Acute Calcium Ingestion Attenuates Exercise-Induced Disruption of Calcium Homeostasis


Medicine & Science in Sports & Exercise:
doi: 10.1249/MSS.0b013e3181f79fa8
Basic Sciences

Purpose: Exercise is associated with a decrease in bone mineral density under certain conditions. One potential mechanism is increased bone resorption due to an exercise-induced increase in parathyroid hormone (PTH), possibly triggered by dermal calcium loss. The purpose of this investigation was to determine whether calcium supplementation either before or during exercise attenuates exercise-induced increases in PTH and C-terminal telopeptide of Type I collagen (CTX; a marker of bone resorption).

Methods: Male endurance athletes (n = 20) completed three 35-km cycling time trials under differing calcium supplementation conditions: 1) 1000 mg of calcium 20 min before exercise and placebo during, 2) placebo before and 250 mg of calcium every 15 min during exercise (1000 mg total), or 3) placebo before and during exercise. Calcium was delivered in a 1000-mg·L−1 solution. Supplementation was double-blinded, and trials were performed in random order. PTH, CTX, bone-specific alkaline phosphatase (BAP; a marker of bone formation), and ionized calcium (iCa) were measured before and immediately after exercise.

Results: CTX increased and iCa decreased similarly in response to exercise under all test conditions. When compared with placebo, calcium supplementation before exercise attenuated the increase in PTH (mean ± SE: 55.8 ± 15.0 vs 74.0 ± 14.2 pg·mL−1, P = 0.04); there was a similar trend (58.0 ± 17.4, P = 0.07) for calcium supplementation during exercise. There were no effects of calcium on changes in CTX, BAP, and iCa.

Conclusions: Calcium supplementation before exercise attenuated the disruption of PTH. Further research is needed to determine the effects of repeated increases in PTH and CTX on bone (i.e., exercise training) and whether calcium supplementation can diminish any exercise-induced demineralization.

Author Information

1Department of Medicine, Division of General Internal Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO; 2Division of Geriatric Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO; 3Department of Preventive Medicine and Biometrics, University of Colorado, Anschutz Medical Campus, Aurora, CO

Address for correspondence: Daniel W. Barry, M.D., Mail Stop B179, 12631 E. 17th Ave. Room 8213, Aurora, CO 80045; E-mail:

Submitted for publication March 2010.

Accepted for publication August 2010.

©2011The American College of Sports Medicine