INTRODUCTION:
Oxygen uptake (V̇O2) at a given submaximal running intensity is higher in the high hormone (HH; Days 18-24) phase of the menstrual cycle compared to the low hormone (LH; Days 2-5) phase. Whether this inefficiency also occurs during cycling and how this might impact the cardiovascular system has not been evaluated. This study compared gas exchange and cardiovascular responses to severe-intensity continuous cycling exercise in eumenorrheic females within the LH and HH phases of their menstrual cycle.
METHODS:
Nine young, healthy females (20 ± 1 years, 164 ± 7 cm, 64.6 ± 14.3 kg) with normal cycle lengths (28 ± 1 days) completed 3 visits: a step-ramp-step cycling test to determine power output at the respiratory compensation point (RCP), and two identical 14 minute and 15 seconds severe-intensity continuous cycling bouts at ~110%RCP performed within their LH and HH menstrual phases. For each severe-intensity bout, participants cycled on an electromagnetically braked ergometer during which breath-by-breath gas exchange was continuously monitored by mass spectrometer and pneumotach. Cardiac output (Q̇) was measured every 3 minutes using open-circuit acetylene breathing. Blood samples were drawn before and after exercise to measure intravascular volumes and hemoglobin (Hb) mass in conjunction with a post-exercise carbon monoxide rebreathing test.
RESULTS:
Paired t-test revealed that natural (LH: 103 ± 44 pmol/L vs. HH: 326 ± 200 pmol/L; p<0.05) or synthetic estrogen (LH: 0.0 ± 0.0 mg vs. HH: 0.2 ± 0.0 mg; p<0.001) and natural progesterone (LH: 1.3 ± 0.6 nmol/L vs. HH: 24.7 ± 15.9 nmol/L; p<0.05) were higher in the HH phase compared to the LH phase, whereas testosterone (LH: 1.4 ± 0.6 nmol/L vs. HH: 1.2 ± 0.4 nmol/L; p=0.2) and synthetic progestin (LH: 0.0 ± 0.0 mg vs. HH: 1.3 ± 1.6 mg; p>0.05) did not differ across menstrual phases. Neither Hb mass (LH: 585 ± 73 g vs. HH: 582 ± 76 g; p=0.9) nor blood volume (LH: 4225 ± 654 mL vs. HH: 4194 ± 665 mL; p=0.8) were different between phases. Cycling power output was 123±28 W. At the end of the cycling bouts, neither V̇O2 (LH: 2.0 ± 0.5 L/min vs. HH: 1.9 ± 0.5 L/min; p=0.3) nor Q̇ (LH: 15.7 ± 4.6 L/min vs. HH: 15.7 ± 3.3 L/min; p=0.9) differed between menstrual phases. Additionally, there were no between-phase differences in ratings of perceived exertion, cycling cadence, arteriovenous oxygen difference, heart rate, stroke volume, systolic blood pressure, diastolic blood pressure, mean arterial pressure, total peripheral resistance, nor rate-pressure product (all p>0.2). The ΔQ̇ (HH-LH; 0.05 ± 2.0 L/min) was not correlated with ΔHb mass (-3 ± 49 g; r=-0.028, p=0.9) nor Δblood volume (-31 ± 433 mL; r=-0.099, p=0.8).
CONCLUSION:
Neither gas exchange nor cardiovascular responses to severe-intensity exercise differed between the LH and HH phases, suggesting that the cardiovascular stress in response to higher intensity exercise is consistent over the menstrual cycle in young, healthy females.