Elisa Robey

Sleep quantity and quality in elite youth soccer players: A pilot study

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.

Sleep, anxiety and electronic device use by athletes in the training and competition environments

Abstract 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.

Sleep patterns and injury occurrence in elite Australian footballers

OBJECTIVES To examine the potential relationship between sleep duration and efficiency and injury incidence in elite Australian footballers. DESIGN Prospective cohort study. METHODS Australian footballers (n=22) from one AFL club were studied across the 2013 competitive season. In each week sleep duration and efficiency were recorded via actigraphy for 5 nights (the 3 nights preceding a game, the night of the game and the night after the game). Injury incidence was monitored and matched with sleep data: n=9 players suffered an injury that caused them to miss a game. Sleep in the week of the injury (T2) was compared to the average of the previous 2 weeks (T1). A two-way repeated measures ANOVA was used to determine any effect of sleep duration and efficiency on injury. Significance was accepted at p<0.05. RESULTS Injury incidence was not significantly affected by sleep duration, sleep efficiency or a combination of these factors. Analysis of individual nights for T2 versus T1 also showed no differences in sleep quality or efficiency. However, a main effect for time was found for sleep duration and efficiency, with these being slightly, but significantly greater (p<0.05) at T2 (437±61min and 82±7%) than T1 (414±64min and 79±7%). CONCLUSIONS No significant effect of sleep duration and efficiency on injury occurrence was found in elite Australian footballers.

Effect of postexercise recovery procedures following strenuous stair-climb running.

This study compared the effects of hot/cold water immersion, static stretching, and no recovery (control) interventions on leg strength, rowing performance, and indicators of muscle soreness/damage in the 72 hours following strenuous stair-climb running. Club (n = 14) and elite (Sports Institute) (n = 6) rowers performed the training run on three separate occasions. After each run, participants completed a randomly assigned 15-minute recovery treatment, either hot/cold, static stretching, or control, which were repeated at 24 and 48 hours postrun. No significant strength or performance differences existed between the three recovery treatments for either group. Muscle soreness for both groups remained significantly elevated (p < 0.05) above baseline at 72 hours postrun. At 48-hours postrun serum creatine kinase levels had returned to baseline and at 72 hours postrun were below baseline in both groups. In conclusion, neither hot/cold nor static stretching accelerated recovery at 72 hours beyond that achieved by the control condition.

Evidence for Shear Stress–Mediated Dilation of the Internal Carotid Artery in Humans

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 subjects at rest and during hypercapnia (6% carbon dioxide). Middle cerebral artery velocity increased significantly (69±10–103±17 cm/s; P<0.01) along with shear in both the internal (316±52–518±105 1/s; P<0.01) and common (188±40–275±61 1/s; P<0.01) carotids. Diameter also increased (P<0.01) in both carotid arteries (internal: +6.3±2.9%; common: +5.8±3.0%). Following hypercapnia onset, there was a significant delay between the onset of internal carotid shear (22±12 seconds) and diameter change (85±51 seconds). This time course is associated with shear-mediated dilation of larger conduit arteries in humans. There was a strong association between change in shear and diameter of the internal carotid (r=0.68; P<0.01). These data indicate, for the first time in humans, that shear stress is an important stimulus for hypercapnic vasodilation of the internal carotid artery. The combination of a hypercapnic stimulus and continuous noninvasive, high-resolution assessment of internal carotid shear and dilation may provide novel insights into the function and health of the clinically important extracranial arteries in humans.

Effect of Evening Postexercise Cold Water Immersion on Subsequent Sleep

PURPOSE This study investigated the effect of cold water immersion after evening exercise on subsequent sleep quality and quantity in trained cyclists. METHODS In the evenings (~1900 h) on three separate occasions, male cyclists (n = 11) underwent either no exercise (control, CON), exercise only (EX), or exercise followed by cold water immersion (CWI). EX comprised cycling for 15 min at 75% peak power, then a 15-min maximal time trial. After each condition, a full laboratory-based sleep study (polysomnography) was performed. Core and skin temperature, heart rate, salivary melatonin, ratings of perceived fatigue, and recovery were measured in each trial. RESULTS No differences were observed between conditions for any whole night sleep measures, including total sleep time, sleep efficiency, sleep onset latency, rapid eye movement onset latency, wake after sleep onset, or proportion of the night spent in different sleep stages. Core temperature in EX and CWI trials was higher than CON, until it decreased below that of EX and CON until bedtime in CWI. After bedtime, core temperature was similar for all conditions throughout the night, except for a 90-min period where it was lower for CWI than EX and CON (3.5-4.5 h postexercise). Heart rates for EX and CWI were both significantly higher than CON postexercise until bedtime, whereas skin temperature after CWI was significantly lower than EX and CON, remaining lower than EX until 3 h postexercise. Melatonin levels and recovery ratings were similar between conditions. Fatigue ratings were significantly elevated after exercise in both CWI and EX conditions, with EX still being elevated compared with CON at bedtime. CONCLUSION Whole night sleep architecture is not affected by evening exercise alone or when followed by CWI.

Relationship between monocyte‐platelet aggregation and endothelial function in middle‐aged and elderly adults

Low‐grade inflammation, endothelial dysfunction, and platelet hyper‐reactivity to agonists are associated with an increased risk of cardiovascular events. In vitro and animal studies infer an inverse mechanistic relationship between platelet activation and the production of endothelium‐derived nitric oxide and prostacyclin. This concept is supported by evidence of an inverse relationship between endothelial function and platelet activation in high‐risk cardiac patients. The aim of this study was to investigate what relationship, if any, exists between platelet and endothelial function in healthy, middle‐aged, and elderly adults. In 51 participants (18 male, 33 post menopausal female), endothelial function was assessed by flow‐mediated dilation (FMD). Platelet function was assessed by flow cytometric determination of glycoprotein IIb/IIIa activation (measured by PAC‐1 binding), granule exocytosis (measured by surface P‐selectin expression), and monocyte‐platelet aggregates (MPAs), with and without stimulation by canonical platelet agonists adenosine diphosphate (ADP), arachidonic acid (AA), and collagen. Correlation analysis indicated there was no significant (all P => 0.05) relationship between FMD and any marker of in vivo platelet activation (MPAs R = 0.193, PAC‐1 R = −0.113, anti‐CD62P R = −0.078) or inducible platelet activation by ADP (MPA R = −0.128, anti‐CD62P R = −0.237), AA (MPA R = −0.122, PAC‐1 R = −0.045, anti‐CD62P R = −0.142), or collagen (MPA R = 0.136, PAC‐1 R = 0.174, anti‐CD62P R = −0.077). Our findings contrast with two previous studies performed in high‐risk cardiac patients, which reported inverse relationships between platelet activation and endothelial function, suggesting that some compensatory redundancy may exist in the relationship between platelet and endothelial function in preclinical populations.

Impact of commonly prescribed exercise interventions on platelet activation in physically inactive and overweight men

The exercise paradox infers that, despite the well‐established cardioprotective effects of repeated episodic exercise (training), the risk of acute atherothrombotic events may be transiently increased during and soon after an exercise bout. However, the acute impact of different exercise modalities on platelet function has not previously been addressed. We hypothesized that distinct modalities of exercise would have differing effects on in vivo platelet activation and reactivity to agonists which induce monocyte‐platelet aggregate (MPA) formation. Eight middle‐aged (53.5 ± 1.6 years) male participants took part in four 30 min experimental interventions (aerobic AE, resistance RE, combined aerobic/resistance exercise CARE, or no‐exercise NE), in random order. Blood samples were collected before, immediately after, and 1 h after each intervention, and incubated with one of three agonists of physiologically/clinically relevant pathways of platelet activation (thrombin receptor activating peptide‐6 TRAP, arachidonic acid AA, and cross‐linked collagen‐related peptide xCRP). In the presence of AA, TRAP, and xCRP, both RE and CARE evoked increases in MPAs immediately post‐exercise (P < 0.01), whereas only AA significantly increased MPAs immediately after AE (P < 0.01). These increases in platelet activation post‐exercise were transient, as responses approached pre‐exercise levels by 1 h. These are the first data to suggest that exercise involving a resistance component in humans may transiently increase platelet‐mediated thrombotic risk more than aerobic modalities.

Beneficial impacts of regular exercise on platelet function in sedentary older adults: Evidence from a randomized 6-month walking trial

Platelet activation, including the formation of monocyte platelet aggregates (MPAs), contributes to atherosclerosis, thrombus formation, and acute coronary syndromes. Regular participation in exercise can lower cardiovascular risk, but little is known regarding the impact of exercise training on platelet function. We investigated the effect of 6 mo of walking exercise on platelet function in sedentary older adults without significant cardiovascular disease. Twenty-seven participants were randomly allocated to 6 mo of either: no-exercise ( n = 13) or 3 × 50 min/wk of supervised center-based walking ( n = 14). Circulating and agonist-induced MPAs were assessed using flow cytometry before [ month 0 (0M)] and after [ month 6 (6M)] the intervention. Circulating MPAs increased from 0M (3.7 ± 1.0%) to 6M (4.7 ± 1.6%) in the no-exercise group ( P = 0.009), whereas a nonsignificant decrease was observed in the walking group (0M 4.3 ± 1.7 vs. 6M 3.7 ± 1.2 %, P = 0.052). The change in MPAs between groups was significant ( P = 0.001). There were no differences between groups in platelet responses to agonists across the interventions (all P > 0.05). Collectively, these data suggest that the absence of regular exercise may increase MPAs, which are cellular mediators involved in atherosclerosis, while regular walking inhibits such increases. The thrombotic function of platelets appears to be relatively unaltered by exercise training. This study provides novel data related to the cardioprotective effects associated with participation in exercise. NEW & NOTEWORTHY Monocyte-platelet aggregates contribute to atherosclerosis and exercise can lower cardiovascular risk. This is the first study to discover that a lack of regular physical activity is associated with increased monocyte-platelet aggregates over a 6-mo intervention period. In contrast, walking exercise inhibits increased monocyte-platelet aggregates in the circulation. This study highlights a novel pathway by which regular participation in exercise exerts its cardioprotective effects.

Acute Impact of Different Exercise Modalities on Arterial and Platelet Function

Purpose Acute coronary syndromes and ischemic stroke are associated with arterial events involving platelets, the endothelium, and atherosclerosis. Although regular physical activity is associated with lower risk of cardiovascular events and mortality, risk is transiently increased during and immediately after participation in an acute bout of exercise. No previous study has investigated the acute impact of exercise on platelet activation and arterial function in the same participants; it is also unknown if responses are dependent on exercise modality. We hypothesized that commonly adopted, yet physiologically distinct, modalities of exercise (“aerobic” vs “resistance”) have differing effects on in vivo platelet activation and conduit artery diameter. Methods Eight apparently healthy middle-age (53.5 ± 1.6 yr) male subjects took part in four 30-min experimental interventions (aerobic exercise, resistance exercise, combined aerobic/resistance exercise, or no-exercise), in random order. Blood samples were collected, and the measurement of brachial artery diameter by ultrasound was performed before, immediately after, and 1 h after each intervention. Platelet activation was determined by the positive binding of antibodies to surface receptors exposed on activated platelets (anti-CD62P and PAC-1). Results Brachial artery diameter increased immediately after all three exercise modalities (P < 0.001) and remained above preexercise levels 1 h after resistance exercise and after combined aerobic/resistance exercise. No changes were observed in markers of in vivo platelet activation with any experimental protocol. Conclusions These data suggest that postexercise enhancement in arterial function may mitigate the acute impact of exercise on platelet activation.