The use of oral contraceptive (OC) agents is widespread, yet there is no current consensus as to whether the hormonal fluctuation associated with specific phases of the OC cycle affects swimming performance. The combined monophasic OC contains a constant dose of the exogenous hormones, ethinyl estradiol (EE) and progestogen and is the preparation predominantly used among athletes because it allows easy menstrual cycle manipulation for competition or travel. The hormones are commonly taken for 21 days (OC consumption phase), followed by 7 days of placebo and sugar tablets. Exogenous EE and progestogen (family of natural and synthetic hormones that have progestational effects) act to suppress endogenous estrogen and progesterone production (8). Therefore, during a single cycle, acute hormonal change occurs when active OC use is ceased (the withdrawal phase), circulating exogenous hormone levels decline, and endogenous hormone production varies (8).
Prior work has suggested that estrogen alters the regulation of substrate metabolism during exercise by increasing lipid and reducing carbohydrate oxidation (1). Therefore, high-intensity exercise performance may be enhanced during OC withdrawal when circulating levels of estrogen are the lowest and carbohydrate metabolism is upregulated. High-intensity exercise performance may also be improved during the withdrawal phase as a result of a reduction in progestogen levels, which has been linked with increased aldosterone activity (because progestogen is an antagonist at the aldosterone receptor site). Consequently, when progestogen is lowered during OC withdrawal, the increased circulating aldosterone could potentially increase fluid and electrolyte retention, H+ buffering and anaerobic capacity (9). Anaerobic capacity refers to the maximal amount of adenosine triphosphate resynthesized via anaerobic metabolism during a specific bout of short-duration exercise (11) and is an important performance parameter for swimmers and water polo players who compete and test over distances ranging from 100 to 400 m.
Only 1 previous study (20) has investigated the variation in sustained high-intensity performance or anaerobic capacity throughout an OC cycle. The authors determined that for 5 well-trained rowers taking a triphasic OC, performance during a 1,000-m rowing time trial was significantly better during OC withdrawal compared with that during OC consumption (226.5 ± 1.3 vs. 230.6 ± 1.4 seconds), when exogenous EE and progestogen levels were lowest. This finding was attributed to the secondary cellular effects of EE and progestogen on substrate use and buffering capacity.
Earlier research has examined swimming performance throughout the menstrual cycle (2,4); however, to the best of our knowledge, no data exist concerning the impact of the OC cycle. Hence, this study was designed to examine whether 200-m swimming performance and associated measures of heart rate, blood lactate, pH, and blood glucose were affected by the acute hormonal fluctuation of a monophasic OC cycle. It was hypothesized that swimming performance would be optimal during OC withdrawal when circulating exogenous hormones are reduced, potentially facilitating carbohydrate metabolism and improved buffering and anaerobic capacity. Although this study replicates a test of brief, high-intensity exercise performance, it differs from previous research (20) in exercise mode, use of a monophasic vs. a triphasic OC preparation, and the assessment of 3 OC cycle phases vs. 2. The results should assist female swimmers and coaches make informed decisions about the effect of OC cycle phase on swimming performance and whether it is necessary to manipulate the cycle to coincide with major competition. It will also educate coaches and scientists as to whether they should control for OC cycle phase with respect to routine physiological testing.
Experimental Approach to the Problem
We quantified whether 200-m swimming time trial performance would be affected at 3 different phases of the monophasic OC cycle. Test order was randomized and counterbalanced, and testing times were standardized for each participant. This distance was selected because successful performance has a heavy reliance on anaerobic capacity, a variable that can potentially be affected by the hormones contained in a monophasic OC. In addition, this distance has been commonly used in elite testing protocols, and the subjects were familiar with the pacing strategies involved (10). Split times and stroke rates were analyzed to confirm the pacing strategy used for each test. Other physiological variables, including heart rate, blood lactate, pH, and blood glucose were also assessed. These parameters reflect sustained high-intensity performance and are often reported during routine testing to assess adaptation to training. It was therefore important to determine whether they fluctuate between the OC cycle phase.
A monophasic OC cycle consists of 21 active pills containing a constant concentration of estradiol and progestogen and 7 inactive/sugar pills. Three test times were selected to represent the varied hormonal profiles seen within a normal monophasic OC cycle. This included 1 test between days 17 and 21 of the active OC consumption phase (CONS), when circulating levels of exogenous hormones are high. The 2 remaining tests were during the OC withdrawal phase when exogenous hormone intake ceases, 2–3 days postactive pill cessation (WITH1) and 6–7 days postactive pill cessation (WITH2). Two withdrawal phases were selected because of the exogenous steroids having different half lives and therefore variable impact on the endogenous hormones throughout the withdrawal phase (18).
All the subjects consented to participate in the experiment after being informed of the purpose and protocol of the study, and each provided written informed consent. The study was approved by the ethics committee of the University of Western Australia. Six competitive swimmers and water polo players taking a monophasic OC (30 μg EE, 150 μg levonorgestrel) were familiarized with test procedures and participated in the study. Characteristics including age, sport, representative status, preferred stroke, and time taking OC are presented in Table 1. All the subjects were at the end of a general preparatory training phase and were completing between 7 and 10 training sessions per week. During the testing period, the subjects were required to maintain a regular diet and training regime and were to avoid sustained high-intensity activity in the 48 hours before testing. Before each test, the participants completed a 3-day food diary, a weekly training monitor and a health questionnaire to ensure that dietary intake and hydration status were appropriate and consistent. Dietary intakes confirmed that a minimum amount of carbohydrate was consumed in the 24 hours before testing (5 g·kg−1 of body mass).
The subjects reported to the laboratory before each performance test, completed the aforementioned food diary, training history, and health questionnaire and provided a resting venous blood sample (∼8 mL). This blood sample was immediately centrifuged, stored in a freezer, and later analyzed for endogenous serum hormones estradiol and progesterone (Path West, Laboratory Medicine, WA, USA), using a 1-step chemiluminescent competitive immunoassay (% CV—estradiol 4.7, progesterone 5.6). In addition, body mass (±0.05 kg, A&D, Australia) and sum of skinfold thickness (millimeters) at 7 different sites were assessed using Harpenden skinfold calipers (17).
All performance tests were completed in a 10-lane, 50-m swimming pool with water temperature maintained at 27.0 ± 0.4°C (Challenge Stadium, Perth, Australia). Before each time trial, swimmers completed a standardized individual warm-up (1,000–1,500 m) and commenced the 200-m time trial within approximately 5 minutes. The swimmers completed the test in their preferred competition stroke and were given no instruction with regard to pacing but were simply asked to swim the fastest 200-m time possible. During the time trial, split times and stroke rates were recorded each 50 m. Immediately after the time trial, the heart rate was assessed using a specific swimming polar heart rate monitor (Polar Vantage NV, Polar Electro Oy, Kempele, Finland) and at 1- and 3-minute intervals posttest, 2 capillary blood samples were taken from a hyperemic earlobe. A 5 μL blood sample was immediately analyzed for blood lactate using a Lactate Pro (Shiga, Japan) and a 90 μL blood sample was collected in a heparinized tube, capped, and placed on ice for subsequent blood pH analysis (ABL™ 700 Series, Radiometer Medical A/S, Copenhagen, Denmark). For all blood measures, the peak results from the 2 samples (1- and 3-minute posttest) were used in further analysis.
A prospective statistical power analysis was determined using PASS 2008 software (NCSS, LLC, Kaysville, UT, USA). On the basis of a desired power >0.80, with alpha and beta errors set at 0.05 and 0.20, respectively, the sample size of 6 subjects was acceptable based on the repeated measures design. Descriptive statistics (mean ± SD) were used to characterize the data. Performance parameters were analyzed using a 1-way within-subjects repeated measures analysis of variance (RMANOVA) to determine any difference between the OC cycle phases. For results that were of statistical significance, planned comparisons were tested between particular phases of the repeated measures design (Statistica Version 5, '97 edition). For all the tests, the statistical significance was preset at p ≤ 0.05 and where significant differences are reported, these are the only phase differences.
In addition to traditional statistics, inferential statistics were used to determine the practical importance of the findings. These statistics describe the effect of each OC cycle phase on dependent variables and emphasize the precision of estimation rather than null-hypothesis testing (12). The uncertainty in the effect was expressed as 90% confidence limits and as possibilities that the true value of the effect represents substantial change (harm or benefit). If the confidence interval spanned the thresholds for positive and negative changes, the effect was deemed unclear. All the measures were log transformed before analysis to reduce nonuniformity of error and to express effects as percent changes. The smallest clinically or practically important performance change was set at the percent typical error for each variable (0.7% for the 200-m time trial).
Individual subject results for primary variables are presented in Figure 1. The mean and SD for measured variables, during each OC phase are documented in Table 2. No significant difference was observed between OC phases for 200-m swim time, mean stroke rate, peak heart rate, blood glucose, and body composition (p > 0.05). Mean peak blood lactate was significantly lower during WITH2 (9.9 ± 3.0 mmol·L−1) compared with CONS (12.5 ± 3.0 mmol·L−1) and mean pH higher during WITH2 (7.183 ± 0.111) compared with CONS (7.144 ± 0.092). There was no difference in endogenous progesterone concentration between OC cycle phases, although serum estradiol was significantly higher in WITH2 (80 ± 13 pmol·L−1) compared with that in WITH1 and CONS (47 ± 12 and 47 ± 12 pmol·L−1, respectively) (p < 0.05).
In contrast to our hypothesis, the results demonstrated no significant difference in 200-m swimming time trial performance throughout the OC cycle. This finding is supported by the inferential statistics, which found the practical importance of the variation between OC phases to be trivial. Consistent with the RMANOVA results, a reduction in peak blood lactate was deemed ‘very likely’ in WITH2 compared with CONS and in addition ‘likely’ in WITH2 compared with WITH1. Higher pH values were also deemed ‘likely’ in WITH2 compared with that in CONS. These results are presented in Table 3. For all other measures, the practical importance of the variation between OC phases was trivial and a full description of these results has been omitted.
The aim of this study was to determine whether 200-m swimming performance was affected by the acute hormonal fluctuation of a monophasic OC cycle. We hypothesized that swimming performance would be optimal during OC withdrawal, when circulating exogenous hormones are lowered, because of the facilitation of carbohydrate metabolism and potentially improved buffering and anaerobic capacity. The results refuted this hypothesis, and there was no significant clinical or practical difference in 200-m time trial performance between the 3 phases of the OC cycle. Despite there being no difference in performance, there was a reduction in peak blood lactate in the withdrawal phase (when progestogen is lowest) and an increase in the pH at the end of the withdrawal phase compared with during OC consumption.
Previous research has confirmed that varied levels of estrogen can alter acute exercise metabolism (3,5). An increased concentration of estrogen is specifically linked to inhibited gluconeogensis and glycogenolysis, resulting in glycogen sparing and increased lipid availability and use (5,14). Our research found no difference in blood glucose between OC phases, and blood lactate was greater during OC consumption when estrogen levels are the highest. Given that blood lactate is a by-product of carbohydrate metabolism, our findings do not support glycogen sparing as a result of increased estrogen. It is possible that the duration and the intensity of exercise activity is a significant factor in determining whether the OC cycle phase has an impact on high-intensity exercise performance. The majority of support for altered substrate metabolism because of hormonal effects refers to aerobic or submaximal exercise (1). With a shorter, more intense performance test there may be less opportunity (time) for exogenous steroids to exert their influence on substrate metabolism, alternatively the demands of higher intensity exercise may override any hormonal effects (6).
Given that our blood lactate findings do not support the secondary cellular effects of estrogen on substrate use during exercise, the difference in blood lactate between OC phases is likely to be the result of something other than altered substrate metabolism. Prior studies have reported that changes in anaerobic capacity may be because of a variation in buffering capacity, attributed to the secondary effects of progestogen (20). A fall in progestogen level is associated with increased aldosterone activity because progesterone is an antagonist at the aldosterone receptor site (13). Thus, when progestogen is significantly lowered during OC withdrawal, the increased circulating aldosterone could potentially increase fluid and electrolyte retention and improve plasma volume maintenance (9). Increased plasma volume may translate to cellular alkalosis and improved buffering capacity. Lactate concentration is known to be affected by changes in plasma volume (21). In our study, an increase in plasma volume because of diminished progestogen levels may have resulted in a reduced peak blood lactate level that does not necessarily reflect the glycolytic activity involved. The higher mean pH values during WITH2 (7.183 ± 0.111) compared with those during CONS (7.144 ± 0.092) also support the likelihood of cellular alkalosis during OC withdrawal.
Despite the potential for increased buffering capacity, there was no resultant improvement in 200-m swimming performance during the withdrawal phase. Prior studies (7,15,16) have also reported no difference in high-intensity exercise performance throughout the OC cycle, but the results are difficult to compare because of differences in OC type used, mode of exercise, training status of subjects, and the definition of OC cycle phases. Redman et al. (20) conducted the only research to have reported a significant difference in high-intensity exercise performance during an OC cycle. They determined that performance during a 1,000-m rowing time trial was significantly better during OC withdrawal compared with consumption (226.5 ± 1.3 vs. 230.6 ± 1.4 seconds) when exogenous EE and progestogen levels were the lowest. The most distinct difference between the Redman et al. (20) research and the others is the mean test duration, approximately 228 seconds (20) vs. 143 seconds (this study), 33 seconds (15), 31 seconds (7), and repeated 20-second efforts (16). This may suggest that for shorter duration, higher intensity tests, there may be insufficient time for exogenous steroids to exert an influence on substrate metabolism or buffering capacity.
The lactate finding in this study is supported by previous research (19) on endurance performance and OC cycle phase, which reported a significantly higher mean blood lactate during CONS (6.2 ± 2.7 mmol·L−1), compared with WITH1 (5.1 ± 1.9 mmol·L−1). Altered substrate metabolism could not be substantiated and because of the unlikely physiological significance of a 1 mmol·L−1 blood lactate change, the finding was dismissed or unexplained. Protocol length has been discussed, but other major differences between this study and that of Redman et al. (20) was the assessment of 3 OC phases as opposed to 2 and the use of a monophasic OC vs. triphasic. Earlier research has reported that exogenous hormones contained in the OC have different half lives and variable impact on the endogenous hormones during the withdrawal phase (18). In this study, endogenous estrogen was significantly higher in WITH2 (80 ± 13 pmol·L−1) compared with in WITH1 and CONS (47 ± 12 and 47 ± 12 pmol·L−1, respectively), whereas Redman et al. (20) reported no difference between OC consumption and withdrawal (60 ± 10 and 60 ± 8 pmol·L−1, respectively). Therefore, the difference in anaerobic performance and blood lactate findings between studies may be partly because of the difference in withdrawal phase definition. It is also possible that the OC types (monophasic vs. triphasic) containing different exogenous hormone concentrations exert variable suppression effects on the endogenous hormones and therefore total hormone levels (endogenous and exogenous) and subsequent performance.
In conclusion, this study shows that for monophasic OC users, the OC cycle phase does not impact 200-m swimming performance. However, there was a reduction in mean peak blood lactate during the withdrawal phase and an increased pH late in the withdrawal phase, possibly because of an increase in fluid retention, plasma volume, and cellular alkalosis. These results challenge previous findings and speculation pertaining to substrate metabolism and high-intensity exercise performance. Further research is necessary to determine the effect of protocol duration, OC type, the total of exogenous and endogenous hormones, and ratio of these hormones on high-intensity exercise performance.
The results of this study suggest that female 200-m swimmers taking a monophasic OC need not be concerned by the phase of their cycle with regard to competition and optimizing performance. Given that there is no impact on performance, female swimmers may or may not manipulate their cycle according to their individual preference. The assessment of blood lactate is common during routine training sessions and testing protocols for elite swimmers and water polo players. Coaches and scientists have commonly used peak lactate results and lactate curves to evaluate athlete condition and adaptation to training. Based on the findings of this study, we recommend that coaches and scientists exercise caution when interpreting blood lactate results obtained from swimming tests and consider controlling for cycle phase for athletes taking an OC.
The authors would like to thank the Western Australian Institute of Sport for the provision of testing equipment and facilities and Dr. Carmel Goodman for her assistance in the research design. There are no competing interests in relation to the submission of this manuscript and no external funding was involved.
1. Ashley CD, Kramer ML, Bishop P. Estrogen and substrate metabolism—A review of contradictory research. Sports Med 29: 221–227, 2000.
2. Bale P, Nelson G. The effects of menstruation on performance of swimmers. Aust J Sci Med Sport: 19–21, 1985.
3. Bonen A, Haynes FW, Watson-Wright W, Sopper MM, Pierce GN, Low MP, Graham TE. Effects of menstrual cycle on metabolic responses to exercise. J Appl Physiol: Respir Environ Exerc Physiol 55: 1506–1513, 1983.
4. Brooks-Gunn J, Gargiulo JM, Warren MP. The effect of cycle phase on the performance of adolescent swimmers. Phys Sportsmed 14: 182–192, 1986.
5. Bunt JC. Metabolic actions of estradiol: Significance for acute and chronic exercise responses. Med Sci Sports Exerc 22: 286–290, 1990.
6. Burrows M, Peters CE. The influence of oral contraceptives on athletic performance in female athletes. Sports Med 37: 557–574, 2007.
7. De Bruyn-Prevost P, Masset C, Sturbois X. Physiological response from 18–25 years women to aerobic and anaerobic physical fitness tests at different periods during the menstrual cycle. J Sports Med 24: 144–148, 2002.
8. Fotherby K. Bioavailability of orally administered sex steroids used in oral contraception and hormone replacement therapy. Contraception 54: 59–69, 1996.
9. Gaebelein CJ, Senay LC Jr. Vascular volume dynamics during ergometer exercise at different menstrual phases. Eur J App Physiol 50: 1–11, 1982.
10. Gore C. Test Methods Manual: Sport Specific Guidelines for the Physiological Assessment of Elite Athletes (3rd ed.). Canberra, Australia: Australian Sports Commission, 1998 .
11. Green S, Dawson B. Measurement of anaerobic capacities in humans. Definitions, limitations and unsolved problems. Sports Med 15: 312–327, 1993.
13. Laidlaw JC, Ruse JL, Gornall AG. The influence of estrogen and progesterone on aldosterone excretion. J Clin Endocrinol Metab 22: 161–171, 1962.
14. Lebrun CM. Effect of the different phases of the menstrual cycle and oral contraceptives on athletic performance. Sports Med 16: 400–430, 1993.
15. Lebrun CM, Petit MA, McKenzie DC, Taunton JE, Prior JC. Decreased maximal aerobic capacity with use of a triphasic oral contraceptive in highly active women: A randomised controlled trial. Br J Sports Med 37: 315–320, 2003.
16. Lynch NJ, De Vito G, Nimmo MA. Low dosage monophasic oral contraceptive use and intermittent exercise performance and metabolism in humans. Eur J Appl Physiol 84: 296–301, 2001.
17. Norton K, Olds T. Anthropometrica. Sydney, Australia: University of New South Wales Press, 1996.
18. Rechichi C, Dawson B. Effect of oral contraceptive cycle phase on performance in team sport players. J Sci Med Sport 12: 190–195, 2009 .
19. Rechichi C, Dawson B, Goodman C. Oral contraceptive phase has no effect on endurance test. Int J Sports Med 29: 277–281, 2008.
20. Redman LM, Weatherby RP. Measuring performance during the menstrual cycle: A model using oral contraceptives. Med Sci Sports Exerc 36: 130–136, 2004.
21. Weinstein Y, Bediz C, Dotan R, Falk B. Reliability of peak-lactate, heart rate, and plasma volume following the Wingate test. Med Sci Sports Exerc 30: 1456–1460, 1998.
Copyright © 2012 by the National Strength & Conditioning Association.