PURPOSE: We examined the catecholamine response to exercise in five eumenorrheic (EU) and five amenorrheic (AM) athletes, matched by age (mean ± SEM: EU = 29.8 ± 2.5 yr and AM = 31.0 ± 4.3 yr) and running volume (EU = 56.4 ± 8.1 km·wk(-1) and AM = 61.5 ± 6.4 km·wk(-1)). 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 (VO(2peak)). 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 VO(2peak) (EU = 57.3 ± 2.3 mL·kg(-1)·min(-1) and AM = 54.1 ± 1.2 mL·kg(-1)·min(-1). 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 VO(2peak) (EU = 7784.5 ± 582.9 pg·mL(-1) and AM = 3626.1 ± 271.4 pg·mL(-1) at VO(2peak)). Epinephrine (EU = 1470.3 ± 275.1 pg·mL(-1) and AM = 416.9 ± 67.5 pg·mL(-1)) and blood lactate (EU = 10.1 ± 1.2 mmol·L(-1) and AM = 6.7 ± 0.9 mmol·L(-1)) were lower at VO(2peak) 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.
PURPOSE: We examined the catecholamine response to exercise in five eumenorrheic (EU) and five amenorrheic (AM) athletes, matched by age (mean ± SEM: EU = 29.8 ± 2.5 yr and AM = 31.0 ± 4.3 yr) and running volume (EU = 56.4 ± 8.1 km·wk(-1) and AM = 61.5 ± 6.4 km·wk(-1)). 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 (VO(2peak)). 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 VO(2peak) (EU = 57.3 ± 2.3 mL·kg(-1)·min(-1) and AM = 54.1 ± 1.2 mL·kg(-1)·min(-1). 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 VO(2peak) (EU = 7784.5 ± 582.9 pg·mL(-1) and AM = 3626.1 ± 271.4 pg·mL(-1) at VO(2peak)). Epinephrine (EU = 1470.3 ± 275.1 pg·mL(-1) and AM = 416.9 ± 67.5 pg·mL(-1)) and blood lactate (EU = 10.1 ± 1.2 mmol·L(-1) and AM = 6.7 ± 0.9 mmol·L(-1)) were lower at VO(2peak) 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.
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