This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.RationaleAlthough it is generally true that exercise is beneficial for bone health,1 under certain conditions exercise can be associated with loss of bone mineral density (BMD). In this pilot study, we will evaluate the impact of calcium (Ca) loss through sweating on bone density. One study of calcium loss and bone density in athletes4 found that male college basketball players had significant decreases in total BMD over the course of a season. When the same athletes were given supplemental Ca in the form of a Ca-fortified sports drink the following competitive season, there was an increase in BMD rather than a loss.To further explore the potential role of calcium loss through sweat, we have chosen to conduct the study in competitive road cyclists. Their high training volume (10-15 h/wk or more) is expected to generate a large sweat Ca loss. Also, the training/competitive season for road cycling is relatively long (Jan to Sept), which is suitable for determining the effects on bone metabolism. Another reason we chose to study road cyclists is because they appear to be at increased risk for low BMD.6-12We will examine the loss of calcium through sweat in this pilot study as one potential mechanism of loss of BMD. However, strenuous exercise has also been found to disrupt sex and stress hormone levels in humans.13-16 Strenuous exercise may also result in systemic inflammation.17-19 These alterations may also effect bone metabolism.
Aims and Hypotheses:The primary goal of this Pilot Study is to evaluate in a prospective, controlled fashion a potential mechanism by which vigorous, prolonged exercise (both in terms of length of an exercise bout and duration of the training/competitive season) may promote bone loss. Our hypotheses are as follows: H1: Dermal Ca loss as a result of prolonged, vigorous exercise training is a significant determinant of bone loss in competitive road cyclists over a season of training and competition.H2: Increasing Ca intake to higher than currently recommended levels (2000 mg/d) will attenuate the loss of bone in competitive road cyclists over a season of training and competition. Methods:To address these hypotheses, we will study 20 competitive cyclists over a season of training and competition. Participants will be men aged 18-35 yr who have been racing for 2 or more seasons and train 10 or more hours/week. They will have baseline calcium intakes at or below the recommended daily allowance of 1000mg/day. They will be randomized to take placebo or supplemental calcium to 1800-2000mg/day or maintain their usual intake of 1000-1200mg/day. Participants will perform a 2 hour simulated training ride on a stationary trainer at baseline, mid-season, and after the season ends. BMD will be measured at these visits, and estimates of their sweat calcium loss will be determined by measuring sweat calcium concentrations and determining sweat loss (estimated from change in body weight corrected for water consumption and urine production). Analysis:Our primary outcome measure is BMD in the placebo non-supplemented vs. the calcium supplemented group. We will attempt to control for confounders such as changes in sex and stress hormones, inflammatory makers, and change in body weight through the season.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
2M01RR000051-46
Application #
7604451
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
2007-07-01
Project End
2008-03-31
Budget Start
2007-07-01
Budget End
2008-03-31
Support Year
46
Fiscal Year
2007
Total Cost
$27,266
Indirect Cost
Name
University of Colorado Denver
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
041096314
City
Aurora
State
CO
Country
United States
Zip Code
80045
Millstein, Richard J; Pyle, Laura L; Bergman, Bryan C et al. (2018) Sex-specific differences in insulin resistance in type 1 diabetes: The CACTI cohort. J Diabetes Complications 32:418-423
Martin, Maureen P; Naranbhai, Vivek; Shea, Patrick R et al. (2018) Killer cell immunoglobulin-like receptor 3DL1 variation modifies HLA-B*57 protection against HIV-1. J Clin Invest 128:1903-1912
Nowak, Kristen L; You, Zhiying; Gitomer, Berenice et al. (2018) Overweight and Obesity Are Predictors of Progression in Early Autosomal Dominant Polycystic Kidney Disease. J Am Soc Nephrol 29:571-578
Haas, David W; Bradford, Yuki; Verma, Anurag et al. (2018) Brain neurotransmitter transporter/receptor genomics and efavirenz central nervous system adverse events. Pharmacogenet Genomics 28:179-187
Venuto, Charles S; Lim, Jihoon; Messing, Susan et al. (2018) Inflammation investigated as a source of pharmacokinetic variability of atazanavir in AIDS Clinical Trials Group protocol A5224s. Antivir Ther 23:345-351
Li, Binglan; Verma, Shefali S; Veturi, Yogasudha C et al. (2018) Evaluation of PrediXcan for prioritizing GWAS associations and predicting gene expression. Pac Symp Biocomput 23:448-459
Hayden, Kathleen M; Baker, Laura D; Bray, George et al. (2018) Long-term impact of intensive lifestyle intervention on cognitive function assessed with the National Institutes of Health Toolbox: The Look AHEAD study. Alzheimers Dement (Amst) 10:41-48
Shah, V N; Sippl, R; Joshee, P et al. (2018) Trabecular bone quality is lower in adults with type 1 diabetes and is negatively associated with insulin resistance. Osteoporos Int 29:733-739
Jensen, Thomas; Bjornstad, Petter; Johnson, Richard J et al. (2018) Copeptin and Estimated Insulin Sensitivity in Adults With and Without Type 1 Diabetes: The CACTI Study. Can J Diabetes :
Dad, Taimur; Abebe, Kaleab Z; Bae, K Ty et al. (2018) Longitudinal Assessment of Left Ventricular Mass in Autosomal Dominant Polycystic Kidney Disease. Kidney Int Rep 3:619-624

Showing the most recent 10 out of 1065 publications