|Van Loan, Marta|
Submitted to: American College of Sports Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/20/2010
Publication Date: 1/20/2011
Citation: Schaal, K., Van Loan, M.D., Cassazza, G.A. 2011. Reduced catecholamine response to exercise in amenorrheic athletes. American College of Sports Medicine. 43:34-43. Interpretive Summary: Over the last decade research related to sports performance has focused on female athletes with menstrual dysfunction, known as functional hypothalamic amenorrhea (FHA), with the conclusion that menstrual disruption is due to low energy availability. Little research has been done on other aspects of FHA such as the effect of the cardiovascular system, specifically heart rate, and energy metabolism. We examined two hormones, epinephrine and norepinephrine, that control heart rate response to exercise and glucose and lactate markers of energy use in female runners with and without FHA. Each athlete participated in a maximal effort treadmill test to determine her exercise capacity. Based on each athletes individual maximum capacity she also participated in more endurance treadmill tests at varying levels of effort (70%, 80% and 85%) relative to her maximum capacity. During the treadmill test we examined blood markers of energy metabolism, e.g. glucose, lactate and for heart rate responsiveness, e.g. epinephrine and norepinephrine. We found that at each level of exercise athletes with FHA had lower levels of lactate and epinephrine than the athletes without FHA. These results suggest that FHA athletes with suppressed epinephrine response may not be able to elicit as high a heart rate during exercise or maximize available energy for the exercise thus overall performance may be reduced.
Technical Abstract: Studies have found an array of endocrine disturbances related to energy deprivation in women with functional hypothalamic amenorrhea. Purpose: We examined the catecholamine response to exercise in five eumenorrheic (EU) and five amenorrheic (AM) athletes, matched by age (mean T SEM: EU = 29.8 T 2.5 yr and AM = 31.0 T 4.3 yr) and running volume (EU = 56.4 T 8.1 kmIwkj1 and AM = 61.5 T 6.4 kmIwkj1). Methods: Subjects performed a maximal treadmill test followed by a 30-min recovery and then a submaximal running test, consisting of 4-min stages at 60%, 70%, and 80% and 15 min at 85% of peak oxygen consumption (V' O2peak). Blood was drawn after each stage to measure glucose, lactate, epinephrine, norepinephrine, and cortisol concentrations. HR, blood pressure, and rate of perceived exertion were also measured at each stage. Results: There were no differences between groups in body composition or VO2peak (EU = 57.3 T 2.3 mLIkgj1Iminj1 and AM = 54.1 T 1.2 mLIkgj1Iminj1). Resting HR and mean arterial pressure were significantly (P < 0.05) lower in AM. Norepinephrine was lower in AM at 70%, 80%, 85%, and 100% of VO2peak (EU = 7784.5 T 582.9 pgImLj1 and AM = 3626.1 T 271.4 pg/mL at VO2peak). Epinephrine (EU = 1470.3 T 275.1 pg/mL and AM = 416.9 T 67.5 pg/mL) and blood lactate (EU = 10.1 T 1.2 mmol/L and AM = 6.7 T 0.9 mmol/L) were lower at VO2peak in AM. Conclusions: Our results demonstrate a reduced adrenergic response to intense exercise in AM athletes as indicated by reduced blood lactate and catecholamine concentrations. A suppressed catecholamine response could decrease performance by reducing the sympathetic drive essential for the cardiovascular and metabolic adjustments needed to maintain high intensities of exercise