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Effects of sleep deprivation on performance during submaximal and maximal exercise

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Abstract

The effect of 42 h sleep deprivation on selected cardiorespiratory, metabolic, and psychological measures was studied in eight healthy volunteers. Exercise was performed on a bicycle ergometer at constant work loads requiring 25%, 50%, 75%, and 100% of the V̇O2max before and after sleep loss. During exercise after sleep loss work time to exhaustion was reduced by an average of 7.7% (p < 0.05). Heart rate was significantly reduced after sleep loss during rest, exercise, and recovery conditions (p < 0.05). Exercise at work loads requiring 50% and 75% of V̇O2max resulted in significantly greater RPE after sleep loss (p < 0.05). Despite no alteration in submaximal exercise V̇(E), V̇O2 and V̇CO2 after sleep loss (p < 0.05), measures of maximal V̇(E), V̇O2, and V̇CO2 were significantly reduced (p < 0.05).

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... La privation de sommeil diminue l'endurance de 3 à 22 % dans des exercices corps entier comme la marche, la course ou le vélo (94)(95)(96)(97)(98)(99)(100)(101)(102). Selon les études, il existe (96,99,(103)(104)(105) ou non (94,101,106) une altération du VO2 max après une privation de sommeil aiguë. La privation de sommeil, ne modifie pas la fréquence cardiaque maximale, le quotient respiratoire ou la saturation artérielle en oxygène (101). ...
... L'altération du VO2 max après privation de sommeil n'est pas systématiquement retrouvée dans la littérature (94,96,99,101,(103)(104)(105)(106). En revanche, les épreuves d'endurance de marche ou de pédalage réalisées à charge constante et élevée (> 75 % de la puissance maximale aérobie), montrent une diminution de l'endurance sans modification du VO2 (94,95). ...
... Ces afférences musculaires peuvent inhiber la commande motrice soit par rétrocontrôle central (activation thalamique et insulaire) (165)(166)(167), soit par réflexe rachidien projetant sur le motoneurone et diminuant sa fréquence de décharge (93,162). Or, la privation de sommeil augmente la perception de l'effort musculaire périphérique modéré à important (50 et 75 % du VO2 max) et respiratoire (94,96,103,106). ...
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Introduction : En réanimation, le sommeil est déstructuré, fragmenté et non réparateur. Ce mauvais sommeil est associé à une augmentation de la morbi-mortalité et de la durée du sevrage de la ventilation mécanique. Le sevrage ventilatoire est une période critique qui se complique dans 15% des cas. Les échecs de sevrage ventilatoire ont une physiopathologie complexe et le mauvais sommeil pourrait être impliqué en diminuant l’autonomie respiratoire des patients. Objectifs : (1) Evaluer l’impact de la privation de sommeil sur l’endurance musculaire inspiratoire et manuelle ; (2) Explorer les mécanismes physiologiques en cause chez le sujet sain ; (3) Evaluer chez le patient de réanimation la pertinence des mécanismes mis en évidence chez le sujet sain et proposer des mesures protectrices du sommeil en réanimation. Matériel et Méthodes : Chez le sujet sain, ce travail de thèse a comparé l’endurance inspiratoire et manuelle après sommeil normal et après privation aiguë de sommeil, en explorant la commande cérébrale musculaire, le muscle squelettique et les afférences musculaires. Chez le patient de réanimation, la commande cérébrale inspiratoire a été comparée entre les patients réussissant et les patients échouant leur sevrage ventilatoire. Enfin, la capacité d’un algorithme à distinguer les états de veille et de sommeil des patients de réanimation a été évaluée.Résultats : Une privation aiguë de sommeil diminuait l’endurance inspiratoire de 50% et manuelle de 11% chez des hommes sains. Cette perte d’endurance musculaire était associée à une altération de la commande musculaire corticale prémotrice et à une augmentation de la dyspnée et des afférences motrices pour un effort équivalent. Chez les patients de réanimation, une augmentation de 0,425 µV d’amplitude des potentiels prémoteurs inspiratoires prédisait l’échec de sevrage ventilatoire avec une sensibilité de 100% et une spécificité de 87%. L’analyse automatique de polysomnographies de réanimation par un algorithme de détection automatique du sommeil était bien corrélée à la lecture humaine. Conclusions : Lors d’un exercice, la privation aiguë de sommeil entraine une augmentation des afférences musculaires, inhibant la commande prémotrice corticale et réduisant l’endurance des muscles striés squelettiques. La mesure des potentiels prémoteurs inspiratoires prédit efficacement l’échec de sevrage ventilatoire d’un patient intubé. Ainsi, le mauvais sommeil nuit au sevrage ventilatoire des patients. Mais la détection en direct du sommeil de ces patients ouvre la voie à une protection du sommeil tout au long du nycthémère.
... In two studies, mean and standard deviation were calculated (Excel, Microsoft, USA) based on individual data presented in the full text (Holland, 1968;Martin, 1981). In one study (Bond et al., 1986), endurance performance data were extracted from the graph in triplicate using an online tool (Web Plot Digitizer, Version 4.1, USA). The average of three extractions was retained for analysis. ...
... The mechanisms that underlie the deleterious effect of sleep deprivation on endurance performance were not within the present study's aims. However, we noted that sleep deprivation caused either no change (Azboy & Kaygisiz, 2009;Konishi et al., 2013;Omiya et al., 2009;Rae et al., 2017;Vaara et al., 2018) or a decrease (Bond et al., 1986;Chen, 1991;Mougin et al., 1991;Omiya et al., 2009;Plyley et al., 1987;Tanabe et al., 1998;Tanabe et al., 1999) in aerobic parameters associated with endurance performance, such as the anaerobic threshold and V̇O 2 max. One possible explanation for such decrease might be the macro-and micro-endothelial dysfunction generated by sleep deprivation (Holmer et al., 2021), which could compromise the oxygen delivery to skeletal muscle and, consequently, the aerobic energy supply during exercise (Chen, 1991;Vaara et al., 2018). ...
... One possible explanation for such decrease might be the macro-and micro-endothelial dysfunction generated by sleep deprivation (Holmer et al., 2021), which could compromise the oxygen delivery to skeletal muscle and, consequently, the aerobic energy supply during exercise (Chen, 1991;Vaara et al., 2018). Moreover, we also noted that eight out of 10 studies that measured perceived effort reported a sleep deprivation-increasing effect (Bond et al., 1986;Martin, 1981;Oliver et al., 2009;Plyley et al., 1987;Roberts et al., 2019aRoberts et al., , 2019bRodrigues et al., 2021;Souissi et al., 2020b;Temesi et al., 2013;Vaara et al., 2018). Such observation suggests that sleep deprivation might alter mechanisms specifically involved in the perceived effort formation. ...
Article
We conducted a systematic review and meta-analysis to investigate the effect of sleep deprivation on endurance performance, as well as possible effect-modifying factors. Searches were done in Pubmed, Web of Science, Embase, and Scopus on 12 July 2022. We additionally searched the bibliographic references and citations on Google Scholar of the papers whose full text was analyzed. Eligible studies were randomized and non-randomized controlled trials that compared sleep deprivation and habitual-sleep night effects on endurance performance in healthy humans. The studies’ quality was examined by the Cochrane Collaboration’s risk of bias tool. We calculated the pooled standardized mean differences (pooled SMD) and 95% confidence interval (95%CI) by a random-effects model. A mixed-effects model analyzed subgroups. Thirty-one studies were analyzed (n = 478), generating 38 effect sizes in full. The overall risk of bias was low in 8% of the studies, unclear in 74%, and high in 18%. Sleep deprivation in general had a moderate negative effect on endurance performance (polled SMD [95%CI] = -0.52 [-0.67; -0.38]). Training status, sleep deprivation magnitude, assessment time, exercise mode, and endpoint type did not influence the sleep deprivation effect, whereas longer exercises (>30 min) were more affected by sleep deprivation than shorter ones (P = 0.035). Therefore, the available evidence supports that sleep deprivation's deleterious effect on endurance performance is of moderate size and depends on exercise duration. This information can be useful to estimate the performance decrement of endurance exercise practitioners under sleep deprivation in training routines and competitions. PROSPERO registration number CRD42021229717.
... 24-36 h of sleep loss)), such as heart rate, oxygen uptake, ventilation and respiratory exchange ratio (Azboy & Kaygisiz, 2009;Martin & Haney, 1982;Martin, 1981;Mougin et al., 1989Mougin et al., , 1991Oliver et al., 2009;Plyley et al., 1987) and in thermoregulatory function (Dewasmes et al., 1993;Oliver et al., 2009;Sawka et al., 1984) . Different experiments have also shown that decrements in endurance exercise performance might be associated with increments in ratings of perceived exertion during time to exhaustion tests at constant intensities and steady state exercises (Bond et al., 1986;Martin, 1981;Martin & Gaddis, 1981;Symons et al., 1988;Temesi et al., 2013) , more specifically at high intensities rather than low intensities (Martin & Gaddis, 1981) . Moreover, despite significant decrements in the distance covered during a 30-min self-paced run following 30 h of sleep deprivation, no differences in ratings of perceived exertion have been found (Oliver et al., 2009) indicating that perception of effort would have been higher if running speeds were equal. ...
... Moreover, the reasons why SD might negatively affect endurance exercise performance are also still unclear. Several findings have shown significant negative effects on RPE (Bond et al., 1986;Martin, 1981;Martin & Gaddis, 1981;Oliver et al., 2009;Symons et al., 1988;Temesi et al., 2013) and no evident cardio-respiratory parameters alterations following SD (Azboy & Kaygisiz, 2009;Martin & Haney, 1982;Martin, 1981;Mougin et al., 1989Mougin et al., , 1991Oliver et al., 2009;Plyley et al., 1987) , suggesting that perception of effort might be the limiting factor of endurance exercise performance during a sleep-deprived state (Temesi et al., 2013 1996; Drummond et al., 2006;Lorenzo et al., 1995;Rosa et al., 1983;Rupp et al., 2009;Wesensten et al., 2005b) . However, the effects of recovery sleep on endurance exercise performance following SD have never been tested as yet. ...
... Sleep deprivation is a mentally fatiguing condition characterized by continuous and prolonged lack of sleep (Ackerman, 2011;Boonstra et al., 2007;Jones & Harrison, 2001) , which is very common in ultra-endurance sporting disciplines. Although findings in the literature are still controversial (Fullagar et al., 2015) , it has been demonstrated that sleep deprivation also negatively affects both, perception of effort and endurance exercise performance (Bond et al., 1986;Martin, 1981;Martin & Gaddis, 1981;Oliver et al., 2009;Symons et al., 1988;Temesi et al., 2013) . At present, stimulants such as caffeine (McLellan et al., 2004b;McLellan et al., 2007) and modafinil (Wesensten et al., 2002), as well as naps (Blanchfield et al., 2018;Waterhouse et al., 2007) bouts of sleep deprivation (sleep deprivation training, SDT) to make the brain more resilient to the negative effects of sleep deprivation on perception of effort and endurance exercise performance. ...
Thesis
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Mental fatigue and sleep deprivation are two common conditions in our modern societies, affecting millions of healthy people. Whereas mental fatigue is considered a psychobiological state caused by prolonged and demanding cognitive activities, sleep deprivation can be defined as a brain state caused by at least 24 hours of wakefulness. The first aim of this thesis was to investigate the acute effects of mental fatigue, sleep deprivation and subsequent recovery sleep on endurance exercise performance. The second aim was to evaluate the effects of two innovative training interventions, Brain Endurance Training (BET) and Sleep Deprivation Training (SDT) on endurance performance. It was hypothesized that: 1) 50-min of mentally-demanding cognitive task and 25-h of sleep deprivation would impair endurance performance and that the following night of recovery sleep would be enough to restore rested endurance performance; 2) six weeks of BET (alone) and six weeks of SDT (combined with physical training) would improve endurance performance. The first and second study do not provide reliable evidence that mental fatigue and sleep deprivation reduce endurance performance during a half-marathon and a 20-min cycling time trial, respectively. However, an alternative statistical analysis used in study one, suggests that the hypothesis that mental fatigue is harmful cannot be rejected. The third study shows that BET is not effective in physically-inactive males. The fourth study reveals that SDT in combination with physical training might be beneficial to counteract the effects of sleep deprivation on endurance performance. In conclusion, the findings do not provide statistical evidence of a negative effect of mental fatigue and sleep deprivation on endurance performance. However, it might be prudent to avoid them prior to races. The use of BET alone does not enhance endurance performance. Nonetheless, the combination of SDT with a physical training program might be beneficial in preparation for an endurance/ultra-endurance event. Mental Fatigue and Sleep Deprivation: Effects, Mechanisms, and Countermeasures in Endurance Exercise Performance.
... Collectively, the previous studies, assessing the effect of SD on aerobic performance, have shown a tendency to a decreased time to exhaustion in most (Martin, 1981;Martin and Chen, 1984;Chen, 1991;Azboy and Kaygisiz, 2009;Temesi et al., 2013) but not all studies (Goodman et al., 1989;Racinais et al., 2004). Moreover, indices of aerobic performance such as heart rate and respiratory parameters have shown more controversial findings both at submaximal and maximal levels (Martin, 1981;Martin and Gaddis, 1981;Martin and Chen, 1984;Bond et al., 1986;Plyley et al., 1987;Chen, 1991). A recent review concluded that although the results remain somewhat mixed, there is evidence suggesting that SD may induce detrimental effects on physical performance (Fullagar et al., 2015). ...
... Similar to the present study findings, an earlier study has shown time to exhaustion to be unchanged after 60-h SD (Goodman et al., 1989). However, some studies have shown reduced time (Martin, 1981;Martin and Chen, 1984;Bond et al., 1986;Chen, 1991;Azboy and Kaygisiz, 2009;Temesi et al., 2013). Furthermore, previous studies have observed contradictory findings in maximal VO 2, ventilation and RER in regard to maximal aerobic performance after SD showing either decreases (Bond et al., 1986;Plyley et al., 1987;Chen, 1991) or no changes (Martin and Gaddis, 1981;Goodman et al., 1989). ...
... However, some studies have shown reduced time (Martin, 1981;Martin and Chen, 1984;Bond et al., 1986;Chen, 1991;Azboy and Kaygisiz, 2009;Temesi et al., 2013). Furthermore, previous studies have observed contradictory findings in maximal VO 2, ventilation and RER in regard to maximal aerobic performance after SD showing either decreases (Bond et al., 1986;Plyley et al., 1987;Chen, 1991) or no changes (Martin and Gaddis, 1981;Goodman et al., 1989). In addition, no change in maximal heart rate was observed in the present study, which is in line with some earlier studies (Plyley et al., 1987;Goodman et al., 1989) and contradictory to the other ones (Martin and Gaddis, 1981;Bond et al., 1986;Chen, 1991). ...
Article
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The effect of 60-h sleep deprivation (SD) on physical performance and motor control was studied. Twenty cadets were measured for aerobic performance (VO2) before and immediately after the SD period. Maximal strength and EMG of the knee extensor muscles were measured before and after 60 h of SD. Balance, reaction times and motor control were assessed every evening and morning during the SD period. Main effects were observed for heart rate (p = 0.002, partial eta squared: 0.669), VO2 (p = 0.004, partial eta squared: 0.621), ventilation (p = 0.016, partial eta squared: 0.049), and lactate concentration (p = 0.022, partial eta squared: 0.501), whereas RER remained unaltered (p = 0.213, partial eta squared: 0.166). Pairwise comparisons revealed decreased values at submaximal loads in heart rate, VO2, ventilation (all p < 0.05) but not in RER, whereas all of their respective maximal values remained unchanged. Moreover, pairwise comparisons revealed decreased lactate concentration at maximal performance but only at 8-min time point during submaximal workloads (p < 0.05). Pairwise comparisons of maximal strength, EMG and rate of force development revealed no change after SD. Main effects were observed for motor and postural control, as well as for reaction times (all p < 0.05), whereas pairwise comparison did not reveal a consistent pattern of change. In conclusion, motor control can mostly be maintained during 60-h SD, and maximal neuromuscular and aerobic performances are unaffected. However, submaximal cardiorespiratory responses seem to be attenuated after SD.
... However, it was shown that when the sleep schedule changes, it indirectly affects on athletic performance. But the results of research done in this case has less integrity and often are contradictory (Bond et al., 1986Hill. 1992Holland., 1986Johnson., 1982. ...
... ct of sleep deprivation on athletic performance, often have been less studied. However, it was shown that when the sleep schedule changes, it indirectly affects on athletic performance. But the results of research done in this case has less integrity and often are contradictory (Bond et al., 1986Hill. 1992Holland., 1986Johnson., 1982. For example, (Bond. 1986) demonstrated that sleep deprivation reduces maximum oxygen consumption, while Martin and Gdys (Hill., 1992) stated that there are no changes in VO2 following sleep deprivation (Bryant et al., 1992). In addition, most previous studies have shown that heart rate at a given workload by sleep deprivation is not affected (Hill., 1992Holland ...
... 86) demonstrated that sleep deprivation reduces maximum oxygen consumption, while Martin and Gdys (Hill., 1992) stated that there are no changes in VO2 following sleep deprivation (Bryant et al., 1992). In addition, most previous studies have shown that heart rate at a given workload by sleep deprivation is not affected (Hill., 1992Holland., 1986. (Bond. 1986) reported that heart rate after sleep deprivation decreases. These differences can result from different research methods, including sleep deprivation period, measuring techniques and training methods, so the investigation can add some information about the effect of sleep on performance. Another test, on six patients, sleep deprivation ...
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The aim of this study is to determine the effect of sleep deprivation on the dribbling skills of football players. To this end, 22 students of Sahand University, with age range (20-24 years) performed dribbling skill in the pre-test and post test stages. In this study to assess this skill, the test "Mor - Christian" has been used. In the first step, subjects conducted the dribble test as pre-test after 8 hours sleep a night. 10 days later, to ensure the validity of tests and test results on the learning effect, subjects did the same test again after 8 hours sleep a night. In the third stage, 36 hours of sleep deprivation as an independent variable imposed on the subjects and then the test was repeated and experimental test results were compared as recorded using paired t-test. The findings showed that 36 hour sleep deprivation decreases dribble implementation skills (p
... (Martin 1981;Martin & Gaddis 1981;Horne & Pettit 1984;McMurray & Brown 1984;Scott & McNaughton 2004) Maksimihengityskaasuarvot pysyivät muuttumattomina tässä tutkimuksessa. Aikaisemmissa tutkimuksissa on saatu ristiriitaisia tuloksia maksimi hengitysmuuttujien suhteen niiden joko kasvaessa (Chen 1991), pysyessä samoina (Goodman 1989) tai laskiessa (Bond;Plyley ym. 1987) Hengityskaasujen keskiarvoparametreissa hapenoton suhteelliset ja absoluuttiset arvot laskivat merkitsevästi. ...
... (1987) 64 tunnin valvomisjakson tuloksiin. Toisaalta maksimisykkeen on raportoitu myös laskevan (Martin & Gaddis 1984;Bond 1986;Chen 1991 (Weinberg & Gould 2003, 351-364). Tämän takia submaksimaalisilla kuormilla ei ole tehty kuin vain ja ainoastaan tarvittava määrä työtä kutakin kuormaa kohden. ...
... Tulokset ovat ristiriidassa aikaisempien tutkimusten kanssa, joissa suoritusajat ovat yleisesti laskeneet (Martin 1981;Martin & Gaddis 1981;Home & Pettit 1984;McMurray & Brown 1984;Scott & McNaughton, Chen 1991 (Bond 1986;Plyley 1987, Myles;Martin 1981). RPE-arvioiden pysyminen muuttumattomina valvomisjakson jälkeen vot johtua polkupyöräergometrissä käytetystä testiprotokollasta. ...
... Muitos atletas têm a visão de que a perda ou interrupção do sono é um fator que contribui para o seu fracasso no esporte. A maioria dos estudos que investigaram os efeitos da privação do sono no desempenho físico, focaram primariamente, seus efeitos no desempenho aeróbio submáximo (56)(57)(58)(59) e no consumo máximo de oxigênio (58,60,61) . Outras pesquisas examinaram as respostas neurológicas (62) e a força anaeróbia de indivíduos privados de sono (57,58,60) . ...
... A maioria dos estudos que investigaram os efeitos da privação do sono no desempenho físico, focaram primariamente, seus efeitos no desempenho aeróbio submáximo (56)(57)(58)(59) e no consumo máximo de oxigênio (58,60,61) . Outras pesquisas examinaram as respostas neurológicas (62) e a força anaeróbia de indivíduos privados de sono (57,58,60) . ...
... Os trabalhos que envolveram um período de privação de 30 horas (63,64) até 60 horas (59) não encontraram modificações evidentes. No entanto, o estudo de Bond e colaboradores (57) (1986) encontrou diferenças menores em medidas de ventilação, VCO 2 e VO 2 nos sujeitos privados de sono por 42 horas, quando comparados aos controles nãoprivados, sugerindo, que para uma eficiência máxima do exercício em intensidades acima de 75% do VO 2 máx deveria ser precedido por uma boa noite de sono. A partir desse trabalho houve um consenso entre os pesquisadores de que a privação de sono seria capaz de provocar um pequeno efeito ou até mesmo nenhum, no desempenho aeróbio. ...
Article
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Sleep deprivation can be defined as total or partial suppress of sleep and is associated with alterations in endocrine, metabolic, physical, cognitive functions and modifications of the sleep patterns that compromise health and quality of life. Physical exercise is associated with improvement of cardiovascular, respiratory, muscular, endocrine and nervous system, and a better sleep quality. However, the association of these two conditions is unclear, partly due to the difficulty to obtain volunteers to participate in this type of protocol with no financial compensation. The majority of the studies which investigate the association between physical exercises and sleep deprivation focus on aerobic performance and verify little or no effect of this parameter. Concerning anaerobic power and strength, significant alterations have not been found; however, for prolonged events there may be an interaction between these two factors, which suggests a protection mechanism. Nevertheless, it is important to consider that one of the main alterations caused by sleep deprivation the increase of the subjective perception, which presents a factor to decrease and compromise the physical performance per se, and may represent a masking element of the deleterious effects of sleep deprivation. Thus, the aim of present review is to discuss the different aspects of relationship between physical exercise and sleep deprivation, showing their effects and consequences in physical performance.
... Collectively, the previous studies, assessing the effect of SD on aerobic performance, have shown a tendency to a decreased time to exhaustion in most (Martin, 1981;Martin and Chen, 1984;Chen, 1991;Azboy and Kaygisiz, 2009;Temesi et al., 2013) but not all studies (Goodman et al., 1989;Racinais et al., 2004). Moreover, indices of aerobic performance such as heart rate and respiratory parameters have shown more controversial findings both at submaximal and maximal levels (Martin, 1981;Martin and Gaddis, 1981;Martin and Chen, 1984;Bond et al., 1986;Plyley et al., 1987;Chen, 1991). A recent review concluded that although the results remain somewhat mixed, there is evidence suggesting that SD may induce detrimental effects on physical performance (Fullagar et al., 2015). ...
... Similar to the present study findings, an earlier study has shown time to exhaustion to be unchanged after 60-h SD (Goodman et al., 1989). However, some studies have shown reduced time (Martin, 1981;Martin and Chen, 1984;Bond et al., 1986;Chen, 1991;Azboy and Kaygisiz, 2009;Temesi et al., 2013). Furthermore, previous studies have observed contradictory findings in maximal VO 2, ventilation and RER in regard to maximal aerobic performance after SD showing either decreases (Bond et al., 1986;Plyley et al., 1987;Chen, 1991) or no changes (Martin and Gaddis, 1981;Goodman et al., 1989). ...
... However, some studies have shown reduced time (Martin, 1981;Martin and Chen, 1984;Bond et al., 1986;Chen, 1991;Azboy and Kaygisiz, 2009;Temesi et al., 2013). Furthermore, previous studies have observed contradictory findings in maximal VO 2, ventilation and RER in regard to maximal aerobic performance after SD showing either decreases (Bond et al., 1986;Plyley et al., 1987;Chen, 1991) or no changes (Martin and Gaddis, 1981;Goodman et al., 1989). In addition, no change in maximal heart rate was observed in the present study, which is in line with some earlier studies (Plyley et al., 1987;Goodman et al., 1989) and contradictory to the other ones (Martin and Gaddis, 1981;Bond et al., 1986;Chen, 1991). ...
... Heart rate has been reported either to decrease or to be unaVected by SD (Bond et al. 1986;Burgess et al. 1997;Holmes et al. 2002;Chen 1991;Kato et al. 2000;Ogawa et al. 2003;Zhong et al. 2005). However, very few studies have examined the association between SD and cardiovascular regulation. ...
... Previous studies have reported that HR either decreases or is unaVected by SD (Bond et al. 1986; Burgess et al. 1997; Holmes et al. 2002;Chen 1991;Kato et al. 2000;Ogawa et al. 2003). In the present study, HR decreased during SD. ...
... In the present study, HR decreased during SD. Similarly, Holmes et al. (2002) and Chen (1991) reported a decrease in HR after 30 h of SD, and Bond et al. (1986) after 42 h of SD. Zhong et al. (2005) also reported that HR measured in a supine position decreased after 12 and 36 h of SD, as well as after 24 h in a seated position. ...
Article
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This study examined cardiovascular regulation and body temperature (BT) during 60 h of sleep deprivation in 20 young healthy cadets. Heart rate variability was measured during an active orthostatic test (AOT). Measurements were performed each day in the morning and evening after 2, 14, 26, 38, 50 and 60 h of sleep deprivation. In AOT, in the sitting and standing positions, heart rate decreased (P < 0.001), while high frequency and low frequency power increased (P < 0.05-0.001) during sleep deprivation. Body temperature also decreased (P < 0.001), but no changes were detected in blood pressure. In conclusion, the accumulation of 60 h of sleep loss resulted in increased vagal outflow, as evidenced by decreased heart rate. In addition, BT decreased during sleep deprivation. Thus, sleep deprivation causes alterations in autonomic regulation of the heart, and in thermoregulation.
... After 30 h of continuous wakefulness, Oliver et al. (29) observed a significant decrease in the total distance run in 30 min (6224 vs 6037 m) after 30 min submaximal running. These results are supported by other studies highlighting reduced times to exhaustion during incremental exercise protocols after TSD (3,7,9,39). Fewer studies have been conducted on the effect of TSD on short-term exercise performance (e.g., Wingate test and maximal strength), and the effects are equivocal. ...
... Motor performance and RPE. Our results are in agreement with the majority of studies showing decreased motor performance at submaximal intensity after a period of sleep deprivation (3,7,9,24,26,29,39). This impairment has been observed in various types of exercise such as cycling at constant submaximal intensity (24,26), in incremental tests (3,9), and in submaximal isometric single-joint exercise, as in the present study. ...
Article
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Purpose: To investigate the effects of 6 nights of sleep extension on motor performance and associated neuromuscular function before and after one night of total sleep deprivation (TSD). Methods: Twelve healthy men participated in two experimental conditions (randomized cross-over design): extended sleep (EXT, 9.8 ± 0.1 h time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed 6 nights of either EXT or HAB at-home followed by an assessment of motor performance and neuromuscular function at baseline (D0) and after one night of TSD, i.e. 34-37 h of continuous wakefulness (D1). Maximal voluntary contractions with superimposed femoral nerve electrical and transcranial magnetic stimulations and stimulations on relaxed muscles were investigated before and after submaximal isometric knee extensor exercises performed until task failure. Results: Time to exhaustion was longer in EXT compared to HAB (+3.9 ± 7.7% and +8.1 ± 12.3% at D0 and D1, respectively). Performance at D1 decreased from D0 similarly between conditions (-7.2 ± 5.6% and -3.7 ± 7.3% in HAB and EXT, respectively). At D1, the rating of perceived exertion during exercise was lower in EXT compared to HAB (-7.2 ± 7.5%) with no difference at D0. No difference was observed in voluntary activation between the two conditions. Conclusions: Six nights of sleep extension improved sustained contraction time to exhaustion and this result cannot be explained by smaller reductions in voluntary activation, measured by both nerve and transcranial magnetic stimulation. The beneficial effect on motor performance in the extended sleep condition was likely due to reduced ratings of perceived exertion after TSD.
... In most studies heart rates during submaximal exercises were unaffected by sedentary sleep deprivation: 24 hours of wakefulness and exercise at 80% of ¦O 2 max (2,3), 30 hours and 25, 50 and 75% of ¦O 2 max (4,5), 36 hours and 80% of ¦O 2 max (6), 50 hours and PWC160 (7) and 60 hours and 70% of ¦O 2 max (8). The decreased resting and exercise heart rates after sedentary sleep deprivation were also observed (9)(10)(11)(12)(13). The study with partial 3 hours of sleep deprivation which showed increased heart rate during exercise at intensity of 75% of ¦O 2 max (14) should also be mentioned. ...
... They used an incremental exercise test and recorded depressed heart rates during low and moderate intensities of exercise. Also Bond et al. reported lower heart rates during submaximal exercise (11). Regulation of heart rate is mostly governed by the autonomic nervous system and counterbalancing effects of its sympathetic and parasympathetic components. ...
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In contrast to the well known influence of isolated effects of long lasting exercise and sleep deprivation on physical performance there are few data on effect of those factors combined. Aim of the study was to evaluate the influence of 36 hours of exercise and sleep deprivation on selected physiological factors. Materials and methods. The study was conducted on 11 healthy volunteers at survival camp (age 19±1 (SE) yrs, BMI 21.5±0.7 kg·m-2 , ¦O 2 max 55±2 ml·kg-1 ·min-1). Entry measurements were done the day before the trial: posturography, re-ocardiography in horizontal position and submaximal exercise test (workload increased by 50W every 3 min to 200W). First day of the trial started at 6 AM with gymnastics, followed by running and cycling; overnight there was a mountain trekking lasting 9 hrs; on the second day there was a military training and cycling. The final measurements took place after dinner after 36 hrs without sleep and 24 hrs of exercise of various intensity. Posturography was also performed at 6 AM on the second day. Results. In posturography significant decrease in the sway area with feedback and no changes in maximal sway were recorded. In the final measurements there were significantly lower heart rates at all submaximal workloads (p<0.001) and lower rates of perceived exertion on Borg`s scale at 50 and 100W (p<0.05). In reocardiography there were no significant changes, but a tendency for an increased stroke volume in the final measurement. Conclusion. In young men participating in the study one sleepless night combined with the long lasting exercise caused decrease in heart rate during submaximal exercise, which can be a result of adaptation to adrenergic stimulation.
... Heart rates during submaximal exercise were unaltered by sedentary sleep deprivation: 24 hours of wakefulness and exercise at 80% of ¦O 2 max [4,5], 30 hours and 25, 50 and 75% of VO 2 max [6,7], 36 hours and 80% of ¦O 2 max [8], 50 hours and PWC160 [9] and 60 hours and 70% of ¦O 2 max [10]. The decreased resting and exercise heart rates after sedentary sleep deprivation were also observed [11][12][13][14] but increased heart rate during exercise at intensity of 75% of ¦O 2 max in a study with partial 3 hours of sleep deprivation was reported as well [15]. There are few data on combined sleep deprivation and prolonged exercise. ...
... They used an incremental exercise test and recorded depressed heart rates during low and moderate intensities of exercise. Also Bond et al. [11] reported lower heart rates during submaximal exercise. Moreover, such pattern of heart rate changes is in opposition to the one usually observed during the circadian rhythm [37], emphasizing the influence of the applied procedure on examined factor. ...
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Introduction:There are only few data on influence of combined effects of long lasting exercise and sleep deprivation on physical performance. Objective:To evaluate the influence of 36 hours of sleep deprivation combined with 20 hours of intermittent exercise on selected physiological and psychomotor indices. Methods: Eleven participants of survival camp exercised without sleep and were examined three times (C – before effort, M – after 24 hours, E – after 36 hours) for submaximal heart rate, multiple choice reaction time (MCRT), motion coordination, handgrip force differentiation and shooting accuracy. Results:There were no significant differences in MCRT throughout the whole experiment. Heart rate showed significant decrease between C and M (P < 0.004) and C and E (P < 0.037) trials. Shooting was performed only twice and was significantly less accurate in E than in C (6.71±0.42 vs. 7.71±0.31 respectively, P < 0.001). Handgrip force differentiation was not different between the measurements (C – 6.2±1.8%, M – 5.3±0.9%, E – 4.1±0.9%). Number of mistakes in rotational test increased significantly from session C to M (4.95±0.59 vs. 6.76±0.70; P < 0.001) and C to E (4.95±0.59 vs. 6.90±0.90; P < 0.01). Conclusions:One sleepless night combined with the long lasting exercise caused decrease in heart rate, shooting performance and motion coordination, however it did not affect psychomotor performance and handgrip sensitivity. Such data can be a result of adaptation to adrenergic stimulation unevenly alters phenomena linked with central and peripheral fatigue. Key words: exercise, psychomotor performance, heart rate
... The final data set was formed from the remaining 19 primary journal articles (33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51). A special coding sheet was developed to capture information from these studies. ...
... This subject pool represents a broad range of subjects including both genders and a wide age range. The 19 primary studies were divided approximately equally between the three sleep deprivation categories: four in short-term sleep deprivation (37,42,43,45), six in long-term sleep deprivation (33,35,46,47,50,51), three in both short-term and longterm sleep deprivation (34,36,38) and six in partial sleep deprivation (39)(40)(41)44,48,49). Such a data set is large and provides the opportunity to do meaningful analyses. ...
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To quantitatively describe the effects of sleep loss, we used meta-analysis, a technique relatively new to the sleep research field, to mathematically summarize data from 19 original research studies. Results of our analysis of 143 study coefficients and a total sample size of 1.932 suggest that overall sleep deprivation strongly impairs human functioning. Moreover, we found that mood is more affected by sleep deprivation than either cognitive or motor performance and that partial sleep deprivation has a more profound effect on functioning than either long-term or short-term sleep deprivation. In general, these results indicate that the effects of sleep deprivation may be underestimated in some narrative reviews, particularly those concerning the effects of partial sleep deprivation.
... Deviations in normal sleep may impair an individual's endurance and physical capacity as sleep deprivation has been shown to decrease VO2max in cyclists (Bond et al., 1986), time to exhaustion in volleyball players (Azboy & Kaygisiz, 2009), and decrease in anaerobic Wingate test scores in soccer players, judokas, and judo competitors (Abedelmalek et al., 2013;HajSalem et al., 2013;Souissi et al., 2013). Mah and colleagues showed that basketball players who increased their sleep to at least ten hours per night increased not only physical performance, but also reported higher scores on emotional well-being (Mah et al., 2011). ...
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Injuries in soccer athletes continues to rise and there is a cause for concern. Collegiate athletes have physically demanding workloads and struggle to sleep an adequate amount each night. A potential association is how sleep could play a role in an athletes’ injury. 24 NCAA DI women’s soccer athletes were utilized during the Fall 2019 season. Athletes self-reported their daily hours slept and the athletic trainer tracked and classified athletes’ injury and illness status: no-injury, medical attention injury, or time loss injury. K-mean clustering was utilized to classify the athletes into 3 groups: injury/illness-free group (n=12), mild-to-moderate injury/illness group (n=7), and heavy injury/illness group (n=5). Sleep was statistically significantly lower in the heavy-injury group than other groups and small effect sizes were detected (d31 = .282, p < .001; d32 = .278, p < .001). Based on the data, it appears hours slept plays a factor in female soccer athletes’ risk of injury.
... , whereas athletic performance relying on aerobic capacity seemed to be more negatively affected by sleep loss (Bond et al., 1986;Martin & Chen, 1984;Oliver, Costa, Laing, Bilzon, & Walsh, 2009). ...
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Many athletes sleep poorly due to stress, travel, and competition anxiety. In the present study, we investigated the effects of sleep deprivation on soccer skills (juggling, dribbling, ball control, continuous kicking, 20 and 40 m sprint, and 30 m sprint with changes of direction). In all, 19 male junior soccer players (14–19 years old) were recruited and participated in a cross-balanced experimental study comprising two conditions; habitual sleep and 24 hours sleep deprivation. In both conditions, testing took place between 8 a.m. and 10 a.m. Order of tests was counterbalanced. Each test was conducted once or twice in a sequence repeated three times. The results revealed a negative effect of sleep deprivation on the continuous kicking test. On one test, 30 meter sprint with directional changes, a significant condition × test repetition interaction was found, indicating a steeper learning curve in the sleep deprived condition from Test 1 to Test 2 and a steeper learning curve in the rested condition from Test 2 to Test 3. The results are discussed in terms of limitations and strengths, and recommendations for future studies are outlined.
... 11 Negative effects of sleep deprivation have been reported on explosive athletic tasks such as knee extension peak torque 12 and vertical jump height 13 in some studies, whereas others did not find any negative effects on explosive actions as assessed with the Wingate Anaerobic Power Test [14][15][16] and snatch, clean and jerk, and front squat. 17 Exercises demanding more endurance, like time to exhaustion on ergometer cycling 18 or treadmill walking, 19 are more strongly affected by sleep deprivation. Furthermore, extended sleep has been associated with improved performance of several parameters such as sprints and shooting accuracy in a basketball team. ...
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Objectives: The study aims to evaluate whether 4 weeks with restricted use of electronic media after 22:00 affects sleep, athletic performance, cognitive performance, and mood in high school athletes. Methods: Eighty-five athletes were randomized to either an intervention group (n = 44), who was instructed to not use any electronic media after 22:00, or a control condition (n = 41), where they could act as they preferred in terms of media use. Primary outcomes were sleep habits measured with a sleep diary. Secondary outcomes were (a) physical performance measured with a set of standardized tests (beep test, 20-m linear sprint, chin-up test, hanging sit-ups test, counter movement jump and sit-n-reach test); (b) cognitive performance (response time and response accuracy); and (c) positive and negative affect. Differences between groups were tested with mixed between-within subject analyses of variance. Results and conclusions: Thirty-five and 40 of the athletes in the intervention and control group, respectively, completed the study. Results showed that restricted use of electronic media after 22:00 did not improve sleep habits, athletic performance, cognitive performance, or mood in a group of high school top athletes with already good sleep habits. However, these findings give us knowledge about sleep habits and performance in this population that is of importance when designing future studies.
... Total distance covered during the submaximal exercise part of the protocol was not significantly altered, but distance during the first and last 10 min of the submaximal exercise was reduced [17]. Other studies reported that one night of sleep deprivation reduced the total distance covered during treadmill walking [18], while 42 h of sleep deprivation reduced time to exhaustion in ergometer cycling [19], and sleep deprivation for 36 h [20] and 50 h [21] reduced time to exhaustion on treadmill walking. ...
... [100,101] Interestingly, a higher RPE for a given load has been observed after sleep deprivation. [99,100,102] Some authors [100,101] showed that, after sleep deprivation , subjects ran a shorter distance during a 30-minute self-paced treadmill exercise than did their controls, yet their perception of effort was similar. The authors suggested that altered perception of effort may account for decreased endurance performance after sleep deprivation. ...
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While the industrialized world adopts a largely sedentary lifestyle, ultra-marathon running races have become increasingly popular in the last few years in many countries. The ability to run long distances is also considered to have played a role in human evolution. This makes the issue of ultra-long distance physiology important. In the ability to run multiples of 10 km (up to 1000 km in one stage), fatigue resistance is critical. Fatigue is generally defined as strength loss (i.e. a decrease in maximal voluntary contraction [MVC]), which is known to be dependent on the type of exercise. Critical task variables include the intensity and duration of the activity, both of which are very specific to ultra-endurance sports. They also include the muscle groups involved and the type of muscle contraction, two variables that depend on the sport under consideration. The first part of this article focuses on the central and peripheral causes of the alterations to neuromuscular function that occur in ultra-marathon running. Neuromuscular function evaluation requires measurements of MVCs and maximal electrical/magnetic stimulations; these provide an insight into the factors in the CNS and the muscles implicated in fatigue. However, such measurements do not necessarily predict how muscle function may influence ultra-endurance running and whether this has an effect on speed regulation during a real competition (i.e. when pacing strategies are involved). In other words, the nature of the relationship between fatigue as measured using maximal contractions/stimulation and submaximal performance limitation/regulation is questionable. To investigate this issue, we are suggesting a holistic model in the second part of this article. This model can be applied to all endurance activities, but is specifically adapted to ultra-endurance running: the flush model. This model has the following four components: (i) the ball-cock (or buoy), which can be compared with the rate of perceived exertion, and can increase or decrease based on (ii) the filling rate and (iii) the water evacuated through the waste pipe, and (iv) a security reserve that allows the subject to prevent physiological damage. We are suggesting that central regulation is not only based on afferent signals arising from the muscles and peripheral organs, but is also dependent on peripheral fatigue and spinal/supraspinal inhibition (or disfacilitation) since these alterations imply a higher central drive for a given power output. This holistic model also explains how environmental conditions, sleep deprivation/mental fatigue, pain-killers or psychostimulants, cognitive or nutritional strategies may affect ultra-running performance.
... Furthermore, increased sympathetic activity may lead to decreased leptin levels (Rayner and Trayhurn, 2001;Schafroth et al., 2001;Spiegel et al., 2004b). Notably, the majority of total sleep deprivation studies have shown a heart rate reduction and ⁄ or decreased muscle sympathetic nerve activity (Bond et al., 1986;Chen, 1991;Holmes et al., 2002;Kato et al., 2000;Ogawa et al., 2003;Vaara et al., 2009). Finally, the increase of leptin after less stressful sleep loss is consistent with the potential role of leptin as a novel antidepressant (sleep deprivation improves temporarily the mood of depressed individuals), and with its thermogenic and energy expenditure-promoting effects as sleep loss is associated with decreased body temperature and increased energy expenditure (Horne, 1983;Horne and Pettitt, 1985;Lu, 2007;Mastorakos and Zapanti, 2004;Tuominen et al., 1997). ...
Article
Short-term sleep curtailment associated with activation of the stress system in healthy, young adults has been shown to be associated with decreased leptin levels, impaired insulin sensitivity, and increased hunger and appetite. To assess the effects of one night of sleep loss in a less stressful environment on hunger, leptin, adiponectin, cortisol and blood pressure/heart rate, and whether a 2-h mid-afternoon nap reverses the changes associated with sleep loss, 21 young healthy individuals (10 men, 11 women) participated in a 7-day sleep deprivation experiment (four consecutive nights followed by one night of sleep loss and two recovery nights). Half of the subjects were randomly assigned to take a mid-afternoon nap (14:00-16:00 hours) the day following the night of total sleep loss. Serial 24-h blood sampling and hunger scales were completed on the fourth (predeprivation) and sixth day (postdeprivation). Leptin levels were significantly increased after one night of total sleep loss, whereas adiponectin, cortisol levels, blood pressure/heart rate, and hunger were not affected. Daytime napping did not influence the effects of sleep loss on leptin, adiponectin, or hunger. Acute sleep loss, in a less stressful environment, influences leptin levels in an opposite manner from that of short-term sleep curtailment associated with activation of the stress system. It appears that sleep loss associated with activation of the stress system but not sleep loss per se may lead to increased hunger and appetite and hormonal changes, which ultimately may lead to increased consumption of 'comfort' food and obesity.
... It is not likely that sleep deprivation affected these findings. In recent studies, 36 h of sleep deprivation had no effect on heart rate or stress hormone concentrations during exercise [27], while after 42 h of sleep deprivation there was only a minor increase in heart rate [28]. In our subjects, sleep deprivation was 26 h at the most. ...
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We have studied the effect of dosage time of oxprenolol (Trasicor®) on its pharmacokinetics and pharmacodynamics in six healthy volunteers. The drug effects measured were heart rate and systolic blood pressure during exercise. Oxprenolol was taken orally at 08.00 h, 14.00 h, 20.00 h, and 02.00 h in randomized order, with 1 week between successive doses. There were differences in the pharmacokinetics of oxprenolol for the ratio between the apparent volume of distribution and systemic availability (P=0.04) and for elimination half-life (P=0.006). Both were lowest after administration at 14.00 h (163 (77) l and 1.2 (0.6) h; mean (SD)) and highest after administration at 02.00 h (229 (100) l, and 1.7 (0.6) h). The systolic blood pressure during exercise before oxprenolol did not vary with dosage time, but heart rate during exercise before intake was lowest before dosage time 08.00 h and highest before dosage time 20.00 h (P=0.03). The time-course of heart rate during exercise after oxprenolol was described by a model that incorporated the factors drug concentration and spontaneous diurnal variation. EC50 and Emax did not vary between dosage times. The spontaneous diurnal variation in heart rate during exercise was unaffected by oxprenolol, leading to an apparently greater effect of oxprenolol during the night than during the day.
... Peak oxygen uptake (VO 2peak ) was determined by a one-minute incremental test to exhaustion [3]. After a five-minute warm-up period, subjects began cycling on a stationary cycle ergometer (Monark, Sweden) at a work rate of 70 Watts and increased by 35 Watts´minWatts´Watts´min ±1 until exhaustion was reached. ...
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Participants in the sport of adventure racing often choose to go without sleep for a period of greater than 24 h while partaking in prolonged submaximal exercise. This study examined the effect of 30 h of sleep deprivation and intermittent physical exercise, on the cardiorespiratory markers of submaximal exercise in six subjects. Six subjects with the following physical characteristics participated in the study (mean +/- SD): age 22 +/- 0.3 years, height 180 +/- 5 cm, body mass: 77 +/- 5 kg, VO2peak 44 +/- 5 ml. kg (-1). min (-1). Three subjects engaged in normal sedentary activities while three others cycled on a cycle ergometer at 50 % VO2peak for 20 min out of every two hours during thirty hours of sleep deprivation. One week later sleep deprivation was repeated with a cross over of subjects. Every four hours, subjects completed assessments of cardiorespiratory function during 50 % VO2peak cycling. A 3 x 8 repeated measures ANOVA revealed a significantly lower heart rate with sleep deprivation (p < 0.05), but no other significant effects (p > 0.05) on respiratory gas exchange variables. Neither sleep deprivation, nor a combination of sleep deprivation and five hours of moderate intensity cycling, appear to be limiting factors to the physiological capacity to perform submaximal exercise.
Article
Purpose: Sleep deprivation (SD) reduces time to task failure during endurance exercises. The aim of our work was to study the effect of acute SD on the endurance of a skeletal hand muscle and to investigate cortical motor drive to muscle and perception of effort. Methods: Origin of the early exhaustion after SD might be insufficient cortical motor drive to muscle or motor inhibition because of excessive perception of effort. The supplementary motor area, the medial part of the premotor cortex, links the motor and sensory cortexes, prepares for voluntary movements, and may play a central role in the pathophysiology of impaired muscle endurance after SD. Supplementary motor area can be noninvasively assessed by electromyogram measuring amplitude of premotor potentials before hand movements. We investigated the effect of SD on muscle endurance in healthy volunteers performing moderate hand exercise by monitoring supplementary motor area activation and muscle afferents. Two sessions were performed, in random order, one after a normal sleep night and the other after a sleepless night. Results: Twenty healthy young men were included in this study. Sleep deprivation reduced time to task failure by 11%. Supplementary motor area activation was altered throughout the task and effort perception was increased. Conclusions: Our results suggest that SD reduces skeletal muscle endurance by increasing the effects of muscle afferents on the supplementary motor area. Sleep alterations frequently reported in chronic diseases might reduce patients' capacity to achieve the low-intensity motor exercises required in everyday life. Our results should lead to the search for sleep disorders in patients with chronic pathology.
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Introduction A lack of sleep can pose a risk during military operations due to the associated decreases in physical and cognitive performance. However, fast-acting ergogenic aids, such as ammonia inhalants (AI), may temporarily mitigate those adverse effects of total sleep deprivation (TSD). Therefore, the present study aimed to investigate the acute effect of AI on cognitive and physical performance throughout 36 hours of TSD in military personnel. Methods Eighteen male military cadets (24.1 ± 3.0 y; 79.3 ± 8.3 kg) performed 5 identical testing sessions during 36 hours of TSD (after 0 [0], 12 [–12], 24 [–24], and 36 [–36] hours of TSD), and after 8 [+8] hours of recovery sleep. During each testing session, the following assessments were conducted: Epworth sleepiness scale (ESS), simple reaction time (SRT), shooting accuracy (SA), rifle disassembling and reassembling (DAS), and countermovement jump height (JH). Heart rate (HR) was continuously monitored during the SA task, and a rating of perceived exertion (RPE) was obtained during the JH task. At each time point, tests were performed twice, either with AI or without AI as control (CON), in a counterbalanced order. Results There was faster SRT (1.6%; p < 0.01) without increasing the number of errors, higher JH (1.5%; p < 0.01), lower RPE (9.4%; p < 0.001), and higher HR (5.0%; p < 0.001) after using AI compared to CON regardless of TSD. However, neither SA nor DAS were affected by AI or TSD (p > 0.05). Independent of AI, the SRT was slower (3.2–9.3%; p < 0.001) in the mornings (-24, +8) than in the evening (-12), JH was higher (3.0–4.7%, p < 0.001) in the evenings (-12, -36) than in the mornings (0, -24, +8), and RPE was higher (20.0–40.1%; p < 0.001) in the sleep-deprived morning (-24) than all other timepoints (0, -12, -36, +8). Furthermore, higher ESS (59.5–193.4%; p < 0.001) was reported at -24 and -36 than the rest of the time points (0, -12, and + 8). Conclusion Although there were detrimental effects of TSD, the usage of AI did not reduce those adverse effects. However, regardless of TSD, AI did result in a short-term increase in HR, improved SRT without affecting the number of errors, and improved JH while concurrently decreasing the RPE. No changes, yet, were observed in SA and DAS. These results suggest that AI could potentially be useful in some military scenarios, regardless of sleep deprivation.
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Sleep and exercise influence each other through complex, bilateral interactions that involve multiple physiological and psychological pathways. Physical activity is usually considered as beneficial in aiding sleep although this link may be subject to multiple moderating factors such as sex, age, fitness level, sleep quality and the characteristics of the exercise (intensity, duration, time of day, environment). It is therefore vital to improve knowledge in fundamental physiology in order to understand the benefits of exercise on the quantity and quality of sleep in healthy subjects and patients. Conversely, sleep disturbances could also impair a person’s cognitive performance or their capacity for exercise and increase the risk of exercise-induced injuries either during extreme and/or prolonged exercise or during team sports. This review aims to describe the reciprocal fundamental physiological effects linking sleep and exercise in order to improve the pertinent use of exercise in sleep medicine and prevent sleep disorders in sportsmen.
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A privação do sono é a remoção ou supressão parcial do sono, e esta condição pode causar diversas alterações: endócrinas, metabólicas, físicas, cognitivas, neurais e modificações na arquitetura do sono, que em conjunto comprometem a saúde e a qualidade de vida do sujeito nestas condições. Já o exercício físico praticado regularmente promove benefícios como melhora do aparato cardiovascular, respiratório, endócrino, muscular e humoral, além disso, pode melhorar a qualidade do sono. Entretanto, a associação desses dois parâmetros não tem sido bem explorada, em parte pela dificuldade conseguir voluntários que se submetam a essa condição principalmente sem nenhum tipo de compensação financeira. A maioria dos estudos que investigaram o binômio exercício físico e privação de sono focou os efeitos no desempenho aeróbio. Embora ainda haja controvérsias, os estudos apontam para pequena ou nenhuma alteração desse parâmetro quando as duas situações se fazem presentes. Em relação à potência anaeróbia e força não tem sido encontrados alterações significativas, mas para eventos prolongados, parece haver uma interação entre a privação de sono e o exercício físico, o que sugere um mecanismo de proteção. Entretanto, é importante considerar que uma das alterações mais importantes causadas pela privação do sono é o aumento na percepção subjetiva, que por si só já representa um fator para diminuição e comprometimento do desempenho físico e pode representar um elemento de "mascaramento" dos efeitos deletérios da privação. Assim, o objetivo da presente revisão é o de discutir os diferentes aspectos da relação entre o exercício físico e a privação de sono, evidenciando seus efeitos e reflexos no desempenho físico.
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This study was aimed at investigating the effects of a partial sleep deprivation on the subsequent athletic performance. Eight highly trained cyclists were enrolled for this study. The changes in cardio-vascular, ventilatory and metabolic responses were analysed during and upon completion of physical exercise, taking place after 2 recorded nights, in other words, after a control night and after a night with reduced sleep. Partial sleep deprivation was obtained by waking the subjects for 3 h in the middle of the night. Athletic performance was tested at 2 pm the following day, using an ergometer. The subjects were pedaling at a steady-state submaximal work load (75% of the maximal oxygen uptake) and then at the maximal sustained work load. The analyses of change scores disclosed that there were main significant effects for measures of heart rate, ventilation, oxygen uptake, V̇E/V̇O2 ratio and lactate levels under the observed conditions. Mean exercise duration and maximal sustained work load after partial sleep deprivation were not modified with control. On the other hand, heart rate was significantly greater during sub-maximal, maximal performances, and during recovery after sleep loss. Sleep deprivation significantly increased ventilation at exercise intensities eliciting 75% and 100% of the maximal oxygen uptake (V̇O2 max) and during the recovery, since it significantly decreased V̇O2 during maximal work. The V̇E/V̇O2 ratio was greater at the end of the steady state and at the end of the maximal work load. Lactate levels were altered by sleep loss, undergoing upward drift from the 9th min of the steady state until recovery. These findings suggest that acute sleep loss may contribute to alterations in atlhetic performance.
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Cognitive Behavioural Stress Management (CBSM) has demonstrated favourable changes in psychological and biological stress indicators, consistent with reductions in sports injury, and accelerated recovery following surgery. However, the effects of CBSM on the conditioning of athletes remain speculative. The aim of this study was to assess the effects of a CBSM program on measures of the conditioning process, including stress, recovery and performance. Thirty-two rowers (16 males, 16 females; mean age 20.0 years, range 17 - 29 years) preparing for the 2007 Australian Rowing Championships were recruited and stratified into 16 intervention-control matched pairs based on gender, weight class and performance. They were monitored for 17 weeks with one week of assessment before 3 weeks of CBSM for the intervention group and 3 weeks of normal training for the control group, followed by 13 weeks of their usual training. The intervention consisted of 6 one-hour sessions of instruction on the regular use of CBSM methods in response to daily stressors. Measures of perceived stress and recovery were obtained through the Recovery Stress Questionnaire for Athletes (RESTQ-Sport) (Kellman & Kallus, 2001). Rowing performance was assessed by the average power to complete a maximal 2000m ergometer time-trial in the first week of monitoring, and in the 4th, 9th and 17th week. The CBSM group demonstrated a statistically significant improvement in the REST- Sport General Recovery Scale of Success (Wilks’ Lambda = 0.219, F (14,12) = 3.052, p= 0.03) and Sport Specific Recovery Scale of Burnout/Personal Accomplishment (Wilks’ Lambda = 0.218, F (14,12) = 3.079, p = 0.03) compared to the control group across the time-series. No significant differences in 2000m ergometer performance were demonstrated between groups, but after 17 weeks of training the intervention group’s performance was preserved (0.2 ± 3.7%) whereas the control group showed a 2.7 ± 6.3% decrement. It was concluded that CBSM provided some benefits to the athlete’s psychological state and may be a useful strategy to employ in the conditioning process. Further research using a larger sample size is warranted to fully examine the efficacy of CBSM in high performance athletes.
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The effect of sleep deprivation on male runners (age 18.1 +/- 0.35) and volleyball players (age 17.8 +/- 0.36) has not been investigated. Therefore, we studied the possible effect of sleep deprivation in the sportsmen. The athletes performed spirometric tests at rest and then incremental exercise test on ergometer following one night sleep and one night (25-30 h) sleeplessness. Several standard measurements of spirometric function showed no significant change following sleep loss. Sleep loss raised resting oxygen uptake (VO2) in the runners and resting carbon dioxide production (VCO2) in both the runners and the volleyball players (p < 0.05). However, it left heart rate (HR), respiratory quotient (R), minute ventilation (VE) and arterial oxygen saturation (SaO2) unchanged at rest in both groups. Sleep loss decreased time to exhaustion in the volleyball players (p < 0.01). In the runners and the volleyball players, sleep loss did not alter exercise values of HR, VO2, VCO2, R and SaO2, but it reduced exercise VE (p < 0.05). We suggest that one night sleep deprivation may reduce exercise performance by decreasing exercise VE and time to exhaustion. We also indicate that sleep loss may decrease more the performance of volleyball players than that of runners.
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The effects of 30-h sleep deprivation on cardiorespiratory function either at rest or in exercise were studied in 15 young healthy male volunteers. All subjects performed 1-min incremental exercise tests on a bicycle ergometer until exhaustion and endurance exercise tests at 3/4 of their maximal work rates. Arterialized venous blood samples were withdrawn at rest and during exercise tests to investigate the influence of sleep loss on blood gases. In addition, resting plasma catecholamine levels were also measured in ten subjects. The results showed that 1) resting heart rate, plasma catecholamine levels, and blood pH were decreased while minute ventilation (VI) and CO2 production (VCO2) were increased after 30 h of sleep loss (P less than 0.05), and 2) the maximal exercise performance was reduced by sleeplessness, as indicated by the decreases in the maximal heart rate, peak VI, peak VCO2, peak O2 consumption, and time to exhaustion (P less than 0.05). However, no significant changes in exercise endurance, arterialized venous pH, and PCO2 were found in exercise after sleep deprivation either. We therefore conclude that 30-h sleep loss alters cardiorespiratory function at rest and the ability to perform maximal exercise but not exercise endurance.
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This report provides information supporting the conclusion that sleep deprivation produces only very small biomedical effects. It nonetheless concludes that chronic partial sleep deprivation may contribute to gastrointestinal disorders, cardiovascular disease, and other medical conditions that occur more often in shiftworkers than in permanent dayworkers.
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The purpose of this study was to determine the effect of one night's sleep loss on the performance of high-intensity exercise and on the contribution of anaerobic and aerobic energy systems to the exercise. Seven males and seven females performed an all-out cycling exercise test during baseline testing and then on three consecutive days after a sleepless night. The work rates were 5.0 W kg-1 for the females and 6.0 W kg-1 for the males. The aerobic contribution was determined based on measured VO2 and the anaerobic contribution was determined by subtraction of the aerobic contribution from the total amount of work performed. The results of baseline tests and of tests performed following sleep loss were compared for evidence of an effect of sleep deprivation. The 25-30 h of sleep deprivation did not affect total work, the anaerobic contribution or the aerobic contribution (all P > 0.1), although there was a tendency (P = 0.13) for mean VO2 to decrease after the sleepless night. There were no interaction effects involving sex on total work, the anaerobic contribution or the aerobic contribution (all P > 0.1). The mean (+/- S.E.M.) values for total work (kJ) performed were: baseline, 21.9 +/- 2.7; after sleep loss, 21.1 +/- 2.5 (day 1), 21.7 +/- 2.5 (day 2), and 21.9 +/- 2.7 (day 3). It is concluded that, in both males and females, there are no changes in the contributions of the aerobic and anaerobic energy systems to high-intensity exercise performed following the loss of one night's sleep.
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Synchronized human sleep has been shown to decrease activation of the sympathetic nervous system, resulting in reduced levels of oxygen consumption. This is in direct conflict with sympathetic arousal, which coincides with the initiation of exercise. Although a considerable body of research has investigated the effects of sleep deprivation on exercise performance, the effects of an acute bout of sleep on exercise response have not been previously reported. This question appears relevant considering the occurrence of acute sleep bouts among athletes competing in prolonged multi-event competition (e.g. swimming, track and field). To investigate the effects of an acute bout of sleep on submaximal (running economy) and maximal oxygen consumption, seven male volunteers participated in a continuous, progressive treadmill test to volitional exhaustion immediately following a 1-h bout of sleep (SB) or no sleep (Control). The subjects served as their own controls and the order of trials was randomized. A MANOVA with repeated measures indicated no difference between groups for running economy or VO2 (P < 0.05). However, a significant interaction effect was observed in which SB resulted in greater running economy (lower VO2) through the first two stages of the protocol, while the control treatment yielded a greater economy throughout the remaining stages. While the implications of the findings are uncertain, they may indicate differences in psychological arousal or anxiety as a result of treatments or the possibility of a delayed sympathetic arousal in the early stages of exercise following sleep.
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Fatigue has often been confused with sleepiness and has received little study as an independent symptom of sleep disturbance. To investigate if fatigue is a common and severe symptom in sleep disordered individuals, the Fatigue Severity Scale (FSS) was administered to 206 patients over a 12-month period at a sleep disorder center. Our sample averaged 4.8 on the 7-point FSS, which is in the severe fatigue range. High fatigue was present in a broad range of sleep disorders, but was particularly high among individuals diagnosed with psychophysiological insomnia. A number of variables predicted fatigue (being female, being a smoker, high BMI, low sleep efficiency percent, and high MMPI average clinical scale score), but surprisingly daytime sleepiness (as measured by the multiple sleep latency test) did not. Apparently, daytime sleepiness and perceived fatigue are independent phenomena. We discussed the importance of attributing credence to the complaint of fatigue and suggested some areas for future study including further study of fatigue in insomnia, expanded consideration of sleep variables causing fatigue, and testing objective measures of fatigue.
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We examined the effects of nasal continuous positive airway pressure (CPAP) on exercise performance in patients with obstructive sleep apnea (OSA). Six patients were treated with nasal CPAP on seven successive days and underwent overnight sleep studies and multiple sleep latency test (MSLT) at the beginning and after the last day of the treatment. The subjects also performed incremental exercise testing using a bicycle ergometer followed by 0-w, 25-w, 50-w,--(3 minutes each) until maximum level. Arterial oxygen pressure, arterial carbon dioxide pressure at rest while awake, apnea/ hypopnea index, longest apnea duration, the lowest percutaneous oxygen saturation measured by a pulse oximeter and the value of MSLT were significantly improved after nasal CPAP. Moreover, maximal oxygen consumption was significantly increased from 1841 ml/min +/- 350 to 2125 ml/min +/- 351 (p < 0.05); however, other cardiorespiratory parameters did not change significantly. The improvement of exercise performance by short-term nasal CPAP treatment in OSA patients may correlate with the improvement of sleepiness.
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A sample of 32 obstructive sleep apnea patients (27 males, 5 females) was assessed with overnight polysomnography and the Multiple Sleep Latency Test (MSLT), an objective measure of daytime sleepiness. Patients also participated in a maximal exercise test, which served as an objective indicator of physical fatigue. The Fatigue Severity Scale (FSS) was used as a subjective measure of fatigue. Subjective fatigue ratings were significantly correlated with percent of predicted maximum heart rate achieved during exercise testing, suggesting that self-reported fatigue in apnea patients may refer to reduced physical fitness. FSS scores and exercise testing results were not significantly correlated with the MSLT, indicating that daytime fatigue and daytime sleepiness are independent problems in apnea patients. Participants self-reported a high level of fatigue, and exercise testing revealed decreased physical work capacity among apnea patients, but objective and subjective indicators of fatigue were not significantly correlated with apnea severity. A higher percentage of REM sleep predicted greater work capacity.
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The purpose of the study was to investigate the effects of one night's sleep deprivation on the cardiorespiratory responses to exercise during the follicular and luteal phases of the menstrual cycle. We have studied nine, healthy females aged 24-35 years with regular menstrual cycles. Each subject performed spirometric tests at rest and then an incremental exercise testing during 11-13 days of follicular phase and 22-24 days of luteal phase following one normal night's sleep or one night's sleep loss. Compared with resting values exercise produced significant increases in cardiorespiratory variables including oxygen uptake (VO2), carbon dioxide production (VCO2), tidal volume (VT), respiratory rate (RR), minute ventilation (VE), systolic blood pressure, heart rate (HR) and respiratory quotient (R). However, it did not alter significantly diastolic blood pressure, end-tidal PO2 (PETO2), end-tidal PCO2 (PETCO2) and arterial oxygen saturation (SaO2). Spirometric variables which include forced vital capacity (FVC), forced expiratory volume in one s (FEV1), FEV1/FVC%, forced expiratory volume in three s (FEV3), forced expired flow from 25-75% of FVC (FEF 25-75%), forced expired flow at 25% of FVC (FEF 25%), forced expired flow at 50% of FVC (FEF 50%), forced expired flow at 75% of FVC (FEF 75%), forced expired flow from 75-85% of FVC (FEF 75-85%), peak expiratory flow (PEF), expiratory reserve volume (ERV), inspiratory capacity (IC) and maximal voluntary ventilation (MVV) and cardiorespiratory variables were not different between the cycle phases after one normal night's sleep or one night's sleep deprivation. Neither menstrual cycle phase nor sleep deprivation affected spirometric and cardiorespiratory parameters. We suggest that one night's sleep deprivation does not produce alterations in spirometric parameters and cardiorespiratory responses to submaximal incremental exercise during the follicular and luteal phases.
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We sought to determine whether patients with obstructive sleep apnea (OSA) had an objective change in aerobic fitness during cycle ergometry compared to a normal population. The most accurate test of aerobic fitness is measurement of maximum oxygen consumption (VO2max) with cycle ergometry. We performed a retrospective cohort analysis (247 patients with OSA) of VO2max from annual cycle ergometry tests compared to a large control group (normative data from 1.4 million US Air Force tests) in a tertiary care setting. Overall, individuals with OSA had increased VO2max when compared to the normalized US Air Force data (p < .001). Patients with an apnea-hypopnea index of greater than 20 demonstrated a decreased VO2max as compared to normalized values (p < .001). No differences in VO2max were observed after either medical or surgical therapy for OSA. Overall, in a US Air Force population, OSA does not predict a decrease in aerobic fitness as measured by cycle ergometry. However, patients with an apnea-hypopnea index of greater than 20 have a statistically significant decrease in aerobic fitness compared to the normal population. This study demonstrates the effects of OSA on aerobic fitness. Further correlation of fitness testing results with OSA severity and treatment is needed.
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This study examined the effect of interstate travel on sleep patterns and game performance of elite Australian Rules footballers. Nineteen members of a Western Australian-based Australian Football League team participated in the study during the 2004 season. Sleep was assessed on the night before home and away games by measuring sleep duration (SLD), sleep efficiency (SLE), wake time (WT) and number of wakings (NW) via actigraphy. Subjective sleep quality was assessed using a sleep rating (SR) scale. Baseline sleep measurements were obtained over four consecutive non-game nights. Game performance was assessed using a coach's rating (CR) scale and impact ranking (IR) and by player statistics including frequency of possessions (P) and frequency of possessions and team assists (PTA). Compared to baseline, SLD was greater on the nights before home and away games (by 48 and 39 min, respectively, p<0.05). Other sleep measures were unchanged. Sleep rating was poorer before away than home games (p<0.05). CR and IR were greater during home than away games (p<0.05). All other measures of performance were similar at home and away. These results show that prior interstate travel has minimal effect on sleep quality and game performance in elite footballers.
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