Calcium Supplementation Attenuates Disruptions in Calcium Homeostasis during Exercise.

An exercise-induced decrease in serum ionized calcium (iCa) is thought to trigger an increase in parathyroid hormone (PTH), which can stimulate bone resorption. PURPOSE: The purpose of this study was to determine whether taking a chewable calcium (Ca) supplement 30 min before exercise mitigates disruptions in Ca homeostasis and bone resorption in competitive male cyclists. METHODS: Fifty-one men (18 to 45 yr old) were randomized to take either 1000 mg Ca (CA) or placebo (PL) 30 min before a simulated 35-km cycling time trial. Serum iCa and PTH were measured before and immediately after exercise and a marker of bone resorption (C-terminal telopeptide of type I collagen) was measured before and 30 min after exercise. RESULTS: Serum iCa decreased in both groups from before to after exercise (mean ± SD, CA = 4.89 ± 0.16 to 4.76 ± 0.11 mg·dL, PL = 4.92 ± 0.15 to 4.66 ± 0.22 mg·dL, both P ≤ 0.01); the decrease was greater (P = 0.03) in the PL group. There was a nonsignificant (P = 0.07) attenuation of the increase in PTH by Ca supplementation (CA = 30.9 ± 13.0 to 79.7 ± 42.6 pg·mL, PL = 37.1 ± 14.8 to 111.5 ± 49.4 pg·mL, both P ≤ 0.01), but no effect of Ca on the change in C-terminal telopeptide of type I collagen, which increased in both groups (CA = 0.35 ± 0.17 to 0.50 ± 0.21 ng·mL, PL = 0.36 ± 0.13 to 0.54 ± 0.22 ng·mL, both P ≤ 0.01). CONCLUSION: It is possible that ingesting Ca only 30 min before exercise was not a sufficient time interval to optimize gut Ca availability during exercise. Further studies will be needed to determine whether adequate Ca supplementation before and/or during exercise can fully mitigate the exercise-induced decrease in serum iCa and increases in PTH and bone resorption.

Body composition and bone mineral density after ovarian hormone suppression with or without estradiol treatment.

OBJECTIVE: Suppression of ovarian hormones in premenopausal women on gonadotropin-releasing hormone agonist (GnRH(AG)) therapy can cause fat mass (FM) gain and fat-free mass (FFM) loss. Whether this is specifically caused by a decline in serum estradiol (E2) is unknown. This study aims to evaluate the effects of GnRH(AG) with placebo (PL) or E2 add-back therapy on FM, FFM, and bone mineral density (BMD). Our exploratory aim was to evaluate the effects of resistance exercise training on body composition during the drug intervention. METHODS: Seventy healthy premenopausal women underwent 5 months of GnRH(AG) therapy and were randomized to receive transdermal E2 (GnRH(AG) + E2, n = 35) or PL (GnRH(AG) + PL, n = 35) add-back therapy. As part of our exploratory aim to evaluate whether exercise can minimize the effects of hormone suppression, some women within each drug arm were randomized to undergo a resistance exercise program (GnRH(AG) + E2 + Ex, n = 12; GnRH(AG) + PL + Ex, n = 12). RESULTS: The groups did not differ in mean (SD) age (36 [8] and 35 [9] y) or mean (SD) body mass index (both 28 [6] kg/m). FFM declined in response to GnRH(AG) + PL (mean, -0.6 kg; 95% CI, -1.0 to -0.3) but not in response to GnRH(AG) + E2 (mean, 0.3 kg; 95% CI, -0.2 to 0.8) or GnRH(AG) + PL + Ex (mean, 0.1 kg; 95% CI, -0.6 to 0.7). Although FM did not change in either group, visceral fat area increased in response to GnRH(AG) + PL but not in response to GnRH(AG) + E2. GnRH(AG) + PL induced a decrease in BMD at the lumbar spine and proximal femur that was prevented by E2. Preliminary data suggest that exercise may have favorable effects on FM, FFM, and hip BMD. CONCLUSIONS: Suppression of ovarian E2 results in loss of bone and FFM and expansion of abdominal adipose depots. Failure of hormone suppression to increase total FM conflicts with previous studies of the effects of GnRH(AG). Further research is necessary to understand the role of estrogen in energy balance regulation and fat distribution.

Calcium supplementation and parathyroid hormone response to vigorous walking in postmenopausal women.

INTRODUCTION: Disruptions in calcium (Ca) homeostasis during exercise may influence skeletal adaptations to exercise training. In young men, vigorous cycling causes increases in parathyroid hormone (PTH) and bone resorption (C-terminal telopeptides of type I collagen [CTX]); responses are attenuated by Ca supplementation. The study aimed to determine whether vigorous walking causes similar increases in PTH and CTX in older women and how the timing of Ca supplementation before and during exercise influences these responses. METHODS: In experiment 1, 10 women (61 ± 4 yr) consumed 125 mL of either a Ca-fortified (1 g·L) or control beverage every 15 min during exercise starting 60 min before and continuing during 60 min of exercise. In experiment 2, 23 women (61 ± 4 yr) consumed 200 mL of a Ca-fortified (1 g·L) or control beverage every 15 min starting 15 min before and continuing during 60 min of exercise. The exercise was treadmill walking at 75%-80% V˙O2peak. RESULTS: In experiment 1, serum ionized Ca decreased in the control condition (P < 0.001), but not with Ca supplementation. PTH increased after exercise on both days (Ca, P = 0.05; control, P = 0.009) but was attenuated by Ca supplementation (8.3 vs 26.1 pg·mL; P = 0.03). CTX increased only on the control day (P = 0.02). In experiment 2, serum ionized Ca decreased on Ca and control days (Ca and control, P < 0.001), but less so on the Ca day (P = 0.04). PTH (Ca and control, P < 0.001) and CTX (Ca, P = 0.02; control P = 0.007) increased on the Ca and control day, and there were no differences in the changes. CONCLUSION: The timing of Ca supplementation may be a key mediator of Ca homeostasis during acute exercise. Further research is necessary to determine how this influences skeletal adaptations to training.