xvii, 245 p. : ill. A print copy of this thesis is available through the UO Libraries. Search the library catalog for the location and call number. / There has been a lot of research investigating the effects of heat stress and exercise on the physiological adaptations to heat acclimation. It is well documented that heat acclimation improves heat tolerance and performance in a hot environment; however, some of the mechanisms of adaptation are not clear. Furthermore, the role of heat acclimation on exercise performance in cool environments is currently unknown. Therefore, in Chapter IV we aimed to determine the effects of heat acclimation on lactate threshold and maximal oxygen uptake (VO 2max ) in cool and hot conditions. We also sought to investigate the effects of heat acclimation on leg blood flow and oxygen delivery during a single-leg knee extensor exercise. We found that heat acclimation improved lactate threshold and VO 2max in cool and hot environments but did not alter the leg blood flow and oxygen delivery during the leg kicking exercise. In Chapter V we investigated the heat acclimation effects on performance during a 1-hour time trial in hot and cool environmental conditions and the potential mechanisms by which this occurs. A secondary objective was to study whether the pacing strategy was modified during the time trial post-heat acclimation. The results demonstrated that heat acclimation improved time trial performance in both thermal environments by approximately 7% but pacing strategy was not altered. The purpose of the studies in Chapter VI were twofold. First, we sought to investigate how heat acclimation affects the skin blood flow and sweating responses to pharmacological treatment with specific dosages of the muscarinic receptor agonist acetylcholine. Second, we examined the maximal skin blood flow responses to a period of heat acclimation by locally heating the forearm with a water spray device for 45 minutes and measured brachial artery blood flow via ultrasound. We found that heat acclimation increased sweat rate and skin blood flow responses to given concentrations of acetylcholine, suggesting a role for peripheral mechanisms. On the other hand, maximal skin blood flow remained unchanged after heat acclimation. / Committee in charge: Christopher Minson, Chairperson, Human Physiology; John Halliwill, Member, Human Physiology; Andrew Lovering, Member, Human Physiology; Michael Sawka, Member, Not from U of 0; Scott Frey, Outside Member, Psychology

Short-term (3-7 days), high doses of creatine (20g/d) and/or sodium bicarbonate (0.5g/kg body weight) supplementation increase exercise performance during short term high intensity activities; however, it remains unclear whether long-term, low doses of these supplements have a positive impact on exercise performance. The purpose of this study was to determine the effects of long-term (8 weeks), low dose creatine supplementation on exercise performance, and whether combining creatine and sodium bicarbonate supplementation has an additive effect. Sixty-three healthy, habitually active, adults (28 M, 35 W; 22+2 years; 23+ 3 BMI) were randomly assigned by sex to one of three supplement groups: placebo (PL), creatine only (3g/day; Cr), or creatine plus sodium bicarbonate (3g creatine plus 1g sodium bicarbonate; Cr+Sb) for 8 weeks. Before and after supplementation subjects completed two exercise performance tests on separate days. Subjects completed repeated Wingate sprint tests (6 x 10 second sprints) and changes in the slope across the 6 sprints (rate of decline) was analyzed between groups. We also collected 5 km time-trial and the data were analyzed using repeated measures ANOVA. In the repeated sprint test, peak power output slope was significantly decreased (P=0.04) in PL (-83%) and Cr+Sb (-82%) but did not change in Cr alone and was significantly better (P=0.03) than Pl and Cr+Sb. Similarly, mean power output slope significantly decreased (P0.05) in time to completion. However, Cr alone significantly improved time to completion (-3%; P=0.01). Taken together, these data suggest that long-term, low dose creatine supplementation increases exercise performance but adding sodium bicarbonate supplementation has no beneficial impact on exercise performance.

No description available.

A dose response relationship between carbohydrate (CHO) ingestion and exercise performance has not been consistently reported. Additionally the underlying metabolic and neuromuscular explanations for an improvement in performance with increasing doses of CHO have not been fully explained. In Chapter 2 of this thesis 20 male cyclists completed 2 h of submaximal exercise followed by a time trial task (531 ± 48KJ). Three CHO electrolyte beverages, plus a control (water), were administered during a 2 h ride providing 0, 20, 39 or 64 g CHO·h-1 at a fluid intake rate of 1 L·h-1. Performance was assessed by time to complete the time trial task, mean power output sustained, and pacing strategy used. Mean task completion time (min:sec ± SD) for 39 g·h-1 (34:19.5 ± 03:07.1, p=0.006) and 64 g·h-1 (34:11.3 ± 03:08.5 p=0.004) of CHO were significantly faster than control (37:01.9 ± 05:35.0). The mean percentage improvement from control was -6.1% (95% CI: -11.3 to -1.0) and -6.5% (95% CI: -11.7 to -1.4) in the 39 and 64 g·h-1 trials respectively. The 20 g·h-1 (35:17.6 ± 04:16.3) treatment did not reach statistical significance compared to control (p = 0.126) despite a mean improvement of -3.7% (95% CI -8.8 to 1.5%). These data demonstrate that consuming CHO at a rate between 39 to 64 g·h-1 is likely to be optimal for most individuals looking to utilise a single source CHO as an ergogenic aid during endurance performances lasting less than 3 hrs. Attempts have been made to try and understand the acute metabolic regulation that occurs when ingesting increasing amounts of CHO. However, no one study has fully investigated the metabolic mechanisms underlying graded increments of CHO ingestion. In Chapter 3 we aimed to utilise stable isotopes and blood metabolite profiles to examine the integrated physiological responses to CHO ingestion when ingested at rates throughout the range where performance gains appear greatest. Twenty well-trained male cyclists completed 2 h constant load ride (95% lactate threshold, 185 ± 25W) where one of three CHO beverages, or a control (water), were administered every 15 min, providing participants with 0, 20, 39 or 64 g CHO·h-1 at a fixed fluid intake rate of 1L·h-1. Dual glucose tracer techniques (6,6,2H2 glucose and U13C labelled glucose) were used to determine glucose kinetics and exogenous carbohydrate oxidation (EXO) during exercise. Endogenous CHO contribution was suppressed in the second hour of exercise when consuming 39 and 64 g·h-1 in comparison to 0 g·h-1 (-7.3%, 95%CI: -13.1 to -1.6 and -11.2%, 95%CI: -16.9 to -5.5 respectively). Additionally, consuming 64 g·h-1 suppressed the endogenous CHO contribution by -7.2% (95%CI: -1.5 to -13.0) compared to the 20 g·h-1 treatment. Exogenous CHO oxidation rate increased by 0.13 g·min-1 (95%CI: 0.10 to 0.15) and 0.29 g·min-1 (95%CI: 0.27 to 0.31) when consuming 39 and 64 g·h-1 in comparison to 20 g·h-1 of CHO. Peak exogenous CHO oxidation rates were 0.34 (0.06), 0.54 (0.09) and 0.78 (0.19) g·min-1 for 20, 39 and 64 g·h-1 respectively. Plasma NEFA concentration was 0.10 (95%CI: 0.07 to 0.13), 0.12 (95%CI: 0.10 to 0.16) and 0.16 (95%CI: 0.13 to 0.19) mmol.L-1 higher when consuming 0 g·h-1 in comparison to 20, 39 and 64 g·h-1 respectively. Both 39 and 64 g·h-1 were effective at sparing endogenous CHO stores of which it is estimated that most of this is liver glycogen sparing, but the measured response was highly variable between individuals. Consuming 39 g·h-1 of CHO appears to be the minimum ingestion rate required to have a significant metabolic effect that results in an increase in performance. Recent research has indicated a key role of endogenous CHO sensing and oral glucose sensing in maintaining central drive and peripheral function during endurance exercise tasks. Consuming 39 and 64 g·h-1 of CHO elicits the greatest improvements in performance and also demonstrate a similar metabolic response. The improvement in subsequent time trial performance when consuming 39 and 64 g·h-1 coincided with significant alterations in whole body substrate usage that lead to endogenous CHO sparing at the same ingestion rates. In Chapter 4 we aimed to utilise gold standard neuromuscular function assessment techniques, alongside novel measures, to investigate the effect of consuming different rates of CHO on neuromuscular function during and following prolonged cycling exercise. In a double-blind, randomised cross-over design, well-trained male cyclists (n=20, mean±SD, age 34 ± 10 y, mass 75.8 ± 9 kg, peak power output 394 ± 36 W, V̇O2max 62 ± 9 ml·kg-1·min-1) completed 2 familiarisation trials then 4 experimental trials. Trials involved a 2 h submaximal ride followed by a high intensity time trial task lasting approx. 35 min with each of 0, 20, 39 and 64 g·h-1 CHO ingestion rates during submaximal exercise. Each trial involved pre and post exercise assessments (MVC, Mwave twitch potentiation and force, motor unit recruitment and firing rate assessment using high density EMG) and during exercise (gross EMG amplitude). MVC peak torque values were reduced post exercise by -20.4 nM (95%CI: -26.5 to -14.4) in comparison to pre value on all trials with no differences between trials. The firing rates of early recruited motor units significantly increased by 1.55 pps (95%CI: 0.51 to 2.59) following exercise in comparison to pre-exercise rates. Gross EMG during the 2 h cycling bout revealed a main effect of treatment (p<0.01) but post hoc comparisons provided no clarity and likely reflect methodological issues. Consuming CHO at ingestion rates between 20 and 64 g·h-1 had little to no impact on the neuromuscular function of well-trained cyclists when comparing pre and post fatiguing exercise values. Despite differences in time trial completion time between trials, following exercise to fatigue in an endurance task, no post exercise differences were detected.

Cette thèse porte sur l’étude des mécanismes de régulation du niveau de fatigue périphérique à l’exercice et sur les conséquences de cette régulation sur la capacité de performance motrice. Nous avons tout d’abord démontré que la puissance est étroitement régulée au cours de sprints répétés – épreuve au cours de laquelle la commande motrice est recrutée à son niveau maximal volontaire – de sorte qu’un seuil critique de fatigue périphérique ne soit jamais dépassé. Nous avons ensuite montré qu’il existe un lien étroit entre l’atteinte de ce seuil critique de fatigue et l’arrivée à une phase de plateau de puissance développée au cours de sprints répétés, indépendamment de la durée de la récupération entre les sprints. Ces résultats ont permis de démontrer que le niveau d'activité de la commande motrice centrale et la puissance sont régulés au cours de sprints répétés dans le but de limiter le niveau de fatigue périphérique à un niveau seuil. Le rôle de ce mécanisme régulateur est cependant dépendant de la nature de la tâche. Nous avons en effet montré que l’arrêt de l’effort d’un exercice de squat isométrique, conduit jusqu'à épuisement, est associé à une défaillance de l’activation centrale volontaire, qui précède l'atteinte du seuil critique de fatigue. Enfin, l'application de ces données et concepts théoriques à l'exercice réalisé sur une plateforme à instabilité servo-assistée (imoove) a permis de montrer que ce type d’outil permet un recrutement accru des muscles posturaux et de l’équilibre comparé à un exercice réalisé sur une surface stable, sans compromettre la fatigue et le recrutement des muscles locomoteurs, déterminants des adaptations positives à l'entraînement. / This doctorate thesis focused on the mechanisms involved in the control of peripheral fatigue during exercise and on the consequences of this regulation on exercise tolerance. We first demonstrated that performance during repeated sprints – a trial during which the central motor drive is activated at its maximal voluntary level – is tightly regulated to avoid the development of peripheral fatigue beyond a critical threshold. We then showed that the attainment of the plateau phase of performance, characterized by a constant power output until the last sprint, was closely linked to the attainment of the critical threshold of peripheral fatigue, independently of the recovery duration between sprints. These firsts results demonstrated that central motor drive and power output are regulated during repeated sprints in order to limit the development of peripheral fatigue beyond a critical threshold. However, the role of this regulatory mechanism is task-dependent. Indeed, we showed that time to task failure during the first repetitions of a sustained submaximal isometric contraction is likely associated with failure in central activation of motor units, which precede the attainment of the critical threshold of peripheral fatigue. We then developed applied research protocols on imoove, a servo-assisted instability device for training composed by a board that can move in the three-dimensional plans. Because greater trunk and ankle muscles activity was achieved in imoove without compromising lower limb muscles activity and fatigue, this device may provide sufficient muscle overload to simultaneously develop locomotor, postural and balance muscles.

No description available.

Les athlètes utilisent les suppléments nutritionnels avec pour objectif d'améliorer leur performance sportive. La performance sportive dépend de facteurs physiques, mais également de facteurs cognitifs. Les suppléments nutritionnels riches en flavanols issu du cacao (CF) peuvent stimuler la fonction vasculaire, réduire le stress oxydant et améliorer la fonction cognitive. L'objectif de cette thèse est donc d’analyser les effets d'une consommation aigue, ou pendant une semaine, de CF, sur la performance physique et cognitive chez des athlètes, chez des sujets actifs et chez des personnes ayant un diabète de type 1 (DT1). De plus, l’objectif est d’investiguer les effets des CF en altitude simulé, où l’hypoxie limite la performance cognitive et physique.La consommation aigue de 900 mg CF (dont 196 mg d'épicatéchine) suscite une augmentation de l’oxygénation cérébrale, mais pas de la concentration de BDNF sérique et n'a pas d’effet sur la fonction cognitive chez des sportifs sains. L’effet bénéfique des CF sur l’oxygénation cérébrale au repos est dépassé par l’ampleur de l’augmentation de la perfusion et de l’oxygénation cérébrale à l’exercice physique et n'est donc plus visible en post-exercice.En hypoxie (altitude simulée de 4000 m), la consommation aigue de 530 mg CF (dont 100 mg d'épicatéchine) augmente la réponse hémodynamique du cortex préfrontal durant une tâche cognitive, mais n’affecte pas l’activité neuronale. Les CF améliorent la pensée abstraite en normoxie, mais n’améliorent aucun autre domaine des fonctions cognitives. Seule la précision lors du test de Stroop est diminuée par l’hypoxie. De plus, la réponse hémodynamique du cortex préfrontale et l’activité neuronale ne diffèrent pas en hypoxie vs. en normoxie.Le diabète de type 1 (DT1) est associé avec une dysfonction endothéliale, qui constitue un des facteurs de déclin cognitif lié au diabète. Dans une 3ième étude, la fonction cognitive n’est pas altérée chez les patients DT1, en comparaison des sujets sains, alors que l'activation cérébrale diffère entre ces 2 groupes. Cette différence d'activation cérébrale pourrait alors jouer un rôle compensatoire chez les patients DT1. La consommation aigue de CF peut améliorer les fonctions exécutives chez des patients DT1 et des sujets sains, et peut augmenter le signal BOLD dans les régions du cerveau activées par les tâches cognitives.Ainsi, la consommation aigue de CF augmente la vasoréactivité cérébrale. Ces changements sont associés avec une meilleure fonction cognitive chez des patients DT1, alors que ce n’est pas le cas chez des sujets entraînés, ni au niveau de la mer, ni en hypoxie. Malgré ces effets bénéfiques des CF, l’exercice physique semble rester un moyen beaucoup plus efficace pour stimuler la vasoreactivité cérébrale et les fonctions cognitives.Nous nous sommes aussi intéressés aux effets de CF sur la capacité antioxydante, le stress oxydant et la production de NO pendant l’exercice, ainsi que sur les implications pour la performance physique et la récupération, chez des athlètes. La consommation aigue de 903 mg CF augmente la capacité antioxydante au repos et pendant l’exercice, mais sans réduire le stress oxydant et la production de NO. La consommation pendant une semaine de 530 mg CF (dont 100 mg d'épicatéchine) atténue la peroxydation lipidique induite par l’exercice, mais n’influence pas la capacité antioxydante. Les CF ne modifient pas la production et la biodisponibilité du NO pendant un exercice en normoxie et en hypoxie (altitude simulée de 3000 m). La consommation de CF pendant une semaine peut augmenter la fonction endothéliale de repos, et peut réduire les effets nuisibles de l'hypoxie sur l’oxygénation préfrontale au repos et pendant l’exercice modéré. Par contre, cet effet disparait pendant l’exercice intense. La consommation aigue, et pendant une semaine, de CF n’augmente pas la performance physique, ni en normoxie, ni en hypoxie. / Sports performance depends on physical factors, but also on cognitive functioning. Nutritional supplements as potential ergogenic aids can impact muscle, but also the brain. Cocoa flavanols (CF) have antioxidant capacities, can stimulate vascular function, and potentially enhance cognitive function. CF intake might thus improve exercise performance and recovery by reducing oxidative stress, increasing NO availability and/or boosting cognitive function. It is the purpose of this PhD to identify the effects of CF on physical and cognitive performance in healthy athletes at sea level and altitude, as well as in patients with type 1 diabetes. Our systematic review showed that CF can reduce exercise-induced oxidative stress, but without improving exercise performance. Combining CF intake and exercise training improves cardiovascular risk factors and vascular function in healthy and overweight participants, but evidence on the synergistic effects of CF and exercise training on oxidative stress, inflammation and fat and glucose metabolism is lacking.In a randomized, placebo-controlled, double blind cross-over study, we showed that 900 mg CF intake increased prefrontal oxygenation in athletes, but without affecting executive function. BDNF was not affected by CF intake. The effects of high-intensity exercise largely overruled the effects of CF intake: large beneficial effects of exercise on prefrontal oxygenation and cognitive function were observed and CF supplementation did not enlarge these effects. In a 2nd study, the effect of acute CF intake (530 mg CF) on performance on a demanding cognitive test was assessed in normoxia and hypoxia (simulated altitude 4000 m). Electroencephalogram and fNIRS were used to analyse neuronal activity and hemodynamic changes. Acute CF intake improved the neurovascular response, but did not affect neuronal activity and cognitive performance in normoxia and hypoxia. Most cognitive functions, the cerebrovascular response and neuronal activity, were not altered in hypoxia in healthy subjects. In a 3rd study, we found that acute intake of 900 mg CF enhanced cognitive performance on the Flanker test in patients with type 1 diabetes, and their healthy matched controls. CF intake increased the BOLD response in brain areas activated during this specific task. While cognitive performance was not deteriorated in patients with type 1 diabetes, a different brain activation pattern during the cognitive task was observed, compared to healthy controls and this brain activation pattern was altered by CF intake. To conclude, acute CF intake improves prefrontal oxygenation and cerebrovascular responsiveness. This can be associated with better cognitive function in patients with type 1 diabetes, but does not result in improved executive function in healthy persons. Compared to exercise, the magnitude of the CF-induced neurovascular changes is small.Two studies were conducted examining the effects of CF on exercise-induced oxidative stress, NO availability and its implications for exercise performance, in well-trained cyclists. We found that acute CF (900 mg) improved the exercise-induced increase in total antioxidant capacity, but did not reduce the exercise-induced increase in lipid peroxidation. One week CF intake (530 mg CF) improved vascular function at rest, and prefrontal oxygenation at rest and during low-intensity exercise, but did not influence muscular oxygenation. One week CF intake partially restored the hypoxia-induced decline in prefrontal oxygenation during rest and low-intensity exercise, but not during high-intensity exercise. One week CF intake reduced exercise-induced lipid peroxidation, but did not alter total antioxidant capacity. Both acute and 1-week CF intake did not improve exercise performance and recovery and do not change NO production during exercise (in normoxia and hypoxia) in well-trained athletes.

This work aims at creating and verifying the trainig plan which develops dynamic and endurance skills needed for the competition called {\clqq}Ocelový muž``. The dissertation comprises three parts. The first part deals with the competition {\clqq}Ocelový muž``, the problems concerning dynamic and endurance skills, sports training and other interconected aspects. The next part is devoted to compiled training plan and to the testing of dynamic and endurance skills. Acquired knowledge is discussed and its summary is stated in conclusion.