Exercise Endocrinology Laboratory

“Studies conducted in the Exercise Endocrinology Laboratory explore the ways diet and exercise can be used to prevent development of morbidities such as obesity and pre-diabetes. The lab often hosts and collaborates with international scholars and students including countries ranging from Croatia, Iran, PR China, Slovenia, Taiwan, Thailand, and others. The focus of research is on understanding whether modifications in diet and exercise can affect the appetite, high blood sugar concentrations, and loss of bone mineral after menopause through changes in hormone secretion. Clinical studies are designed to translate clinical findings to applications that can impact adult health and quality of daily life.”
Dr. Katarina Borer, Director and Professor of Movement Science

Exercise Endocrinology Laboratory


CCRB 1220
401 Washtenaw Ave.
Ann Arbor, MI 48109-2214
(734) 647-2706
(734) 936-1925



No detection of exercise energy expenditure (Role of exercise in endocrine control of feeding.)

Support: Tanita Healthy Weight Community Trust grant (2005-2006)
NIDDK grant 1 R15 DK066286-01A2

The long-term objective of this research is to arrive at a better understanding of how exercise influences the energy regulatory mechanism. The specific aims of the two proposed experiments are to test the following three hypotheses: that (1) exercise of sufficient volume and intensity will suppress appetite; (2) appetite suppression will show a positive relationship with some, or all, of the postulated endocrine mediators of satiety: hormones insulin, leptin, catecholamines, CCK, and peptide YY, and a negative relationship to the putative orexigenic (appetite-stimulating) hormone ghrelin; and (3) behavioral and endocrine suppression of appetite by exercise will be attenuated by obesity. Answers to these questions should improve currently unsuccessful strategies of combining exercise with eating to achieve body fat loss and will help reduce incidence of national obesity epidemic. The two studies recruit postmenopausal women as this demographically large group displays a high incidence of obesity and inactivity. Exercise that will cause expenditure of about 1000 Kcal in excess of resting metabolic rate is applied either at moderate intensity but with variable timing with respect to meals (Experiment 1), or at two different intensities in normal weight and obese women (Experiment 2). Behavioral measures of hunger and of satiety (fullness, desire to eat, and an estimate of quantity one can eat) are assessed hourly during daytime. Energy expenditure is assessed through indirect respirometry, and blood samples for the measurement of anorexigenic (appetite-suppressing) and orexigenic hormones are drawn at intervals ranging between 15 and 60 minutes, more frequently at the start and end of exercise and meals, and less frequently throughout the rest of the 24-h day. In experiment 1, the effects of exercise are compared under contrasting feeding conditions (exercise before or after meals). In experiment 2, the comparison entails an inactive day versus two days of exercise at different intensities (but same energy expenditure) and two levels of body fatness. In both experiments, subjects serve as their own controls. Hormone concentrations are measured by radioimmunoassays. Preliminary results in experiment 1 provide evidence for appetite suppression by exercise, but not for an effect of meal and exercise timing on the ratings of hunger, and no support for anorexigenic actions of leptin or insulin.

Osteogenic effectiveness of exercise loads and timing

(a pilot study)
Osteoporosis increases bone fragility, contributes in the United States to 1.5 million bone breaks and over 17 billion dollars in health care costs per year and to reduced quality of life. It is imperative to develop therapies that increase bone strength and build bone in areas where the mechanical stresses are the highest particularly in older individuals in whom osteogenesis is reduced. Only physical activity and several hormones including the parathyroid hormone (PTH) secreted intermittently, growth hormone (GH) insulin-like growth factor-I (IGF-I) and estradiol (E2), were found capable of such site-specific strengthening of bones. Therapeutic approaches with bisphosphonates have only antiresorptive action and reduce fracture risk by only 40 to 60% ; with fluoride allow bone deposition in inappropriate locations, and with E2 have other undesirable side effects. The problems with the use of exercise and bone anabolic hormones in the prevention or treatment of osteoporosis are that the parameters of mechanical loading effective for increased bone formation, including the necessity for dynamic loading, suprathreshold stresses, and rapid mechanoreceptor desensitization, were (1) developed in animal models where loading was confined to a segment of the skeleton rather than elicited by exercise where dynamic loading is accompanied by increased secretion of PTH, GH and IGF-I; and (2) have to date not been translated to humans. Therefore the global hypothesis of this proposal is that the best approach to site-specific strengthening of bones in osteopenic postmenopausal individuals is to use dynamic exercise of the intensity, duration, and timing that most effectively increases secretion of PTH, GH, and IGF-I. Our specific aims are to determine (1) effective mechanical loading (2) shortest effective exercise duration; and (3) effective temporal distribution of exercise to elicit increases in plasma concentration of PTH, GH, and IGF-I and in markers of bone formation osteocalcin (OS), osteoprotegerin (OPG), carboxyterminal propeptide of type I procollagen (PICP) and bone-specific alkaline phosphatase (ALKP);. Measurements of markers of bone resorption, immunoactive carboxyterminal telopeptide of type I collagen (ICTP) in plasma and urinary N-telopeptide of type I collagen (NTX) will also be performed.