. In elderly subjects a primary abnormality in metabolism of 25-OH-D to 1,25(OH)(2)D, analagous to that seen in aging rats, cannot be excluded.

Intestinal calcium absorption in exogenous hypercortisonism. Role of 25-hydroxyvitamin D and corticosteroid dose.

Pharmacologic doses of corticosteroids impair intestinal calcium absorption and contribute to negative calcium balance. However, the relationship between the impaired calcium absorption and a possible defect in the conversion of vitamin D to its physiologically active form, 1,25-dihydroxyvitamin D, is unknown. We compared fractional calcium absorption (double-isotope method, 100-mg carrier) and serum 25-hydroxyvitamin D (25-OH-D) (Haddad method) in 27 patients receiving pharmacologic doses of prednisone with 27 age-, sex-, and season-matched normal subjects. In patients receiving high daily doses of prednisone (15-100 mg/day), calcium absorption (P < 0.02) and serum 25-OH-D (P < 0.001) were decreased. However, in patients receiving low doses (8-10 mg/day) or high doses (30-100 mg) of prednisone on an alternate-day schedule, both of these parameters were normal. Calcium absorption in the patients treated with daily prednisone correlated inversely with the dose of corticosteroids (r = -0.52, P < 0.025) and, in all steroid-treated patients, correlated directly with serum 25-OH-D (r = 0.58, P < 0.01). In four patients who received high-dose corticosteroid therapy for an average of 4 wk, serum 25-OH-D decreased by 35.5% from pretreatment values. Administration of a physiologic or near-physiologic dose of synthetic 1,25-dihydroxyvitamin D(3) (0.4 mug daily for 7 days) to patients receiving high-dose corticosteroids led to an increase in calcium absorption in all patients. These results suggest that calcium malabsorption in the corticosteroid-treated patients is due to a dose-related abnormality of vitamin D metabolism and not to a direct effect of corticosteroids on depressing transmucosal intestinal absorption of calcium.

Changes in markers of bone formation and resorption in a bed rest model of weightlessness.

To study the mechanism of bone loss in physical unloading, we examined indices of bone formation and bone resorption in the serum and urine of eight healthy men during a 7 day -6 degrees head-down tilt bed rest. Prompt increases in markers of resorption--pyridinoline (PD), deoxypyridinoline (DPD), and hydroxyproline (Hyp)/g creatinine--during the first few days of inactivity were paralleled by tartrate-resistant acid phosphatase (TRAP) with significant increases in all these markers by day 4 of bed rest. An index of formation, skeletal alkaline phosphatase (SALP), did not change during bed rest and showed a moderate 15% increase 1 week after reambulation. In contrast to SALP, serum osteocalcin (OC) began increasing the day preceding the increase in Hyp, remained elevated for the duration of the bed rest, and returned to pre-bed rest values within 5 days of reambulation. Similarly, DPD increased significantly at the onset of bed rest, remained elevated for the duration of bed rest, and returned to pre-bed rest levels upon reambulation. On the other hand, the other three indices of resorption, Hyp, PD, and TRAP, remained elevated for 2 weeks after reambulation. The most sensitive indices of the levels of physical activity proved to be the noncollagenous protein, OC, and the collagen crosslinker, DPD. The bed rest values of both these markers were significantly elevated compared to both the pre-bed rest values and the post-bed rest values. The sequence of changes in the circulating markers of bone metabolism indicated that increases in serum OC are the earliest responses of bone to head-down tilt bed rest.

Calcium homeostasis in diabetes mellitus.

Experimentally diabetic rats have low serum 1,25-dihydroxyvitamin D, intestinal malabsorption of calcium, secondary hyperparathyroidism, and bone loss. To examine the hypothesis that abnormalities similar to those in the diabetic rat might explain human diabetic osteopenia, we studied calcium metabolism in 40 healthy control and 82 diabetic patients aged 18--75 yr [47 untreated: fasting plasma glucose (mean +/- SE), 267 +/- 8 mg/dl; 19 treated but hyperglycemic: glucose 305 +/- 24 mg/dl; 16 treated and in better control: glucose, 146 +/- 8 mg/dl]. Serum total calcium, ionic calcium, immunoreactive parathyroid hormone (Arnaud method, GP-1M and CH-12M antisera), 25-hydroxyvitamin D (Haddad method), and 1,25-dihydroxyvitamin D (Lambert method) concentrations were normal in all 3 groups of diabetics and were not significantly different from values in the control group. We determined absorption of calcium from the intestine by a double isotope method (100 mg Ca carrier; normal range, 40--80%) in 11 control and 13 untreated, uncontrolled diabetics (mean plasma glucose, 285 +/- 17 mg/dl). Absorption of calcium in controls was 60 +/- 3% and in diabetics was 56 +/- 3% (not significantly different). We have found no derangement of calcium metabolism in adults with insulin-requiring juvenile- and adult-onset diabetes regardless of treatment status. The experimental diabetic rat model does not appear to be useful for determining the pathogenesis of adult human diabetic osteopenia.

Components of 25-hydroxyvitamin D in serum of young children in upper midwestern United States.

The relative importance of cholecalciferof (vitamin D3) and ergocalciferol (vitamin D2) in maintaining the vitamin D level in children (1/2 to 6 years old) living in the upper midwestern United States was determined by measurement of total 25-hydroxyvitamin D (25-OH-D), its components, and other indices of calcium homeostasis in serum. In 38 normal children, mean (range) serum total 25-OH-D was 32.8 (less than 5 to 53) ng/ml; in 25 of the 28 sera partitioned, the major component was 25-OH-D3. Significant seasonal variation in serum 25-OH-D3 (mean, range: 35.2, 17 to 51 ng/ml in summer and 15.9, less than 5 to 32 ng/ml in winter) was not accompanied by changes in mean serum 25-OH-D2, calcium, phosphorus, or alkaline phosphatase values. However, individual serum total 25-OH-D values correlated with serum phosphorus values (r = 0.37; P less than 0.05). The proportion of the total represented by 25-OH-D3 varied widely, with a a mean of 83% in summer and 67% in winter. Sources of D3, which include both dermal synthesis and intestinal absorption of D3 added to milk, appear to be more important than sources of D2 in maintaining vitamin D nutrition of young children throughout the year. However, sources of D2 offset the decrease in total 25-OH-D in winter months.

Serum 25-hydroxyvitamin D in infantile rickets.

In small children with nutritional vitamin D deficiency, the serum concentration of 25-hydroxyvitamin D (25-OH-D), the major circulating metabolite of vitamin D, was correlated with the stage of clinical disease. It was low (16 to 20 ng/ml) but within the normal range in the earliest (hypocalcemic) stage of the deficiency syndrome and decreased (less than 15 ng/ml) in the more advanced stages. In patients with familial hypophosphatemia (X-linked dominant), mean serum 25-OH-D concentration was the same as in age-matched normal controls. Evidence is presented that endogenous parathyroid hormone may have a role in the depletion of serum 25-OH0D in deficiency states.

Effect of excess dietary salt on calcium metabolism and bone mineral in a spaceflight rat model.

High levels of salt promote urinary calcium (UCa) loss and have the potential to cause bone mineral deficits if intestinal Ca absorption does not compensate for these losses. To determine the effect of excess dietary salt on the osteopenia that follows skeletal unloading, we used a spaceflight model that unloads the hindlimbs of 200-g rats by tail suspension (S). Rats were studied for 2 wk on diets containing high salt (4 and 8%) and normal calcium (0.45%) and for 4 wk on diets containing 8% salt (HiNa) and 0.2% C (LoCa). Final body weights were 9-11% lower in S than in control rats (C) in both experiments, reflecting lower growth rates in S than in C during pair feeding. UCa represented 12% of dietary Ca on HiNa diets and was twofold higher in S than in C transiently during unloading. Net intestinal Ca absorption was consistently 11-18% lower in S than in C. Serum 1,25-dihydroxyvitamin D was unaffected by either LoCa or HiNa diets in S but was increased by LoCa and HiNa diets in C. Despite depressed intestinal Ca absorption in S and a sluggish response of the Ca endocrine system to HiNa diets, UCa loss did not appear to affect the osteopenia induced by unloading. Although any deficit in bone mineral content from HiNa diets may have been too small to detect or the duration of the study too short to manifest, there were clear differences in Ca metabolism from control levels in the response of the spaceflight model to HiNa diets, indicated by depression of intestinal Ca absorption and its regulatory hormone.

Circulating parathyroid hormone and calcitonin in rats after spaceflight.

Parathyroid hormone and calcitonin, two major calcium-regulating hormones, were measured in the plasma of five experimental groups of rats to evaluate postflight calcium homeostasis after the 14-day COSMOS 2044 flight. Parathyroid hormone values were slightly higher in the flight animals (F) than in the appropriate cage and diet controls (S) (44 +/- 21 vs. 21 +/- 4 pg/ml, P less than 0.05), but they were the same as in the vivarium controls (V), which had different housing and feeding schedules. Neither V nor S showed the increase in plasma creatinine phosphorus and magnesium found in F, features of early renal insufficiency. F showed the lowest mean plasma calcitonin that was statistically different from V only. This difference in F and V (22 +/- 11 vs. 49 +/- 16 pg/ml, P less than 0.05) was most likely due to failure of circulating calcitonin in F to show the normal age-dependent increase we demonstrated in age-matched controls in a separate experiment. Basal values for parathyroid hormone and calcitonin were unchanged after 2 wk of hindlimb suspension, a flight simulation model, in age-matched and younger rats. From a time course experiment serum calcium was higher and parathyroid hormone lower after 4 wk than in ambulatory controls. Postflight circulating levels of parathyroid hormone appear to reflect disturbances in calcium homeostasis from impaired renal function of undetermined cause, whereas levels of calcitonin reflect depression of a normal growth process.

Factors in daily physical activity related to calcaneal mineral density in men.

To determine the factors in daily physical activity that influence the mineral density of the calcaneus, we recorded walking steps and the type and duration of exercise in 43 healthy 26-to 51-yr-old men. Areal (g.cm-2) calcaneal bone mineral density (CBMD) was measured by single energy x-ray densitometry (SXA, Osteon, Inc., Wahiawa, HI). Subjects walked a mean (+/- SD) of 7902 (+/- 2534) steps per day or approximately 3.9 (+/- 1.2) miles daily. Eight subjects reported no exercise activities. The remaining 35 subjects spent 143 (2-772) (median and range) min.wk-1 exercising. Twenty-eight men engaged in exercise activities that generate single leg peak vertical ground reaction forces (GRFz) of 2 or more body weights (high loaders, HL), and 15 reported exercise or daily activities that typically generate GRFz less than 1.5 body weights (low loaders, LL). CBMD was 12% higher in HL than LL (0.668 +/- 0.074 g.cm-2 vs 0.597 +/- 0.062 g.cm-2, P < 0.004). In the HL group, CBMD correlated to reported minutes of high load exercise (r = 0.41, P < 0.03). CBMD was not related to the number of daily walking steps (N = 43, r = 0.03, NS). The results of this study support the concept that the dominant factor in daily physical activity relating to bone mineral density is the participation in site specific high loading activities, i.e., for the calcaneus, high calcaneal loads.

Musculoskeletal adaptations to weightlessness and development of effective countermeasures.

A Research Roundtable, organized by the American College of Sports Medicine with sponsorship from the National Aeronautics and Space Administration, met in November 1995 to define research strategies for effective exercise countermeasures to weightlessness. Exercise was considered both independently of, and in conjunction with, other therapeutic modalities (e.g., pharmacological nutritional, hormonal, and growth-related factors) that could prevent or minimize the structural and functional deficits involving skeletal muscle and bone in response to chronic exposure to weightlessness, as well as return to Earth baseline function if a degree of loss is inevitable. Musculoskeletal deficits and countermeasures are described with respect to: 1) muscle and connective tissue atrophy and localized bone loss, 2) reductions in motor performance, 3) potential proneness to injury of hard and soft tissues, and 4) probable interaction between muscle atrophy and cardiovascular alterations that contribute to the postural hypotension observed immediately upon return from space flight. In spite of a variety of countermeasure protocols utilized previously involving largely endurance types of exercise, there is presently no activity-specific countermeasure(s) that adequately prevent or reduce musculoskeletal deficiencies. It seems apparent that countermeasure exercises that have a greater resistance element, as compared to endurance activities, may prove beneficial to the musculoskeletal system. Many questions remain for scientific investigation to identify efficacious countermeasure protocols, which will be imperative with the emerging era of long-term space flight.

Noninvasive determination of bone mechanical properties using vibration response: a refined model and validation in vivo.

Accurate non-invasive mechanical measurement of long bones is made difficult by the masking effect of surrounding soft tissues. Mechanical response tissue analysis (MRTA) offers a method for separating the effects of the soft tissue and bone; however, a direct validation has been lacking. A theoretical analysis of wave propagation through the compressed tissue revealed a strong mass effect dependent on the relative accelerations of the probe and bone. The previous mathematical model of the bone and overlying tissue system was reconfigured to incorporate the theoretical finding. This newer model (six-parameter) was used to interpret results using MRTA to determine bone cross-sectional bending stiffness, EIMRTA. The relationship between EIMRTA and theoretical EI values for padded aluminum rods was R2 = 0.999. A biological validation followed using monkey tibias. Each bone was tested in vivo with the MRTA instrument. Postmortem, the same tibias were excised and tested to failure in three-point bending to determine EI3-PT and maximum load. Diaphyseal bone mineral density (BMD) measurements were also made. The relationship between EI3-PT and in vivo EIMRTA using the six-parameter model is strong (R2 = 0.947) and better than that using the older model (R2 = 0.645). EIMRTA and BMD are also highly correlated (R2 = 0.853). MRTA measurements in vivo and BMD ex vivo are both good predictors of scaled maximum strength (R2 = 0.915 and R2 = 0.894, respectively). This is the first biological validation of a non-invasive mechanical measurement of bone by comparison to actual values. The MRTA technique has potential clinical value for assessing long-bone mechanical properties.

Postural responses of head and foot cutaneous microvascular flow and their sensitivity to bed rest.

To explore the mechanism for facial puffiness, headache, and nasal congestion associated with microgravity and cephalad fluid shifts, the postural responses of the cutaneous microcirculation in the forehead and dorsum of the foot of eight healthy men were studied by changing body position on a tilt table and measuring blood flows with a laser-Doppler flowmeter. Increasing arterial pressure in the feet by moving from a -6 degree head-down tilt to a 60 degrees head-up posture decreased foot cutaneous flow by 46.5 +/- 12.0% (mean +/- S.E.; p less than 0.05). Raising arterial pressure in the head by tilting from the 60 degree head-up to -6 degree head-down posture increased forehead cutaneous flow by 25.5 +/- 7.2% (p less than 0.05). To investigate the possibility that these opposite responses could be modified by simulated microgravity, tilt tests were repeated after 7 d of -6 degrees head-down tilt bed rest. On the 1st and 2nd days after bed rest, flows in the foot were decreased by 69.4 +/- 8.8% and 45.8 +/- 18.7%, respectively, and increased in the head by 39.3 +/- 8.6% and 15.5 +/- 5.9%, respectively. These responses were not significantly different from those recorded before bed rest. Therefore, cutaneous microcirculatory flow in the feet is well regulated to prevent edema when shifting to an upright position, whereas there is less regulation in the head microcirculation. The lack of regulation in the forehead cutaneous microcirculation increases capillary flow, and consequently increases fluid filtration. This phenomenon helps explain the facial edema associated with the stimulated or actual microgravity environment.

Dietary salt and urinary calcium excretion in a human bed rest spaceflight model.

BACKGROUND: Dietary salt is known to increase the excretion of urinary calcium (Ca). To determine the potential role of dietary sodium (Na) on the calciuria associated with a spaceflight simulation model, we evaluated urinary Ca in two groups of bed rest subjects fed either high or low normal amounts of salt. METHODS: We analyzed urinary Ca excretion expressed in terms of creatinine (UCa/Cr), fractional Ca excretion (FECa), and urinary cAMP (UCAMP) as an index of parathyroid function, in the urine of 30-50-yr-old male volunteers for 6 degrees head down tilt bed rest studies. Dietary Na was in the high normal range (190 mmol x d(-1)) in 8 men for 7 d (HiNa), and in the low normal range (114 mmol x d(-1)) in 11 men for 30 d (LoNa) bed rest. Dietary Ca averaged 20 mmol x d(-1) in both studies. RESULTS: Within the first 3 bed rest days, subjects in the HiNa study showed increases in UCa/Cr (0.1130 +/- 0.05 to 0.161 +/- 0.05, p < 0.002) and in FECa (1.95 +/- 0.70 to 3.19 +/- 0.93, p < 0.001); those in LoNa showed no change in UCa/Cr (0.125 +/- 0.06 to 0.121 +/- 0.07, NS) or FECa (1.93 +/- 0.75 to 2.22 +/- 0.63). After the 5th bed rest day UCa/Cr stabilized at similar levels in both dietary groups. UCAMP decreased 20% during the first week of bed rest with HiNa, but not until the third week with LoNa diets (p < 0.05). CONCLUSION: These findings implicate high salt diets in Ca excretion in a spaceflight model and suggest that low normal salt diets may reduce early calciuria associated with spaceflight.

Effects of 1-week head-down tilt bed rest on bone formation and the calcium endocrine system.

To understand the potential early responses of human bone and the calcium endocrine system to spaceflight, we studied 8 healthy men, aged 35-44 years before, during, and after bed rest in a -6 degrees head-down tilt model for microgravity. Based on a novel single-dose labeling schedule, average rates of bone formation in the iliac crest were reduced in 6, unchanged in 1, and increased in 1 following the bed rest period. The decrease was greatest for subjects whose daily walking miles were highest (r = -0.762, p less than 0.05, n = 7). Before a measurable increase in ionized serum calcium the sixth bed rest day, there was increased excretion of urinary calcium and sodium, evident the first 2 bed-rest days and parallel for the entire week (r = 0.92, p less than 0.001). Reduced excretion of phosphorus and 3', 5' cyclic adenosine monophosphate on the first and second bed rest days was followed by an increase in serum phosphorus by the sixth bed rest day. Depressed serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D were manifest by the sixth and seventh bed rest days. The similarity of the response of bone and the calcium endocrine system of healthy men after only 7 days to results of longer term bed rest studies emphasizes the responsiveness of the adult human skeleton to biomechanical stimuli induced by changes in activity and/or position.