GE decreases during time-trial exercise. Unfortunately, the cause of the decrease remains uncertain. Future modeling studies should consider using a declining instead of a constant GE. In sport situations, the declining GE has to be taken into account when selecting a pacing strategy.

Cerebrovascular reactivity (CVR) is reduced in patients with cognitive decline. Women with a history of preeclampsia are at increased risk for cognitive decline. This study examined an association between pregnancy history and CVR using a subgroup of 40 age- and parity-matched pairs of women having histories of preeclampsia (n=27) or normotensive pregnancy (n=29) and the association of activated blood elements with CVR. Middle cerebral artery velocity was measured by Doppler ultrasound before and during hypercapnia to assess CVR. Thirty-eight parameters of blood cellular elements, microvesicles, and cell-cell interactions measured in venous blood were assessed for association with CVR using principal component analysis. Middle cerebral artery velocity was lower in the preeclampsia compared with the normotensive group at baseline (63±4 versus 73±3 cm/s; =0.047) and during hypercapnia (=0.013-0.056). CVR was significantly lower in the preeclampsia compared with the normotensive group (2.1±1.3 versus 2.9±1.1 cm·s·mm Hg; =0.009). Globally, the association of the 7 identified principal components with preeclampsia (=0.107) and with baseline middle cerebral artery velocity (=0.067) did not reach statistical significance. The interaction between pregnancy history and principal components with respect to CVR (=0.084) was driven by a nominally significant interaction between preeclampsia and the individual principal component defined by blood elements, platelet aggregation, and interactions of platelets with monocytes and granulocytes (=0.008). These results suggest that having a history of preeclampsia negatively affects the cerebral circulation years beyond the pregnancy and that this effect was associated with activated blood elements.

Purpose Previous work has shown nitric oxide (NO) contributes to ~15% of the hyperemic response to dynamic exercise in healthy humans. This NO-mediated vasodilation occurs, in part, via increases in intracellular cyclic guanosine monophosphate (cGMP), which is catabolized by phosphodiesterase. We sought to examine the effect of phosphodiesterase-5 (PDE-5) inhibition on forearm blood flow (FBF responses to dynamic handgrip exercise in healthy humans and the role of NO. We hypothesized exercise hyperemia would be augmented by sildenafil citrate (SDF, PDE-5 inhibitor). We further hypothesized any effect of SDF on exercise hyperemia would be abolished with intra-arterial infusion of the NO synthase (NOS) inhibitor L-NG-monomethyl arginine (L-NMMA). Methods FBF (Doppler ultrasound) was assessed at rest and during 5 minutes of dynamic forearm handgrip exercise at 15% of maximal voluntary contraction under control (saline) conditions and during 3 experimental protocols: 1) oral SDF (n=10), 2) intra-arterial L-NMMA (n=20), 3) SDF and L-NMMA (n=10). FBF responses to intra-arterial sodium nitroprusside (NTP, NO donor) were also assessed. Results FBF increased with exercise (p<0.01). Intra-arterial infusion of L-NMMA resulted in a reduction in exercise hyperemia (17±1 to 15±1 mL/dL/min, p<0.01). Although the hyperemic response to NTP was augmented by SDF (Area under the curve: 41±7 vs 61±11 AU, p<0.01), there was no effect of SDF on exercise hyperemia (p=0.33). Conclusions Despite improving NTP-mediated vasodilation, oral SDF failed to augment exercise hyperemia in young, healthy adults. These observations reflect a minor contribution of NO and the cGMP pathway during exercise hyperemia in healthy young humans.

Scientific interest in pacing goes back >100 years. Contemporary interest, both as a feature of athletic competition and as a window into understanding fatigue, goes back >30 years. Pacing represents the pattern of energy use designed to produce a competitive result while managing fatigue of different origins. Pacing has been studied both against the clock and during head-to-head competition. Several models have been used to explain pacing, including the teleoanticipation model, the central governor model, the anticipatory-feedback-rating of perceived exertion model, the concept of a learned template, the affordance concept, the integrative governor theory, and as an explanation for “falling behind.” Early studies, mostly using time-trial exercise, focused on the need to manage homeostatic disturbance. More recent studies, based on head-to-head competition, have focused on an improved understanding of how psychophysiology, beyond the gestalt concept of rating of perceived exertion, can be understood as a mediator of pacing and as an explanation for falling behind. More recent approaches to pacing have focused on the elements of decision making during sport and have expanded the role of psychophysiological responses including sensory-discriminatory, affective-motivational, and cognitive-evaluative dimensions. These approaches have expanded the understanding of variations in pacing, particularly during head-to-head competition.