S mall cerebral arteries and arterioles (eg, pial vessels) respond rapidly to changes in their metabolic milieu and are highly sensitive to the partial pressure of arterial carbon dioxide (PaCO 2 ).1 Vasomotor responsiveness to PaCO 2 , termed CO 2 reactivity, is integral to stabilizing blood pH levels, and previous studies have associated lower CO 2 reactivity to increased cardiovascular and all-cause mortality.2 Recent magnetic resonance imaging studies in humans have revealed that vasomotor changes also occur in the middle cerebral artery (MCA) 3-5 and basilar artery 6 across the hypo-and hypercapnic range. These studies demonstrate the involvement of larger cerebral arteries in the PaCO 2 reactivity response, 7 findings consistent with well-controlled, animal studies. 8 Other recent studies using Duplex ultrasound have investigated extracranial artery responses during hypo-and hypercapnia.9,10 These studies provide direct evidence that changes in end-tidal CO 2 (PETCO 2 ) are associated with directionally similar, and dosedependent, changes in internal carotid artery (ICA) diameter. The mechanism(s), however, mediating these changes in extracranial ICA diameter remain unclear.Significant and rapid changes in extracranial artery blood flow occur across the hypo-and hypercapnic range. [9][10][11] In peripheral conduits such as the radial and brachial arteries, such changes in flow and attendant arterial shear stress represent potent vasoactive stimuli.12,13 Although Pohl et al 14 and Rubanyi et al 15 were the first to identify that flow-mediated dilation (FMD) is endothelium dependent, it is now well established that this phenomenon occurs in humans and that NO plays a significant role. [16][17][18][19] The widely used FMD test 13 relies on dilation of small arteries and arterioles in the limbs, as a consequence of cuff-induced ischemia, to induce an increase in upstream conduit artery shear stress and dilation. In the context of these studies, it is conceivable that rapid and profound dilation of intracranial vessels in response to hypercapnia induces extracranial (ICA) dilation as a consequence of increased shear stress. The aim of this study was to identify whether hypercapnia induces shear-mediated dilation in the carotid arteries. Using high-resolution Duplex ultrasound combined with novel, edge-detection software, we assessed simultaneous common Abstract-Increases in arterial carbon dioxide tension (hypercapnia) elicit potent vasodilation of cerebral arterioles. Recent studies have also reported vasodilation of the internal carotid artery during hypercapnia, but the mechanism(s) mediating this extracranial vasoreactivity are unknown. Hypercapnia increases carotid shear stress, a known stimulus to vasodilation in other conduit arteries. To explore the hypothesis that shear stress contributes to hypercapnic internal carotid dilation in humans, temporal changes in internal and common carotid shear rate and diameter, along with changes in middle cerebral artery velocity, were simultaneously assessed in 18 su...

Whole night sleep architecture is not affected by evening exercise alone or when followed by CWI.

This study subjectively assessed sleep quality and quantity, state anxiety and electronic device use during a 7-day training week (TRAIN) and a 7-day competitive tournament (COMP). Eight state-level netball players used wrist-watch actigraphy to provide indirect sleep measures of bedtime, wake time, sleep duration, sleep onset latency, sleep efficiency, wake after sleep onset and fragmentation index. State anxiety was reported using the anxiety sub-scale in the Profile of Mood States-Adolescents. Before bed duration of electronic device use and the estimated time to sleep after finishing electronic device use was also recorded. Significant main effects showed that sleep efficiency (p = 0.03) was greater in COMP as compared to TRAIN. Furthermore, the bedtime and wake time were earlier (p = 0.01) during COMP. No further differences existed between conditions (p > 0.05). However, strong negative associations were seen between state anxiety and the sleep quality rating. Here, sleep efficiency was likely greater in COMP due to the homeostatic need for recovery sleep, resulting from the change in environment from training to competition. Furthermore, an increased anxiety before bed seems to influence sleep quality and should be considered in athletes portraying poor sleep habits.

This study examined the effect of early evening high-intensity training on the sleep of elite male youth soccer players (n = 12) using wrist actigraphy. High-intensity training (TRAIN) nights were compared with a home environment (HOME) condition, created by averaging sleep variables on the night before and after TRAIN nights. Additionally, after TRAIN athletes alternately used cold water immersion (TRAIN+CWI) or none, to assess whether cold water immersion (CWI) had any impact on sleep quality and quantity. Ratings of perceived exertion, fatigue and recovery were recorded after training. Actigraphy sleep measures were bedtime, wake time, sleep duration, sleep onset latency, sleep efficiency and wake after sleep onset. Self-rated scores of sleepiness at bedtime and wake, plus overall sleep quality were also recorded. Only fatigue ratings were higher in TRAIN compared to TRAIN+CWI at bedtime, there were no other differences in training data. Both TRAIN and TRAIN+CWI conditions had significant later (07:45 ± 1:09 h p < 0.01 and 07:34 ± 1:20 h p = 0.01) wake times than HOME (06:44 ± 0:41 h). The TRAIN condition had a significantly higher (7 ± 2; p < 0.01) rating of sleepiness at bedtime compared to HOME (6 ± 1), but no further differences were found in any of the sleep (actigraphy and self-reported) measures. Across all conditions, time spent asleep was ∼7:30 (±0:52) h:min and sleep efficiency was ∼89% (±6.1). In conclusion, early evening high-intensity training had no impact on subsequent sleep quality and quantity, nor was there any effect on sleep after performing CWI post-training.