An acute bout of prolonged sitting (PS) impairs the popliteal artery flow-mediated dilation (FMD) response. Despite equivocal reductions in mean shear rate, young women demonstrate an attenuated decline in popliteal FMD versus young men. However, it is uncertain whether popliteal endothelial-dependent vasoconstrictor responses [low-flow-mediated constriction (L-FMC)] are similarly affected by PS and/or whether sex differences exist. We tested the hypothesis that women would have attenuated reductions in both popliteal FMD and L-FMC responses following an acute bout of PS. Popliteal FMD and L-FMC responses were assessed via duplex ultrasonography before and after a 3-h bout of PS. These responses were then compared between 10 men (24 ± 2 yr) and 10 women (23 ± 2 yr) with similar ( P > 0.13) levels of objectively measured habitual physical activity (via PiezoRx) and sedentary time (via activPAL). At baseline, men and women exhibited similar ( P > 0.46) popliteal FMD (4.8 ± 1.2 vs. 4.5 ± 0.6%) and L-FMC (–1.7 ± 1.0 vs. –1.9 ± 0.9%) responses. Both sexes experienced identical (group: P > 0.76; time: P < 0.001) PS-induced impairments in popliteal FMD (–2.8 ± 1.4 vs. –2.6 ± 0.9%) and L-FMC (1.3 ± 0.7% vs. 1.4 ± 0.7%). In young adults, sex did not influence the negative PS-induced FMD, L-FMC, or microvascular responses in the lower limb. As such, our findings suggest that young men and women are similarly susceptible to the acute negative vascular effects of PS. Future studies should extend these findings to older, less physically active adults and/or patients with vascular disease. NEW & NOTEWORTHY We compared changes in popliteal artery endothelial function to a single 3-h bout of sitting between young men and women. Both groups exhibited similar endothelial-dependent vasodilation (i.e., flow-mediated dilation) and endothelial-dependent vasoconstrictor responses (i.e., low-flow-mediated constriction) at baseline and equivocal impairments in these measures of endothelial function following prolonged sitting. These findings demonstrate that acute impairments in conduit artery endothelial health associated with uninterrupted sitting are not influenced by sex in young, healthy adults.

Purpose It is unclear if high-intensity interval training (HIIT) elicits superior improvements in brachial artery (BA) flow-mediated dilation (FMD) responses (i.e., endothelial-dependent vasodilation) than moderate-intensity continuous training (MICT) or resistance training (RT) in otherwise healthy older adults. Whether HIIT enhances lower-limb FMD responses and/or augments low flow-mediated constriction (L-FMC) (endothelial-dependent vasoconstriction) responses more than MICT or RT is also unknown. We tested the hypothesis that HIIT would improve BA and popliteal artery (POP) FMD and L-FMC responses more than MICT or RT in healthy older adults. Methods Thirty-eight older adults (age, 67 ± 6 yr) performed 6 wk of either HIIT (2 × 20 min bouts alternating between 15-s intervals at 100% of peak power output [PPO] and passive recovery [0% PPO]; n = 12), MICT (34 min at 60% PPO; n = 12), or whole-body RT (8 exercises, 2 × 10 repetitions; n = 14). The L-FMC and FMD were measured before and after training using high-resolution ultrasound and quantified as the percent change in baseline diameter during distal cuff occlusion and after cuff release, respectively. Results Resting BA blood flow and vascular conductance (both, P < 0.003) were greater after HIIT only. The HIIT and MICT similarly increased BA-FMD (pre–post: both, P < 0.001), but only HIIT improved BA L-FMC (P < 0.001). Both HIIT and MICT similarly enhanced POP FMD and L-FMC responses (both, P < 0.045). Resistance training did not impact FMD or L-FMC responses in either artery (all, P > 0.20). Conclusions HIIT and MICT, but not RT, similarly improved lower-limb vasodilator and vasoconstrictor endothelial function in older adults. Although HIIT and MICT groups enhanced BA vasodilator function, only HIIT improved resting conductance and endothelial sensitivity to low-flow in the BA. In the short-term, HIIT may be most effective at improving peripheral vascular endothelial function in older adults.

Uninterrupted sitting can impair popliteal flow-mediated dilation (FMD) responses in young, premenopausal females when endogenous or exogenous estrogen levels are low. However, it is unknown if sitting-induced FMD responses are altered when estrogen levels are elevated in females who naturally menstruate (NAT) or those using combined, monophasic oral-contraceptive-pills (OCP). This study tested the hypothesis that the decline in popliteal FMD following an acute bout of prolonged sitting would be attenuated during the later versus earlier phases of a natural menstrual or OCP cycle. Popliteal FMD was measured before and after 3-h of sitting in NAT-females (n=9; 23±3 years) and OCP-females (n=9; 23±3 years) during both of their respective phases. At pre-sit, relative FMD was greater in the later phase versus earlier phase in NAT (4.6±1.6% to 5.8±1.5%; P=0.002), but not between pill phases among OCP (4.4±1.2% to 4.8±1.6%; P=0.32). Both groups exhibited similar prolonged sitting-induced impairments in popliteal FMD (Pre-Post Sitting Time: P<0.001; Group ΔFMD: P=0.66; Phase ΔFMD: P=0.42; Interaction ΔFMD: P=0.72), regardless of menstrual cycle phase (earlier: -2.5±1.5%; later: -2.4±1.0%) or pill phase (inactive-pill: -2.4±1.4%; active-pill: -2.1±1.1%). Our findings demonstrate that lower-limb arterial endothelial-dependent vasodilatory function was enhanced in the later versus earlier menstrual phase among NAT, but unaffected by combined, monophasic pill phases in OCP. Furthermore, healthy, young females exhibited pronounced negative lower-limb vascular effects in response to prolonged sitting regardless of whether they were in the earlier or later phases of a natural menstrual or contraceptive pill cycle.

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Heterogeneous flow-mediated dilation (FMD) and low-flow-mediated constriction (L-FMC) responses have been reported between upper- and lower-limb arteries. Radial artery L-FMC, but not FMD, responses are blunted when endothelial-derived hyperpolarizing factors (EDHF) or prostaglandin production are inhibited in young adults. However, it is unknown if these mechanisms similarly impact endothelial-dependent responses in the brachial (BA) and popliteal (POP) arteries. We tested the hypotheses that BA-L-FMC and POP-L-FMC would be attenuated following independent EDHF and prostaglandin inhibition. Eighteen participants (23 ± 3years; 6♀) completed 3 randomized and double-blinded ultrasound assessments following ingestion of an opaque capsule containing maltodextrin (Control), 150mg Fluconazole (EDHF inhibition) or 500mg Aspirin (prostaglandin inhibition). POP resting diameter was reduced following Fluconazole administration (6.13±0.63 mm versus 6.19±0.65 mm in Control, P=0.03). Compared to Control, Fluconazole also blunted the relative L-FMC responses in both the BA (-2.1 ± 0.8% versus -0.8 ± 1.0%, P=0.001) and POP (-1.7±1.1% versus -0.8±0.9%, P=0.009). In contrast, Aspirin did not impact either the BA (-1.9±0.7%) or POP-L-FMC (-1.3±0.6%) responses (both, P>0.35). The FMD response was unchanged following Fluconazole or Aspirin administration in either artery (both, P>0.36). Our findings demonstrate that EDHF mediates L-FMC responses in both the brachial and popliteal arteries. Complementary to the nitric oxide-mediated FMD response, L-FMC appears to provide information regarding the EDHF pathway. Future research should uncover if these mechanisms impact older adults and/or patient populations characterized by vascular endothelial dysfunction associated with low aerobic fitness and habitual physical activity levels.