Effects of oral contraceptives on peak exercise capacity

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Effects of oral contraceptives on peak exercise capacity

Gretchen A. Casazza, Sang-Hoon Suh, Benjamin F. Miller, Franco M. Navazio and George A. Brooks J Appl Physiol 93:1698-1702, 2002. doi:10.1152/japplphysiol.00622.2002 You might find this additional info useful... This article cites 24 articles, 5 of which can be accessed free at: /content/93/5/1698.full.html#ref-list-1 This article has been cited by 6 other HighWire hosted articles, the first 5 are: Resting and exercise ventilatory chemosensitivity across the menstrual cycle Meaghan J. MacNutt, Mary Jane De Souza, Simone E. Tomczak, Jenna L. Homer and A. William Sheel J Appl Physiol, March 1, 2012; 112 (5): 737-747. [Abstract] [Full Text] [PDF] Lipid oxidation in fit young adults during postexercise recovery Calvin C. Kuo, Jill A. Fattor, Gregory C. Henderson and George A. Brooks J Appl Physiol, July , 2005; 99 (1): 349-356. [Abstract] [Full Text] [PDF]

Menstrual cycle phase and oral contraceptive effects on triglyceride mobilization during exercise Gretchen A. Casazza, Kevin A. Jacobs, Sang-Hoon Suh, Benjamin F. Miller, Michael A. Horning and George A. Brooks J Appl Physiol, July , 2004; 97 (1): 302-309. [Abstract] [Full Text] [PDF] No effect of menstrual cycle phase on lactate threshold Teresa M. Dean, Leigh Perreault, Robert S. Mazzeo and Tracy J. Horton J Appl Physiol, December , 2003; 95 (6): 2537-2543. [Abstract] [Full Text] [PDF] Updated information and services including high resolution figures, can be found at: /content/93/5/1698.full.html Additional material and information about Journal of Applied Physiology can be found at: http://www.the-aps.org/publications/jappl

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Journal of Applied Physiology publishes original papers that deal with diverse areas of research in applied physiology, especially those papers emphasizing adaptive and integrative mechanisms. It is published 12 times a year (monthly) by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2002 by the American Physiological Society. ISSN: 0363-6143, ESSN: 1522-1563. Visit our website at http://www.the-aps.org/.

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Fatty acid reesterification but not oxidation is increased by oral contraceptive use in women Kevin A. Jacobs, Gretchen A. Casazza, Sang-Hoon Suh, Michael A. Horning and George A. Brooks J Appl Physiol, May , 2005; 98 (5): 1720-1731. [Abstract] [Full Text] [PDF]

J Appl Physiol 93: 1698–1702, 2002; 10.1152/japplphysiol.00622.2002.

Effects of oral contraceptives on peak exercise capacity GRETCHEN A. CASAZZA, SANG-HOON SUH, BENJAMIN F. MILLER, FRANCO M. NAVAZIO, AND GEORGE A. BROOKS Exercise Physiology Laboratory, Department of Integrative Biology, University of California, Berkeley, California 94720 Received 11 July 2002; accepted in final form 31 July 2002

menstrual cycle; sex hormones; oxygen consumption; physical fitness and exertion

PARTICIPATION BY WOMEN IN both recreational and competitive sports has increased dramatically over the last two decades. In addition, the US Surgeon General’s Report on Physical Activity and Health recommends that women of all ages, not just athletes, include a minimum of 30 min of moderate-intensity exercise on most days of the week (25). However, dietary energy insufficiency associated with high-intensity exercise training and competition can increase a woman’s risk of experiencing an abnormal menstrual cycle (3, 13). Abnormal menstrual cycles, with chronically low ovarian hormones, may increase the risk for osteopenia, osteoporosis, and fractures (7). Oral contraceptives (OCs) are used for birth control in normally menstruating young women, and, although controversial, OCs have been used to prevent bone loss in amenorrheic athletes (8, 16). However, there is concern among athletes that these exogenous ovarian hormones affect exercise performance.

Address for reprint requests and other correspondence: G. A. Brooks, Dept. of Integrative Biology, 3060 VLSB, Univ. of California, Berkeley, CA 94720-3140 (E-mail: [email protected]). 1698

˙ O2 peak) is considered the Peak oxygen consumption (V “standard” for assessing aerobic exercise capacity (23), ˙ O2 peak in women could vary owing to ovarian and V hormone influences on stroke volume, pulmonary minute ventilation, oxygen-carrying capacity, blood flow, and muscle oxygen utilization. Although the cyclic endogenous ovarian hormone fluctuations across the normal menstrual cycle do not appear to affect ˙ O2 peak (1, 6, 12), low-dose administration of exogeV nous estrogen and progesterone may have a greater influence on exercise capacity. Only a few studies have examined the effects of exogenous steroids on exercise performance by use of longitudinal study designs. Although short-term OC use (21 days) did not affect ˙ O2 peak (2), 6 mo of monophasic OC use was associated V ˙ O2 peak in endurancewith a significant decrease in V trained women (18). To our knowledge, no longitudinal studies have examined peak exercise capacity in moderately trained women before and after triphasic OC use. With monophasic OCs, the estrogen and progestin components remain constant throughout the pill cycle. In contrast, in triphasic OCs the amounts of estrogen and/or progestin vary across the pill cycle and more closely mimic the ovarian hormone variation that occurs during the normal menstrual cycle. Triphasic OCs contain lower per-cycle progestin levels to provide better cycle control and reduce the incidence of androgenic side effects such as alterations in carbohydrate and lipid metabolism (4) and therefore may not have the same influence on exercise capacity as monophasic OCs. The purpose of this investigation was to examine the effects of menstrual cycle phase (endogenous ovarian hormones) and triphasic OC use (exogenous ovarian hormone analogs) on peak exercise capacity, as ˙ O2 peak. measured by V MATERIALS AND METHODS

Subjects. Eight subjects were recruited from the University of California, Berkeley campus, to participate in a series of experiments to examine the effects of ovarian hormones on cardiorespiratory function and substrate utilization during peak and prolonged submaximal exercise. Results from the submaximal exercise trials on normally menstruating

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Casazza, Gretchen A., Sang-Hoon Suh, Benjamin F. Miller, Franco M. Navazio, and George A. Brooks. Effects of oral contraceptives on peak exercise capacity. J Appl Physiol 93: 1698–1702, 2002; 10.1152/japplphysiol.00622. 2002.—We examined the effects of menstrual cycle phase and oral contraceptive (OC) use on peak oxygen consumption ˙ O2 peak). Six moderately active, eumenorrheic women (V (25.5 ⫾ 1.5 yr) were studied before and after 4 mo of OC. Subjects were tested during the follicular and luteal phases before OC and the inactive and high-dose phases after OC. Before OC, there were no significant differences between the follicular and luteal phases in any of the variables studied. There were also no differences between the inactive and high-dose phases. Dietary composition, exercise patterns, and peak heart rate, minute ventilation, and respiratory exchange ratio did not change with OC use. However, OC use significantly (P ⱕ 0.05) increased body weight (59.6 ⫾ 2.3 to 61.2 ⫾ 2.6 kg) and fat mass (13.3 ⫾ 1.3 to 14.5 ⫾ 1.3 kg) and ˙ O2 peak (⫺11%, 2.53 ⫾ 0.21 to 2.25 ⫾ 0.18 l/min). decreased V In conclusion, 1) endogenous ovarian steroids have little ˙ O2 peak, but 2) the exogenous ovarian steroids in effect on V OC decrease peak exercise capacity in moderately physically active young women.

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Table 1. Physical characteristics of young women before and after 4 mo of OC Before OC*

After OC

Variable

FP

LP

IP

HP

Age, yr Height, cm Weight, kg Body fat, % Lean body mass, kg Fat mass, kg

25.5 ⫾ 1.5 163.8 ⫾ 1.9 59.4 ⫾ 2.3 21.8 ⫾ 1.3 46.4 ⫾ 1.5 13.0 ⫾ 1.2

59.8 ⫾ 2.3 22.5 ⫾ 1.5 46.2 ⫾ 1.4 13.6 ⫾ 1.3†

61.1 ⫾ 2.6†‡ 23.2 ⫾ 1.5† 46.8 ⫾ 1.8 14.3 ⫾ 1.3†‡

61.2 ⫾ 2.5†‡ 23.8 ⫾ 1.4†‡ 46.6 ⫾ 1.8 14.6 ⫾ 1.2†‡

Values are means ⫾ SE for 6 women. FP, follicular phase; LP, luteal phase; IP, inactive phase; HP, high dose phase; OC, oral contraceptives. * Includes some of the same subjects as a previous report (22). † Significantly different from FP; ‡ significantly different from LP, P ⱕ 0.05.

˙ O2 peak were reashormones. Physical work capacity and V sessed during the week of the inactive pills (IP) and during the second week of active pill ingestion (HP). Subjects were instructed to refrain from exercise, caffeine, and medications 24 h before testing, to eat a light meal 3 h before arriving at the laboratory, and to maintain constant diet and exercise regimens throughout the entire experimental period. Three-day dietary records were collected and analyzed before and after the 4 mo of OC using the Nutritionist III program (N-Squared Computing, Salem, OR). Peak exercise tests. Before each peak exercise test, subjects were weighed and body composition was determined (six-site skinfolds with a Harpenden skinfold caliper) (9). A continuously graded exercise test was conducted on an electronically braked cycle ergometer (Monark Ergometric 839E, Vansbro, Sweden). The workload began at 75 W and was increased by 25 W every 3 min until volitional exhaustion. The test was considered maximal if respiratory exchange ratio values exceeded 1.1. Respiratory gases were continuously collected and analyzed via an open-circuit indirect calorimetry system (Ametek S-3A1 O2 and Ametek CD-3A CO2 analyzers, Pittsburgh, PA), and respiratory parameters were recorded every minute by a real-time, on-line personal computer-based system. Heart rate was continuously monitored by a Quinton Q750 electrocardiograph (Bothell, WA). Blood sampling and analyses. Blood was sampled at rest and immediately transferred to collection tubes containing EDTA for hormone determination. Plasma estradiol and progesterone concentrations were determined by 125I radioimmunoassay (Coat-A-Count kits; Diagnostic Products, Los Angeles, CA). All samples for each subject were analyzed together. The intra-assay coefficients of variation were 1–5%. Statistical analyses. Repeated-measures ANOVA and Fisher’s protected least significant difference post hoc tests were used to determine phase differences in body weight, body composition, diet composition, estradiol and progesterone concentrations and peak power output, heart rate, pulmonary minute ventilation, oxygen consumption rate, carbon

Table 2. Ovarian hormone profiles before and after 4 mo of OC Before OC*

After OC

Variable

FP

LP

IP

HP

Day of cycle Days past ovulation Estradiol, pg/ml Progesterone, ng/ml

7 ⫾ 0.7

21 ⫾ 1.1 8 ⫾ 0.6 73.9 ⫾ 15.3 10.6 ⫾ 2.4

27 ⫾ 2.0

19 ⫾ 0.3

14.6 ⫾ 1.3† 0.26 ⫾ 0.02†

10.5 ⫾ 0.8† 0.26 ⫾ 0.03†

34.1 ⫾ 10.6† 0.38 ⫾ 0.04†

Values are means ⫾ SE for 6 women. Day of cycle, days after start of menses before OC and day of pill cycle with OC. * Includes some of the same subjects as a previous report (22). † Significantly different from LP, P ⱕ 0.05. J Appl Physiol • VOL

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women (22) are reported separately. Retrospective blood analyses revealed that two of the subjects failed to meet the ovarian hormone concentration criteria for the follicular and luteal phases of the menstrual cycle and thus were excluded from data analysis. The final subject pool, for peak exercise analysis, consisted of six healthy, nonsmoking, female subjects (25.5 ⫾ 1.5 yr). Subjects habitually exercised 2–6 h/wk (3.5 ⫾ 0.6 h/wk) but were not competitive athletes. The women were nulliparous; had been diet, weight, and exercise stable; and had not taken OCs for at least 6 mo. All subjects reported consistently normal menstrual cycles (22–32 days) and were injury and disease free as determined by health history questionnaire and physical examination. Informed, written consent was provided, and the University of California Committee for the Protection of Human Subjects approved the study protocol (no. 2001-8-132). ˙ O2 peak Experimental design. Physical work capacity and V were tested, in a randomized order, during the early follicular (FP, 4–8 days after the start of menses) and midluteal (LP, 17–25 after the start of menses and 6–9 days after ovulation) phases of the menstrual cycle before OC use. Ovulation was determined by using urine ovulation predictor kits (First Response, Carter Products, New York, NY). FP and LP were confirmed by plasma estradiol and progesterone concentrations from blood samples taken at rest before the peak exercise test or from blood sampled at rest on the same day of the next menstrual cycle. Progesterone levels above 3 ng/ml were used for verification of the luteal phase (21). Peak exercise testing was completed within one to two sequential menstrual cycles. After completion of the menstrual cycle phase testing, each subject began taking the same triphasic OC (one pill per day) for four complete cycles (28 days per cycle). For days 1–7 each pill contained 0.035 mg ethinyl estradiol and 0.18 mg norgestimate, for days 8–14 each pill contained 0.035 mg ethinyl estradiol and 0.215 mg norgestimate, for days 15–21 each pill contained 0.035 mg ethinyl estradiol and 0.25 mg norgestimate, and for days 22–28 the pills were absent of synthetic

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Table 3. Cardiorespiratory parameters at peak exercise before and after 4 mo of OC Before OC*

After OC

Variable

FP

LP

IP

HP

Power output, W Time, min Heart rate, beats/min ˙ E, l/min V ˙ O2, l/min Peak V ˙ O2, ml 䡠 kg⫺1 䡠 min⫺1 Peak V ˙ O2, ml 䡠 kg LBM⫺1 䡠 min⫺1 Peak V ˙ CO2, ml 䡠 kg⫺1 䡠 min⫺1 Peak V RER

175 ⫾ 14.4 14 ⫾ 1.5 192 ⫾ 4.2 78.9 ⫾ 5.3 2.51 ⫾ 0.20 42.3 ⫾ 3.3 54.1 ⫾ 4.1 49.8 ⫾ 3.6 1.18 ⫾ 0.01

175 ⫾ 14.4 14 ⫾ 1.6 191 ⫾ 3.5 81.7 ⫾ 4.8 2.55 ⫾ 0.21 42.6 ⫾ 3.2 55.0 ⫾ 4.1 49.6 ⫾ 3.8 1.17 ⫾ 0.01

150 ⫾ 12.4†‡ 12 ⫾ 1.5†‡ 192 ⫾ 3.6 79.4 ⫾ 2.3 2.25 ⫾ 0.19†‡ 36.9 ⫾ 2.9†‡ 48.1 ⫾ 4.0†‡ 42.3 ⫾ 2.5†‡ 1.16 ⫾ 0.03

150 ⫾ 15.5†‡ 12 ⫾ 1.7†‡ 191 ⫾ 2.8 76.1 ⫾ 3.3 2.25 ⫾ 0.16†‡ 36.9 ⫾ 2.2†‡ 48.6 ⫾ 3.4†‡ 42.5 ⫾ 2.0†‡ 1.16 ⫾ 0.02

˙ O2, oxygen consumption; V ˙ E, pulmonary ventilation; V ˙ CO2, carbon dioxide production; RER, Values are means ⫾ SE for 6 women. V respiratory exchange ratio; LBM, lean body mass. * Includes some of the same subjects as a previous report (22). † Significantly different from FP; ‡ significantly different from LP, P ⱕ 0.05.

dioxide production, and respiratory exchange ratio by use of Statview 5.0.1 (SAS Institute, Cary, NC). Results are expressed as means ⫾ SE throughout the text. The significance level was set at ␣ ⬍ 0.05. RESULTS

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DISCUSSION

This study confirms that, in the absence of OCs, menstrual cycle phase does not affect peak exercise capacity, with no significant changes in body weight, body composition, or cardiorespiratory factors, includ˙ O2 peak, between the follicular and luteal phases. ing V However, 4 mo of a low-dose triphasic OC resulted in a significant increase in body weight and fat mass and a ˙ O2 peak not normalized to significant 11% decrease in V ˙ O2 peak between body mass. There was no change in V the inactive and high-dose phase with OCs, suggesting a persistent synthetic ovarian hormone effect despite a 1-wk cessation of ovarian steroid intake between cycles. That OCs, but not luteal phase menstrual cycle vari˙ O2 peak suggests ations in ovarian hormones, affected V that steroid levels may be involved in suppression of peak exercise capacity. OCs mimic the estrogen profile

˙ O2 peak) before and after 4 mo of Fig. 1. Peak oxygen consumption (V oral contraceptives (OC) for each of the 6 subjects. BOC, before OC (mean ⫽ 42.5 ⫾ 3.3 ml 䡠 kg⫺1 䡠 min⫺1); AOC, after OC (mean ⫽ 36.9 ⫾ 2.6 ml 䡠 kg⫺1 䡠 min⫺1). Some of the same subjects as a previous report (22) were included in the BOC data.

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Subject characteristics. Subject characteristics for the six women that met the ovarian hormone criteria on the day of maximal exercise testing, for all phases, are presented in Table 1. Subject numbers and characteristics vary between the series of reports (22) from our laboratory because not all of the eight subjects met the phase criteria for every experimental protocol. There were no significant differences in body weight or body composition between FP and LP before OCs or between IP and HP with OCs, except a slightly higher fat mass in LP vs. FP. However, there was a small, but significant (P ⬍ 0.05), increase in body weight (3%) and fat mass (9%) after 4 mo of OC use. There were no significant changes in total energy intake (1,920 ⫾ 191 kcal before OC and 1,819 ⫾ 260 kcal after OC), percentage of the energy intake as carbohydrate (58 ⫾ 2.2% before OC and 54 ⫾ 2.9% after OC), percentage of the energy intake as fat (27 ⫾ 2.9% before OC and 31 ⫾ 3.1% after OC), and percentage of the energy intake as protein (15 ⫾ 1.6% before OC and 14 ⫾ 1.3% after OC) with OC use. Day of cycle, days past ovulation, and the ovarian hormone profiles for each phase are shown in Table 2. Criteria for FP (progesterone ⬍ 1 ng/ml) and LP (progesterone ⬎ 3 ng/ml) were met in six subjects before OC use. LP was associated with significantly higher (P ⬍ 0.05) estradiol and progesterone concentrations than all other phases. Both ovarian hormones were low after OC use, validating the suppression of endogenous hormone production by synthetic ovarian steroids. Cardiorespiratory responses. At peak effort, there were no significant differences in any of the cardiorespiratory variables between FP and LP before OC use or between IP and HP with OC (Table 3). However, after 4 mo of OC use, there were significant decreases (P ⬍ 0.05) in time to peak exercise (14%) and in the peak power output attained (8%). There were also ˙ O2 peak measured significant (P ⬍ 0.05) reductions in V

in both liters per minute (11%) and milliliters per kilogram per minute (13%) and in peak carbon dioxide production (15%). There were no significant changes in peak heart rate, pulmonary minute ventilation, and respiratory exchange ratio. All six subjects experienced ˙ O2 peak (ml 䡠 kg⫺1 䡠 min⫺1) after 4 mo of OC a decline in V use (Fig. 1).

ORAL CONTRACEPTIVES AND EXERCISE CAPACITY

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and thyroid hormone play roles in maintaining glucose homeostasis during pregnancy (15), and their importance is more likely exhibited during submaximal prolonged exercise. However, catecholamines are directly involved in hepatic and muscle glycogen mobilization during strenuous exercise. The fetus relies almost exclusively on maternal glucose for growth and development (15), and suppression of epinephrine and norepinephrine release could be a means of preventing maternal liver glycogen depletion and low blood glucose concentrations. Pregnancy is associated with suppressed catecholamine levels during strenuous exercise (15), and exogenous estradiol administration has been shown to decrease SNA at rest (26), decrease catecholamine levels and glucose production and utilization during exercise (20), and increase the levels of the potent vasodilator nitric oxide (5). During exercise, increased SNA and the resultant vasoconstriction in nonactive tissue is essential for increasing blood flow to the working muscle. As exercise intensity increases, some vasoconstriction in the active muscle is also required to maintain mean arterial pressure. Blunting of SNA with high ovarian hormone concentrations, therefore, could limit peak exercise performance. Although oral contraceptives decrease peak exercise capacity in moderately trained young women, effects of these synthetic steroid hormones on prolonged endurance exercise performance in competitive athletes are less obvious and warrant further investigation. The ˙ O2 peak induced by OC use may subside decrement in V over time or become insignificant owing to traininginduced adaptations in highly trained female athletes. In conclusion, these results suggest that 1) endogenous hormones have little effect on exercise perfor˙ O2 peak, but 2) low-dose triphamance as measured by V sic OCs (exogenous ovarian hormones) appear to decrease peak exercise performance in moderately physically active young women. NOTE ADDED IN PROOF

The number of subjects we studied was small, but similar ˙ O2 max are reproducible. results on the effects of OCs on V Since acceptance of our paper, we have learned that the work of Lebrun et al., cited as unpublished, is now in press (Lebrun CM, Petit MA, McKenzie DC, Taunton J, and Prior JC. ˙ O2 max with triphasic oral contraceptive use in Decreased V highly active women: a randomised controlled trial. Br J Sports Med In Press. The authors thank the subjects for their dedication to all aspects of the study. We also thank Joe Vivo, Zinta Zarins, and Christina Chueng for contributions to the data collection and blood analysis. We also thank Rosemary Agostini for commenting on the manuscript. This study was supported by National Institute of Arthritis and Musculoskeletal and Skin Diseases Grant AR-42906. REFERENCES 1. Bemben DA, Salm PC, and Salm AJ. Ventilatory and blood lactate responses to maximal treadmill exercise during the menstrual cycle. J Sports Med Phys Fitness 35: 257–262, 1995.

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during pregnancy, with high levels of ethinyl estradiol (⬎300 pg/ml), levels that are much higher than observed during the normal menstrual cycle (24). As well, the type of contraceptive pill may have an effect on ˙ O2 peak. Our finding of an 11–13% decrease in V ˙ O2 peak V in moderately trained women after 4 mo of triphasic ˙ O2 peak found OCs is greater than the 7% decrease in V in endurance-trained women with 6 mo of monophasic OCs (18). Moreover, C. M. Lebrun (unpublished observations) has observed a similar, small, but statistically ˙ O2 peak with triphasic OC use significant decrease in V in athletic women. And, finally, the duration of OC use may play a role. Longer than 1 mo of OC use appears to be necessary to induce physiological changes because a study examining 1–3 wk of monophasic OCs found no ˙ O2 peak (2). significant effect on V Although the number of subjects was small in our investigation, every subject experienced a drop in ˙ O2 peak with OC use, indicating a significant physioV ˙ O2 peak was depressed during both logical effect. That V IP (ethinyl estradiol levels ⬇ 8 pg/ml) and HP (ethinyl estradiol levels ⬎ 300 pg/ml) phases of OC use is taken to indicate persistence of OC effects (24). In agreement with our findings are those of Lynch et al. (14), who looked at the effects of long-term OC use on intermittent exercise performance in untrained women. ˙ O2 peak include decreases Factors that could reduce V in stroke volume, oxygen-carrying capacity (hemoglobin levels), muscle blood flow, or oxygen extraction or changes in the pattern of substrate utilization. However, most of these do not appear to be candidates for ˙ O2 peak. A decrease an OC-induced negative effect on V in stroke volume is unlikely because estrogen replacement therapy has been shown to increase stroke volume (10) and OC use has been shown to increase the activity of the renin-angiotensin-aldosterone system at rest (19). Decreased hemoglobin concentration is also unlikely because most studies have found no difference in resting blood hemoglobin and ferritin concentrations (11, 17) and an increase in serum iron levels (17) with OC use, presumably owing to a decrease in menstrual blood loss (11). Although we did not directly assess sympathetic nervous system activity (SNA) in this study, decreased SNA and plasma catecholamine concentrations could explain the lower peak oxygen consumption observed with high ovarian hormone concentrations. Consistently high estrogen and progesterone concentrations, such as occur during pregnancy and with exogenous ovarian hormones, may blunt SNA and catecholamine levels as a protective mechanism to maintain blood flow to the uterus and prevent maternal hypoglycemia and uterine contractions (15). Both the sympathetic nervous and endocrine systems play roles in maintaining normal blood glucose concentrations. Because catecholamines do not begin to rise in the circulation until the level of effort be˙ O2 peak), catecholamines comes strenuous (e.g., ⬎65% V are directly involved in glycogen mobilization during strenuous exercise. In contrast, hormones such as human chorionic somatotropin, growth hormone, cortisol,

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15. McMurray RG, Mottola MF, Wolfe LA, Artal R, Millar L, and Pivarnik JM. Recent advances in understanding maternal and fetal responses to exercise. Med Sci Sports Exerc 25: 1305– 1321, 1993. 16. Miller KE and Klibanski A. Amenorrheic bone loss. J Clin Endocrinol Metab 84: 1775–1783, 1999. 17. Mooij PNM, Thomas CMG, Doesburg WH, and Eskes TKAB. The effects of oral contraceptives and multivitamin supplementation on serum ferritin and hematological parameters. Int J Clin Pharmacol Ther 30: 57–62, 1992. 18. Notelovitz M, Zauner C, McKenzie L, Suggs Y, Fields C, and Kitchens C. The effect of low-dose oral contraceptives on cardiorespiratory function, coagulation, and lipids in exercising young women: a preliminary report. Am J Obstet Gynecol 156: 591–598, 1987. 19. Oelkers W, Helmerhorst FM, Wuttke W, and Heithecker R. Effect of an oral contraceptive containing drospirenone on the renin-angiotensin-aldosterone system in healthy female volunteers. Gynecol Endocrinol 14: 204–213, 2000. 20. Ruby BC, Robergs RA, Waters DL, Burge M, Mermier C, and Stolarczyk L. Effects of estradiol on substrate turnover during exercise in amenorrheic females. Med Sci Sports Exerc 29: 1160–1169, 1997. 21. Shepard MK and Senturia YD. Comparison of serum progesterone and endometrial biopsy for confirmation of ovulation and evaluation of luteal function. Fertil Steril 28: 541–548, 1977. 22. Suh SH, Casazza GA, Horning MA, Miller BF, and Brooks GA. Luteal and follicular glucose fluxes during rest and exercise in 3-h postabsorptive women. J Appl Physiol 93: 42–50, 2002. 23. Taylor HE, Buskirk ER, and Henschel A. Maximal oxygen uptake as an objective measure of cardiorespiratory performance. J Appl Physiol 8: 73–84, 1955. 24. Thong FSL, McLean C, and Graham T. Plasma leptin in female athletes: relationship with body fat, reproductive, nutritional, and endocrine factors. J Appl Physiol 88: 2037–2044, 2000. 25. US Department of Health and Human Services. Physical Activity and Health: A Report of the Surgeon General. Atlanta, GA: U. S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996. 26. Weitz G, Elam M, Born J, Fehm HL, and Dodt C. Postmenopausal estrogen administration suppresses muscle sympathetic nerve activity. J Clin Endocrinol Metab 86: 344–348, 2001.

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Downloaded from on July 28, 2014

2. Bryner RW, Toffle RC, Ullrich IH, and Yeater RA. Effect of low dose oral contraceptives on exercise performance. Br J Sports Med 30: 36–40, 1996. 3. Bullen BA, Skrinar GS, Beitins IZ, von Mering G, Turnbull BA, and McArthur JW. Induction of menstrual disorders by strenuous exercise in untrained women. N Engl J Med 312: 1349–1353, 1985. 4. Cedars MI. Triphasic oral contraceptives: review and comparison of various regimens. Fertil Steril 77: 1–14, 2002. 5. Cicinelli E, Ignarro LJ, Matteo MG, Galantino P, Schonauer LM, and Falco N. Effects of estrogen replacement therapy on plasma levels of nitric oxide in postmenopausal women. Am J Obstet Gynecol 180: 334–339, 1999. 6. De Souza MJ, Maguire MS, Rubin KR, and Maresh CM. Effects of menstrual phase and amenorrhea on exercise performance in runners. Med Sci Sports Exerc 22: 575–580, 1990. 7. Drinkwater BL, Nilson K, Chesnut CH III, Bremner WJ, Shainholtz S, and Southworth MB. Bone mineral content of amenorrheic and eumenorrheic athletes. N Engl J Med 311: 277–281, 1984. 8. Hergenroeder AC, Smith EO, Shypailo R, Jones LA, Klish WJ, and Ellis K. Bone mineral changes in young women with hypothalamic amenorrhea treated with oral contraceptives, medroxyprogesterone, or placebo over 12 months. Am J Obstet Gynecol 176: 1017–1025, 1997. 9. Jackson AS, Pollock ML, and Ward A. Generalized equations for predicting body density of women. Med Sci Sports Exerc 12: 175–182, 1980. 10. Kamali P, Muller T, Lang U, and Clapp JF III. Cardiovascular responses of perimenopausal women to hormone replacement therapy. Am J Obstet Gynecol 182: 17–22, 2000. 11. Larsson G, Milsom I, Lindstedt G, and Rybo G. The influence of a low-dose combined oral contraceptive on menstrual blood loss and iron status. Contraception 46: 327–334, 1992. 12. Lebrun CM, McKenzie DC, Prior JC, and Taunton JE. Effects of menstrual cycle phase on athletic performance. Med Sci Sports Exerc 27: 437–444, 1995. 13. Loucks AB, Verdun M, and Heath EM. Low energy availability, not stress of exercise, alters LH pulsatility in exercising women. J Appl Physiol 84: 37–46, 1998. 14. Lynch NJ, DeVito G, and Nimmo MA. Low dosage monophasic oral contraceptive use and intermittent exercise performance and metabolism in humans. Eur J Appl Physiol 84: 296–301, 2001.

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