Effects of the menstrual and oral contraceptive cycle phases on microvascular reperfusion

What is the central question of this study? What are the effects of the menstrual (early follicular and mid-luteal) or monophasic oral contraceptive (inactive- and active-pill) cycle phases on vascular reperfusion of lower limb microvasculature in healthy, active women using the near-infrared spectroscopy (NIRS) vascular occlusion test (VOT) technique? What is the main finding and its importance? We demonstrated that vascular responsiveness in the lower limb microvasculature remained unchanged between the early follicular and mid-luteal phases of the menstrual cycle and inactive- and active-pill phases of the oral contraceptive cycle. These data support that controlling for the cycle phases, within the specific times evaluated in this study, might not be necessary when assessing NIRS-VOT reperfusion rates.

The objective was to examine whether the menstrual or monophasic oral contraceptive cycle phases affect microvascular responsiveness of the lower limb in healthy, active women. During the follicular or inactive-pill phase and the luteal or active-pill phase of the menstrual or oral contraceptive cycle, respectively, 15 non-oral contraceptive users (mean ± SD; 27 ± 6 years of age) and 15 monophasic oral contraceptive users (24 ± 4 years of age) underwent a lower-limb vascular occlusion test (5 min baseline, 5 min occlusion and 8 min post cuff release). Menstrual cycle phases were verified using an ovulation test. Vascular responsiveness was assessed by calculating the near-infrared spectroscopy-derived muscle oxygen saturation (StO₂ ) reperfusion slope (slope 2 StO₂ ) and the post occlusion StO₂ area under the curve (StO_2AUC ) of the tibialis anterior muscle. There were no differences in the reperfusion slope (as a percentage per second; follicular, 1.18 ± 0.48; luteal, 1.05 ± 0.48, inactive-pill, 0.95 ± 0.23; and active-pill, 0.87 ± 0.36; P = 0.09) and area under the curve (as a product of the percentage and seconds; follicular, 1067 ± 562; luteal, 918 ± 414, inactive-pill, 945 ± 702; and active-pill, 750 ± 519; P = 0.09) between the phases of the menstrual or oral contraceptive cycle, regardless of pill generation. The duration of oral contraceptive use was not associated with changes in slope 2 StO₂ (r = 0.02, P = 0.94) or StO_2AUC (r = -0.34, P = 0.22) between cycle phases. In conclusion, vascular responsiveness remained unchanged between the early follicular and mid-luteal phases of the menstrual cycle and the inactive-pill and active-pill phases of the oral contraceptive cycle.