Common methods to prescribe exercise intensity are based on fixed percentages of maximum rate of oxygen uptake (V˙O2max), peak work rate (WRpeak), maximal HR (HRmax). However, it is unknown how these methods compare to the current models to partition the exercise intensity spectrum. Purpose Thus, the aim of this study was to compare contemporary gold-standard approaches for exercise prescription based on fixed percentages of maximum values to the well-established, but underutilized, “domain” schema of exercise intensity. Methods One hundred individuals participated in the study (women, 46; men, 54). A cardiopulmonary ramp-incremental test was performed to assess V˙O2max, WRpeak, HRmax, and the lactate threshold (LT), and submaximal constant-work rate trials of 30-min duration to determine the maximal lactate steady-state (MLSS). The LT and MLSS were used to partition the intensity spectrum for each individual in three domains of intensity: moderate, heavy, and severe. Results V˙O2max in women and men was 3.06 ± 0.41 L·min−1 and 4.10 ± 0.56 L·min−1, respectively. Lactate threshold and MLSS occurred at a greater %V˙O2max and %HRmax in women compared with men (P < 0.05). The large ranges in both sexes at which LT and MLSS occurred on the basis of %V˙O2max (LT, 45%–74%; MLSS, 69%–96%), %WRpeak (LT, 23%–57%; MLSS, 44%–71%), and %HRmax (LT, 60%–90%; MLSS, 75%–97%) elicited large variability in the number of individuals distributed in each domain at the fixed-percentages examined. Conclusions Contemporary gold-standard methods for exercise prescription based on fixed-percentages of maximum values conform poorly to exercise intensity domains and thus do not adequately control the metabolic stimulus.

To examine whether the menstrual or monophasic oral contraceptive cycle phases affect submaximal (oxygen uptake (trueV˙O2) kinetics, maximal lactate steady‐state (MLSS)) and maximal (trueV˙O2max, time‐to‐exhaustion (TTE)) responses to exercise in healthy, active women. During the mid‐follicular or inactive‐pill phase and the mid‐luteal or active‐pill phase of the respective menstrual or oral contraceptive cycle, 15 non‐oral contraceptive users (mean and standard deviation (SD) (±): 27 ± 6 years; 171 ± 5 cm; 65 ± 7 kg) and 15 monophasic oral contraceptive users (24 ± 4 years; 169 ± 10 cm; 68 ± 10 kg) performed: one trueV˙O2 kinetics test; one ramp‐incremental test; two to three 30‐minute constant‐load cycling trials to determine the power output corresponding to MLSS (MLSSp), followed by a TTE trial. The phase of the menstrual or oral contraceptive cycle did not affect the time constant of the trueV˙O2 kinetics response (τtrueV˙O2) (mid‐follicular, 20 ± 5 seconds and mid‐luteal, 18 ± 3 seconds; inactive‐pill, 22 ± 8 seconds and active‐pill, 23 ± 6 seconds), trueV˙O2max (mid‐follicular, 3.06 ± 0.32 L min−1 and mid‐luteal, 3.00 ± 0.33 L min−1; inactive‐pill, 2.87 ± 0.39 L min−1 and active‐pill, 2.87 ± 0.45 L min−1), MLSSp (mid‐follicular, 181 ± 30 W and mid‐luteal, 182 ± 29 W; inactive‐pill, 155 ± 26 W and active‐pill, 155 ± 27 W), and TTE (mid‐follicular, 147 ± 42 seconds and mid‐luteal, 128 ± 54 seconds; inactive‐pill, 146 ± 70 seconds and active‐pill, 139 ± 77 seconds) (P > .05). The rate of perceived exertion (RPE) at minute 30 of the MLSSp trials was greater in the mid‐follicular phase (6.2 ± 1.5) compared with the mid‐luteal phase (5.3 ± 1.4) for non‐oral contraceptive users (P = .022). The hormonal fluctuations between the menstrual and oral contraceptive cycle phases had no detectable effects on submaximal and maximal exercise performance, even when RPE differed.

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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 (StO 2) reperfusion slope (slope 2 StO 2) and the post occlusion StO 2 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 StO 2 (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.

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