BackgroundTo combat historical underrepresentation of female participants in research, guidelines have been established to motivate equal participation by both sexes. However, the pervasiveness of female exclusion has not been examined in vascular exercise physiology research. The purpose of this study was to systematically quantify the sex-specific prevalence of human participants and identify the rationales for sex-specific inclusion/exclusion in research examining the impact of exercise on vascular endothelial function.MethodsA systematic search was conducted examining exercise/physical activity and vascular endothelial function, assessed via flow mediated dilation. Studies were categorized by sex: male-only, female-only, or mixed sex, including examination of the sample size of males and females. Analysis was performed examining sex-inclusion criteria in study design and reporting and rationale for inclusion/exclusion of participants on the basis of sex. Changes in proportion of female participants included in studies were examined over time in 5 year cohorts.ResultsA total of 514 studies were identified, spanning 26 years (1996–2021). Of the total participants, 64% were male and 36% were female, and a male bias was identified (32% male-only vs. 12% female-only studies). Proportions of female participants in studies remained relatively constant in the last 20 years. Male-only studies were less likely to report sex in the title compared to female-only studies (27 vs. 78%, p < 0.001), report sex in the abstract (72 vs. 98%, p < 0.001) and justify exclusion on the basis of sex (15 vs. 55%, p < 0.001). Further, male-only studies were more likely to be conducted in healthy populations compared to female-only studies (p = 0.002). Qualitative analysis of justifications identified four themes: sex-specific rationale or gap in the literature, exclusion of females based on the hormonal cycle or sex-differences, maintaining congruence with the male norm, and challenges with recruitment, retention and resources.ConclusionsThis systematic review provides the first analysis of sex-based inclusion/exclusion and rationale for sex-based decisions in human vascular exercise physiology research. These findings contribute to identifying the impact of research guidelines regarding inclusion of males and females and the perceived barriers to designing studies with equal sex participation, in an effort to increase female representation in vascular exercise physiology research.Systematic Review Registration:CRD42022300388.

Background. Previous research has identified sex differences in substrate oxidation during submaximal aerobic exercise including a lower respiratory exchange ratio (RER) in females compared to males. These differences may be related to differences in sex hormones. Our purpose was to examine the impact of the natural menstrual cycle (NAT) and 2nd and 3rd generation oral contraceptive pill (OCP2, OCP3) cycle phases on substrate oxidation during rest and submaximal aerobic exercise. Methods. Fifty female participants (18 NAT, 17 OCP2, 15 OCP3) performed two experimental trials that coincided with the low (i.e., non-active pill/early follicular) and the high hormone (i.e., active pill/mid-luteal) phase of their cycle. RER and carbohydrate and lipid oxidation rates were determined from gas exchange measurements performed during 10min of supine rest, 5min of seated rest, and two 8min bouts of submaximal cycling exercise at ~40% and ~65% of peak oxygen uptake (V̇O2peak). Results. For all groups, there were no differences in RER between the low and high hormone phases during supine rest (0.73±0.05 vs 0.74±0.05), seated rest (0.72±0.04 vs 0.72±0.04), exercise at 40% (0.77±0.04 vs 0.78±0.04) and 65% V̇O2peak (0.85±0.04 vs 0.86±0.03; p>0.19 for all). Similarly, carbohydrate and lipid oxidation rates remained largely unchanged across phases during both rest and exercise, apart from higher carbohydrate oxidation in NAT versus OCP2 at 40% V̇O2peak (p=0.019) and 65% V̇O2peak (p=0.001). Conclusion. NAT and OCPs do not appear to largely influence substrate oxidation at rest and during acute submaximal aerobic exercise.

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