High intensity interval training is associated with greater impact on physical fitness, insulin sensitivity and muscle mitochondrial content in males with overweight/obesity, as opposed to continuous endurance training: a randomized controlled trial

Objectives: To evaluate the effect of high intensity training (HIT) on physical fitness, basal respiratory exchange ratio (bRER), insulin sensitivity and muscle histology in overweight/obese men compared to continuous aerobic training (CAT). Material and methods: 16 male participants with overweight/obesity (age: 42-57 years, body mass index: 28-36 kg/m2) were randomized to HIT (n=8) or CAT (n=8) for 10 weeks, twice a week. HIT was composed of 10 minutes high intensity, 10 minutes continuous aerobic, 10 minutes high intensity exercises. CAT was composed of three times 10 minutes continuous exercising. Changes in anthropometry, physical and metabolic fitness were evaluated. Muscle histology (mitochondria and lipid content) was evaluated by transmission electron microscopy (TEM). Results: HIT showed a significant increase for peak VO2 (P=0.01), for insulin sensitivity (AUC glucose (P<0,001), AUC insulin (P<0,001), OGTT composite score (P=0.007)) and a significant decrease of bRER (P<0.001) compared to CAT. Muscle mitochondrial content was significantly increased after HIT at the subsarcolemmal (P=0.004 number and P=0.001 surface) as well as the intermyofibrillar site (P<0.001 number and P=0.001 surface). Conclusion: High intensity training elicits stronger beneficial effects on physical fitness, basal RER, insulin sensitivity, and muscle mitochondrial content, as compared to continuous aerobic training

Effect of Intensive Training on Mood With No Effect on Brain-Derived Neurotrophic Factor

Purpose Monitoring mood state is a useful tool for avoiding non-functional overreaching (NFOR). Brain derived neurotrophic factor (BDNF) is implicated in stress-related mood disorders. The purpose of the present study was to investigate the impact of intensified training-induced mood disturbance on plasma BDNF concentrations at rest and in response to exercise.&nbsp; Methods Eight cyclists performed 1 week of normal (NT), 1 week of intensified (INT) and 1 week of recovery (REC) training. Fasted blood samples were collected before and after exercise, on day 7 of each training week and were analyzed for plasma BDNF and cortisol concentrations. A 24-item Profile Of Mood State questionnaire was administered on day 7 of each training week and global mood score (GMS) was calculated. Results Time trial performance was impaired during INT (p=0.01) and REC (p=0.02) compared with NT. Basal plasma cortisol (NT=153&plusmn;16 ng/ml, INT=130&plusmn;11 ng/ml, REC=150&plusmn;14 ng/ml) and BDNF (NT=484&plusmn;122 pg/ml, INT=488&plusmn;122 pg/ml, REC=383&plusmn;56 pg/ml) concentrations were similar between training conditions. Likewise, similar exercise-induced increases in cortisol and BDNF concentrations were observed between training conditions. GMS was 32% greater during INTvs.NT (P&lt;0.001). Conclusion Consistent with a state of functional overreaching (FOR), impairments in performance and mood state with INT were restored after one week of REC. These results support evidence that mood changes before plasma BDNF concentrations as a biochemical marker of FOR and that cortisol is not a useful marker for predicting FOR

Altération des fonctions cognitives & Diabète de Type 1 : quel rôle préventif et curatif de l'exercice physique?

When compared to healthy controls, patients with Type 1 Diabetes (T1D), show a modest, but significant decline in their cognitive function (Brands et al., 2005). This cognitive decline is manifested through a deceleration of mental speed and a diminished mental flexibility. Hence, patients with T1D are less able to flexibly apply acquired knowledge in a new situation (Wessels et al., 2008). Even if the decline in cognitive function is modest, it could significantly influence daily activities of T1D patients, negatively affecting patients’ Quality of Life (QOL). Moreover, EEG studies have shown an increased incidence of abnormalities of brain functions in patients with T1D (Beauquis et al., 2009, Brands et al., 2004). According to the literature, mechanisms for cognitive decline are ascribed to episodes of severe hypoglycaemia, chronic hyperglycemia and C-peptide/insulin deficiency. Because the brain cannot synthesize or store glucose, it requires continuous supply of glucose. Therefore, it is not inconceivable that the disruption of glucose supply by hypoglycaemia and/or chronic hyperglycaemia (expressed as high glycated haemoglobin levels (HbA1c)) will cause disturbances of the cognitive function. Our meta-analysis (Tonoli et al., 2012) successfully demonstrated a reduction in HbA1c induced by aerobic training. Aerobic exercise is well known to enhance insulin action 24h following both acute exercise. Therefore, it is recommended that exercise is performed frequently in order to maintain a constant increase in insulin sensitivity and thus improve HbA1c. While acute aerobic exercise elicits acute marked falls in glycaemia which can often result in episodes of hypoglycaemia, this same meta-analysis revealed that there was a smaller fall of blood glucose levels when acute bouts of High Intensity Exercise (HIE) are added to aerobic training sessions compared to an acute bout of aerobic exercise without HIE. In this way, chronic hyperglycaemia could be prevented by performing regular aerobic exercise while hypoglycaemia could be prevented by adding bouts of HIE to an aerobic exercise session.Furthermore, it is well-known that physical exercise and training has beneficial effects on the cognitive function in humans and that it supports brain plasticity (Berchtold et al., 2005, Knaepen et al., 2010, Colcombe and Kramer, 2003). Physical activity and, in particular, acute exercise and training seem to be key interventions to trigger the processes through which neurotrophins mediate energy metabolism and in turn neural plasticity (Dishman, et al., 2006; Hennigan, et al., 2007; Neeper, et al., 1996; Van Praag, 2008; Vaynman, et al., 2004). The neurotrophin that is most susceptible to physical activity is brain-derived neurotrophic factor (BDNF) (Vaynman et al., 2006). BDNF is an essential neurotrophin and plays a critical role in activity-dependent processes, including synapse development and plasticity and is so involved in memory formation, including learning and behaviour, synaptic plasticity and efficacy and neuronal connectivity, plus it promotes the development of immature neurons and enhances the survival of adult neurons(Knaepen et al., 2010). I Therefore, there exists an upcoming attention in the research area of the effects of physical exercise and training on the functioning of the brain. Besides the special focus on BDNF, an increasing attention to proteins with neurotrophic properties like Insulin-like Growth Factor-1 (IGF-1) exists. If neurotrophins are influenced by physical activity and are positively correlated with cognitive function, we hypothesize that these levels will increase in T1D patients during exercise and so influence the cognitive function of these persons. Until now, no literature can be found on the topic of T1D, exercise and cognitive decline. This PhD project consists of one cross sectional epidemiological study, 2 acute exercise study in which we will analyse the effects of exercise and trainin.Il s’agit de mieux comprendre la nature et l’origine des dysfonctions cognitives chez le DT1 ainsi que l’effet possible de l’exercice aigu et chronique sur les fonctions cognitives en prenant en compte les mécanismes sous-jacents à ces effets, notamment liés aux facteurs neurotrophiques (BDNF, IGF-1) et aux variations glycémiques.Les patients diabétiques de Type 1 (DT1) peuvent présenter un déclin léger, progressif, des fonctions cognitives en comparaison de sujets sains (Brands et coll. 2005 ; Gaudieri et coll. 2008 ; Blasetti et coll. 2011), nommé par certains auteurs Déclin Cognitif Associé au Diabète (DACD) (Mijnhout et coll. 2006). Les fonctions cognitives les plus touchées semblent être l’efficience psychomotrice, l’intelligence, l’attention, la vitesse de traitement des informations, la flexibilité cognitive et la perception visuelle (Brands et coll. 2005). Les mécanismes patho-physiologiques conduisant au DACD ne sont pas clairement élucidés (Figure 3). Les épisodes hypoglycémiques, l’hyperglycémie chronique, le déficit en Peptide C/Insuline, les complications diabétiques, sont souvent cités comme délétères pour le cerveau (Tonoli, Heyman et coll. 2013b).L’effet bénéfique est bien démontré chez le sujet sain, de l’exercice aigu et chronique sur les facteurs neurotrophiques (e.g. BDNF et IGF1) (Knaepen et coll. 2010) et sur les fonctions cognitives (Cassilhas et coll. 2012 ; Lambourne et coll. 2010) notamment exécutives (Colcombe et coll. 2003 ; Tomporowski et coll. 2003) et de mémoire spatiale (Ericksson et coll. 2011). Il est important de prendre en considération l’intensité et la modalité d’exercice puisqu’il a été montré chez le sujet sain, qu’un exercice modéré pouvait améliorer les performances cognitives alors qu’un exercice intermittent de haute intensité les détériorait (Brisswalter et coll. 2002). Il est aussi nécessaire de tenir compte du niveau d’entraînement des sujets puisque lorsque ceux-ci sont entraînés en endurance, l’exercice à haute intensité peut s’avérer au contraire bénéfique sur les fonctions cognitives (Brisswalter et coll. 1997). L’effet bénéfique de l’exercice de haute intensité sur les fonctions cognitives pourrait alors passer par une sécrétion plus importante de catécholamines, lesquelles augmenteraient le niveau d’éveil des sujets (Chmura et coll. 1998). Comme la libération du BDNF dans la circulation sanguine en réponse au stimulus « exercice » semble être dose-dépendant (Knaepen et coll. 2010), notre hypothèse est que des intensités plus élevées d’exercice pourraient susciter des augmentations plus marquées de facteurs neurotrophiques. Notre hypothèse est donc que l’activité physique régulière pourrait réduire ou limiter l’apparition d’un déclin des fonctions cognitives chez les patients DT1 par des mécanismes impliquant une modulation des taux circulants de BDNF et d’IGF-1 (Etude 2 – Exercice chronique & fonctions cognitives du DT1). Néanmoins, l’exercice physique peut être source de variations importantes de la glycémie chez le patient DT1. Ces variations sont importantes à prendre en considération puisqu’elles pourraient également influencer les fonctions cognitives. La meilleure compréhension des effets possibles de l’activité physique sur la fonction cognitive des patients DT1 en lien avec la glycémie (Etude 3 – Exercice aigu & Fonctions cognitives du DT1) pourrait aider à définir des programmes d’activité physique adaptés pour limiter le déclin des fonctions cognitives

Validation and reliability of the Dutch language version of the Modifiable Activity Questionnaire in healthy subjects

International audienceBackground The Modifiable Activity Questionnaire (MAQ) is a physical activity questionnaire shown to be both valid and reliable in French. After translation and adaptation to Dutch, the objective of the study was to see whether this questionnaire was valid and reliable in the Dutch language and thus could be used as a tool for the detection of exercise levels in a Dutch native-speaking population.Methods After translating and back translating the valid French version of the MAQ into Dutch, the final product of the Dutch version was tested twice in the same population (n = 101) interrupted by 1 week for the assessment of the test–retest reliability. To measure concurrent validity, the valid Dutch version of the IPAQ was filled in at the same time as the MAQ. To measure the construct validity of this assessment tool, a smaller sample size (n = 28) of the total population carried an accelerometer for 1 week.Results The intraclass correlation coefficient for the test– retest reliability was 0.78 (p \ 0.01), suggesting a good test–retest reliability. Pearson’s rho correlation coefficient between the IPAQ and the MAQ was 0.41 (p \ 0.01), suggesting a medium concurrent validity. Pearson corre- lation statistics showed a low, non-significant correlation coefficient (r = 0.243, p = 0.213) when measuring con- struct validity.Conclusion The present study shows that the Dutch lan- guage of the MAQ is reliable and has a medium concurrent validity. Although the construct validity is low, these results are in line with previous validation studies of physical activity questionnaires

Acute cocoa flavanol improves cerebral oxygenation without enhancing executive function at rest or after exercise

Acute exercise-induced improvements in cognitive function are accompanied by increased (cerebral) blood flow and increased brain-derived neurotrophic factor (BDNF) levels. Acute cocoa flavanol (CF) intake may improve cognitive function, cerebral blood flow (in humans), and BNDF levels (in animals). This study investigated (i) the effect of CF intake in combination with exercise on cognitive function and (ii) cerebral hemodynamics and BDNF in response to CF intake and exercise. Twelve healthy men participated in this randomized, double-blind, crossover study. Participants performed a cognitive task (CT) at 100 min after acute 903-mg CF or placebo (PL) intake, followed by a 30-min time-trial. Immediately after this exercise, the same CT was performed. Prefrontal near-infrared spectroscopy was applied during CT and exercise to measure changes in oxygenated (Delta HbO(2)), deoxygenated (Delta HHb), and total haemoglobin (Delta Hb(tot)) and blood samples were drawn and analyzed for BDNF. Reaction time was faster postexercise, but was not influenced by CF. Delta HbO(2) during the resting CT was increased by CF, compared with PL. Delta HbO(2), Delta HHb, and Delta Hb(tot) increased in response to exercise without any effect of CF. During the postexercise cognitive task, there were no hemodynamic differences between CF or PL. Serum BDNF was increased by exercise, but was not influenced by CF. In conclusion, at rest, CF intake increased cerebral oxygenation, but not BDNF concentrations, and no impact on executive function was detected. This beneficial effect of CF on cerebral oxygenation at rest was overruled by the strong exercise-induced increases in cerebral perfusion and oxygenation

Effects of different types of acute and chronic (training) exercise on glycaemic control in type 1 diabetes mellitus: a meta-analysis.

International audienceExercise has been accepted and generally recommended for the management of type 1 diabetes mellitus (T1D) and for improving the overall quality of life in affected individuals. This meta-analysis was conducted to determine the overall effects of exercise (acute bouts of exercise and chronic exercise [or training]) on acute and chronic glycaemic control in patients with T1D, the effects of different types of exercise on glycaemic control and which conditions are required to obtain these positive effects. PubMed, ISI Web of Knowledge and SPORTDiscus™ were consulted to identify studies on T1D and exercise. Cohen's d statistics were used for calculating mean effect sizes (ES) as follows: small d = 0.3, medium d = 0.5 and large d = 0.8. Ninety-five percent confidence intervals (95% CIs) were used to establish the significance of our findings. From a total of 937 studies, 33 that met the inclusion criteria were selected. Nine studies were used to calculate the ES of a single bout of aerobic exercise; 13 studies to calculate the ES of aerobic training; 2 studies to calculate the ES of strength training; 4 studies to calculate the ES of combined (aerobic and strength) training and 6 studies to calculate the ES of high-intensity exercise (HIE) and training. ES for exercise on acute glycaemic control were large, while they were small for chronic glycaemic control. Aerobic exercise, resistance exercise, mixed exercise (aerobic combined with resistance training) and HIE acutely decreased blood glucose levels. To prevent late-onset hypoglycaemic episodes, the use of single bouts of sprints into an aerobic exercise can be recommended. This meta-analysis also showed that a regular exercise training programme has a significant effect on acute and chronic glycaemic control, although not all exercise forms showed significant results. Specifically, aerobic training is a favourable tool for decreasing chronic glycaemic control, while resistance training, mixed and HIE did not significantly improve chronic glycaemic control. Although, this meta-analysis showed there was a tendency for improvement in glycaemic control due to resistance training or resistance training combined with endurance training, there were not enough studies and/or subjects to confirm this statistically. Based on this meta-analysis, we can conclude that the addition of brief bouts of high-intensity, sprint-type exercise to aerobic exercise can minimize the risk of sustaining a hypoglycaemic episode. We can also conclude that only regular aerobic training will improve the glycated haemoglobin level of a patient with T1D

Type 1 diabetes-associated cognitive decline: a meta-analysis and update of the current literature

Background: Type 1 diabetes (T1D) can have a significant impact on brain structure and function, which is referred to as T1D-associated cognitive decline (T1DACD). Diabetes duration, early onset disease, and diabetes-associated complications are all proposed as factors contributing to T1DACD. However, there have been no comparisons in T1DACD between children and adults with T1D. To obtain a better insight into the occurrence and effects of T1DACD in T1D, the aim of the present meta-analysis was to investigate differences between children and adults and to analyse factors contributing T1DACD.\ud \ud Methods: Two electronic databases were consulted: PubMed and ISI Web of Knowledge. Literature published up until the end of 2013 was included in the analysis. Effect sizes (Cohen's d), which are standardized differences between experimental and control groups, were calculated.\ud \ud Results: There was a small to modest decrease in cognitive performance in T1D patients compared with non-diabetic controls. Children with T1D performed worse while testing for executive function, full intelligence quotient (IQ), and motor speed, whereas adults with T1D performed worse while testing the full, verbal and performance IQ, part of the executive function, memory, spatial memory, and motor speed. Episodes of severe hypoglycemia, chronic hyperglycemia, and age of onset can be significant factors influencing cognitive function in T1D.\ud \ud Conclusions: The findings in the literature suggest that T1DACD is more severe in adults than children, indicating that age and diabetes duration contribute to this T1DACD

The influence of a mild thermal challenge and severe hypoxia on exercise performance and serum BDNF

Aim: To examine the isolated and combined effects of severe hypoxia and a mild thermal challenge on performance, physiological measures, cognition, and serum brain-derived neurotrophic factor (BDNF).\ud \ud Methods: Nine trained male athletes (age: 23 ± 3 years; W max: 333 ± 45 W) completed four experimental trials (CON: 15 °C/0 m, ALT: 15 °C/3800 m, TEMP: 25 °C/0 m, ALT + TEMP: 25 °C/3800 m) in a double blind, randomized, cross-over design. Subjects cycled for 30 min in a self-paced test starting at 75 % W max, their goal was to 'perform as much work as possible in 30 min.' Power output, heart rate, blood lactate, pulse oximetry, core and skin temperature, thermal sensation, ratings of perceived exertion, reaction time (RT), and BDNF were assessed.\ud \ud Results: The amount of work produced in 30 min was reduced by temperature (F(1,8) = 7.1; p = 0.029; 360 ± 19 kJ in 15 °C; 344 ± 18 kJ in 25 °C) and altitude (F(1,8) = 94.2; p < 0.001; 427 ± 24 kJ at sea level; 277 ± 15 kJ at altitude), yet there was no interaction effect. Altitude increased mean RT (F(1,8) = 8.0; p = 0.022; 281.9 ± 9.4 ms at sea level; 289.3 ± 10.0 ms at altitude) and RT variability (F(1,8) = 8.5; p = 0.020; 44 ± 3 ms at sea level: 50 ± 4 ms at altitude). Exercise increased BDNF (F(1,8) = 15.2; p = 0.005; PRE: 21.8 ± 1.3 ng/mL; POST: 26.5 ± 2.1 ng/mL).\ud \ud Conclusion: Exercise capacity was significantly reduced due to an increase in altitude (3800 m; −34.3 %) or a 10 °C increase in ambient temperature (−3.2 %). The combination of both stressors showed to be additive (−38.0 %). Altitude induced an increase in RT and RT variability presenting a deterioration in cognitive functioning during acute hypoxia. Exercise significantly increased BDNF, but no effect of altitude on the BDNF concentration was observed

BDNF, IGF-I, Glucose and Insulin during Continuous and Interval Exercise in Type 1 Diabetes

Type 1 diabetes (T1D) can have a significant impact on brain function, mostly ascribed to episodes of hypoglycemia and chronic hyperglycemia. Exercise has positive effects on acute and chronic glycemic control in T1D, and has beneficial effects on cognitive function by increasing neurotrophins such as BDNF and IGF-I in non-diabetic humans. The present study examines the effects of different types of exercise intensities on neurotrophins in T1D. 10 participants with type 1 diabetes were evaluated in 3 sessions: high-intensity exercise (10×[60 s 90%Wmax, 60 s 50 W]), continuous exercise (22 min, 70% VO2 max) and a control session. Blood glucose, serum free insulin, serum BDNF and IGF-I were assessed pre/post all the trials and after recovery. Blood glucose significantly decreased after both exercise intensities and BDNF levels increased, with a dose-response effect for exercise intensity on BDNF. IGF-I changed over time, but without a difference between the different exercise protocols. Both exercise intensities change neurotrophins in T1D, but also exhibit a dose response effect for BDNF. The intensity-dependent findings may aid in designing exercise prescriptions fo