Share this article on:

Physical Activity, Heart Rate, Metabolic Profile, and Estradiol in Premenopausal Women


Medicine & Science in Sports & Exercise: June 2008 - Volume 40 - Issue 6 - p 1022-1030
doi: 10.1249/MSS.0b013e318167411f
BASIC SCIENCES: Original Investigations

Purpose: To study whether physical inactive women with a tendency to develop metabolic syndrome have high levels of 17β-estradiol (E2) of importance for breast cancer risk.

Methods: Two hundred and four healthy women of reproductive age were assessed for self-reported leisure-time physical activity (LPA), resting heart rate (HR), blood pressure (BP), anthropometry, and serum glucose, lipids, and insulin [Norwegian Energy Balance and Breast Cancer Aspect (EBBA) study]. E2 was measured in daily saliva samples throughout an entire menstrual cycle. A clustered metabolic risk score [z metabolic syndrome (zMS); total cholesterol-high-density lipoprotein-cholesterol (HDL-C) ratio, insulin resistance, total fat tissue, BP, and triglycerides] was defined. Linear regression and linear mixed models were used, and confounding factors were tested.

Results: Physically active women had lower fat percentage (P trend = 0.003) and HRs (P trend = 0.003) than sedentary women. We estimated an increase in E2 of 1.27 pmol·L−1 [95% confidence interval (CI), 0.06-2.47] for each 11.7 beats·min−1 (1 SD) increase in HR, and this corresponds to the 7% change in mean concentration of E2 for the total group. Associations with E2 were also found for fat tissue, total cholesterol-HDL-C ratio, insulin resistance, and triglycerides. A dose-response relationship was observed among the three levels of LPA and HR and zMS (P trend = 0.03 for LPA; P trend = 0.004 for HR). Women in the highest tertile of the clustered metabolic risk score had average salivary E2profiles that were markedly higher, throughout the cycle, than those of the other groups, with a cycle peak-day difference in E2 of 22-28%.

Conclusion: LPA and HR were associated with metabolic risk score, and this score was associated with daily level of E2, pointing to important biologic mechanisms operating between a sedentary lifestyle and an increased breast cancer risk.

1Department of Oncology, Ullevål University Hospital, Oslo, NORWAY; 2Departments of Biostatistics, Institute of Basic Medical Sciences, University of Oslo, Oslo, NORWAY; 3NORM Surveillance Program for Antimicrobial Resistance in Human Pathogens, Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, NORWAY; 4Faculty of Medicine, Institute of Community Medicine, University of Tromsø, Tromsø, NORWAY; 5Division of Population Health and Information, Alberta Cancer Board, Calgary, Alberta, CANADA; 6Department of Anthropology, Harvard University, Cambridge, MA; 7Department of Epidemiology and Population Studies, Collegium Medicum, Jagiellonian University, Krakow, POLAND; and 8Department of Sports Medicine, Norwegian School of Sport Sciences, Oslo, NORWAY

Address for correspondence: Aina Emaus, Ph.D., Department of Oncology, Ullevål University Hospital HF, 0407 Oslo, Norway; E-mail:

Submitted for publication August 2007.

Accepted for publication January 2008.

©2008The American College of Sports Medicine