Revisiting the Role of Exercise Countermeasure on the Regulation of Energy Balance During Space Flight

A body mass loss has been consistently observed in astronauts. This loss is of medical concern since energy deficit can exacerbate some of the deleterious physiological changes observed during space flight including cardiovascular deconditioning, bone density, muscle mass and strength losses, impaired exercise capacity, and immune deficiency among others. These may jeopardize crew health and performance, a healthy return to Earth and mission’s overall success. In the context of planning for planetary exploration, achieving energy balance during long-term space flights becomes a research and operational priority. The regulation of energy balance and its components in current longer duration missions in space must be re-examined and fully understood. The purpose of this review is to summarize current understanding of how energy intake, energy expenditure, and hence energy balance are regulated in space compared to Earth. Data obtained in both actual and simulated microgravity thus far suggest that the obligatory exercise countermeasures program, rather than the microgravity per se, may be partly responsible for the chronic weight loss in space. Little is known of the energy intake, expenditure, and balance during the intense extravehicular activities which will become increasingly more frequent and difficult. The study of the impact of exercise on energy balance in space also provides further insights on lifestyle modalities such as intensity and frequency of exercise, metabolism, and the regulation of body weight on Earth, which is currently a topic of animated debate in the field of energy and obesity research. While not dismissing the significance of exercise as a countermeasure during space flight, data now challenge the current exercise countermeasure program promoted and adopted for many years by all the International Space Agencies. An alternative exercise approach that has a minimum impact on total energy expenditure in space, while preventing muscle mass loss and other physiological changes, is needed in order to better understand the in-flight regulation of energy balance and estimate daily energy requirements. A large body of data generated on Earth suggests that alternate approaches, such as high intensity interval training (HIIT), in combination or not with sessions of resistive exercise, might fulfill such needs

Movement and heart rate in the Scandinavian brown bear (<i>Ursus arctos</i>)

Background: Understanding animal movement facilitates better management and conservation. The link between movement and physiology holds clues to the basic drivers of animal behaviours. In bears, heart rate increases with the metabolic rate during the active phase. Their movement and heart rate change at seasonal and daily scales, and can also depend on environmental factors. Their behaviour is, therefore, flexible in activity patterns with high individual variations. The aim of this study was to establish the relationship between heart rate and distance travelled, and test whether this relationship was influenced by environmental (e.g., time of year and time of day) and biological (e.g., reproductive status, sex, body mass and age of the bears) factors. We analysed data of distance travelled and heart rate of 15 GPS-collared brown bears, both males and females, equipped with cardiac loggers in the south of Sweden in 2014–2017. Results: Heart rate increased with distances travelled exceeding 50 m in an hour, but this correlation depended on the day-of-year with higher heart rate in August than in May. Bears accompanied by cubs had lower heart rate than solitary bears especially in May. When movement was minimum (< 50 m in an hour), heart rate was not related to distance travelled and was very variable, regardless of the months. Conclusions: Our findings suggest that heart rate increases with long distances travelled, but varies with day-of-year and reproductive status, depending on the metabolic rate. Studying the change in heart rate in bears can help to evaluate their seasonal rhythms and how different factors affect them. This study illustrates the usefulness of combined bio-logging proxies, i.e., movement and heart rates in our case, in animal ecology. Distance travelled, GPS positions, Cardiac bio-logger, Seasonal variation, Reproductive statuspublishedVersio

Acute effects of active breaks during prolonged sitting on subcutaneous adipose tissue gene expression: an ancillary analysis of a randomised controlled trial.

Active breaks in prolonged sitting has beneficial impacts on cardiometabolic risk biomarkers. The molecular mechanisms include regulation of skeletal muscle gene and protein expression controlling metabolic, inflammatory and cell development pathways. An active communication network exists between adipose and muscle tissue, but the effect of active breaks in prolonged sitting on adipose tissue have not been investigated. This study characterized the acute transcriptional events induced in adipose tissue by regular active breaks during prolonged sitting. We studied 8 overweight/obese adults participating in an acute randomized three-intervention crossover trial. Interventions were performed in the postprandial state and included: (i) prolonged uninterrupted sitting; or prolonged sitting interrupted with 2-minute bouts of (ii) light- or (iii) moderate-intensity treadmill walking every 20 minutes. Subcutaneous adipose tissue biopsies were obtained after each condition. Microarrays identified 36 differentially expressed genes between the three conditions (fold change ≥0.5 in either direction; p < 0.05). Pathway analysis indicated that breaking up of prolonged sitting led to differential regulation of adipose tissue metabolic networks and inflammatory pathways, increased insulin signaling, modulation of adipocyte cell cycle, and facilitated cross-talk between adipose tissue and other organs. This study provides preliminary insight into the adipose tissue regulatory systems that may contribute to the physiological effects of interrupting prolonged sitting

Effect of physical inactivity on the oxidation of saturated and monounsaturated dietary Fatty acids: results of a randomized trial

OBJECTIVES: Changes in the way dietary fat is metabolized can be considered causative in obesity. The role of sedentary behavior in this defect has not been determined. We hypothesized that physical inactivity partitions dietary fats toward storage and that a resistance exercise training program mitigates storage

Increasing Dietary Fat Elicits Similar Changes in Fat Oxidation and Markers of Muscle Oxidative Capacity in Lean and Obese Humans

In lean humans, increasing dietary fat intake causes an increase in whole-body fat oxidation and changes in genes that regulate fat oxidation in skeletal muscle, but whether this occurs in obese humans is not known. We compared changes in whole-body fat oxidation and markers of muscle oxidative capacity differ in lean (LN) and obese (OB) adults exposed to a 2-day high-fat (HF) diet. Ten LN (BMI = 22.5±2.5 kg/m2, age = 30±8 yrs) and nine OB (BMI = 35.9±4.93 kg/m2, 38±5 yrs, Mean±SD) were studied in a room calorimeter for 24hr while consuming isocaloric low-fat (LF, 20% of energy) and HF (50% of energy) diets. A muscle biopsy was obtained the next morning following an overnight fast. 24h respiratory quotient (RQ) did not significantly differ between groups (LN: 0.91±0.01; OB: 0.92±0.01) during LF, and similarly decreased during HF in LN (0.86±0.01) and OB (0.85±0.01). The expression of pyruvate dehydrogenase kinase 4 (PDK4) and the fatty acid transporter CD36 increased in both LN and OB during HF. No other changes in mRNA or protein were observed. However, in both LN and OB, the amounts of acetylated peroxisome proliferator-activated receptor γ coactivator-1-α (PGC1-α) significantly decreased and phosphorylated 5-AMP-activated protein kinase (AMPK) significantly increased. In response to an isoenergetic increase in dietary fat, whole-body fat oxidation similarly increases in LN and OB, in association with a shift towards oxidative metabolism in skeletal muscle, suggesting that the ability to adapt to an acute increase in dietary fat is not impaired in obesity

Effet de l'inactivité physique sur les balances énergétique et oxydative : inférences sur le rôle de la sédentarité dans l'étiologie de l'obésité

L'obésité est une maladie du stockage des lipides et une vision classique de son étiologie repose sur une incapacité à utiliser les lipides qui serait causale dans la prise de poids. Or l'observation relativement récente d'un alignement étroit de la balanObesity is a fat storage disease and its aetiology is classically viewed as the result of an incapacity to use fat as fuel. However, the recent observation of the tight relationship between energy and lipid balances strongly suggests that the physical ac

Écologie de la santé : la transition globale de l'activité physique

Écologie-éthologi

Effet de l'inactivité physique sur les balances énergétique et oxydative : inférences sur le rôle de la sédentarité dans l'étiologie de l'obésité

L'obésité est une maladie du stockage des lipides et une vision classique de son étiologie repose sur une incapacité à utiliser les lipides qui serait causale dans la prise de poids. Or l'observation relativement récente d'un alignement étroit de la balance lipidique sur la balance énergétique suggère fortement que le niveau d'activité physique, en tant qu élément le plus modulable de la dépense énergétique totale, pourrait jouer un rôle clef dans le devenir des lipides alimentaires. Le corollaire direct de cette observation est que l'incapacité à utiliser les lipides en tant que substrat, observée chez les sujets obèses et post-obèses, pourrait être secondaire à l'adoption généralisée d'un mode de vie sédentaire. Toutefois, nous disposons à ce jour de peu de données concernant la physiologie de l'inactivité physique. Le but majeur de ce travail de thèse a été de déterminer chez l'homme et la femme normo-pondérés si l'inactivité physique altère la régulation des balances énergétique et oxydative des lipides impliquées dans la régulation du poids et de caractériser les mécanismes sous-jacents. Pour cela, nous avons soumis des sujets femme et homme sains sans aucune prédisposition génétique à l'obésité à 2 et 3 mois d'inactivité physique, respectivement, en utilisant le modèle de l'alitement prolongé. Nous avons montré que lors de longues périodes d'inactivité physique, l'énergie ingérée est diminuée proportionnellement à la dépense énergétique totale sous l'effet de signaux satiétogènes dont la leptine. Ainsi la balance énergétique peut-être maintenue sur le long terme. Néanmoins, l'inactivité physique altère l'homéostasie des macronutriments avec une répartition des lipides au profit du stockage et entraîne le développement d'une insulino-résistance. Cette diminution de l'oxydation lipidique totale est probablement due, en partie, à la diminution du transport des acides gras dans le myocyte et la mitochondrie. L'inactivité physique induit aussi une augmentation de l'absorption intestinale et/ou une diminution de la clairance plasmatique des acides gras exogènes résultant en une hypertriglycéridémie et un spill-over accru des acides gras libres provenant de l'hydrolyse des lipoprotéines par la lipoprotéine lipase. De manière intéressante, l'inactivité physique diminue l'oxydation des acides gras alimentaires saturés (palmitate) mais pas celle des acides gras monoinsaturés (oléate). Puisque les acides oléique et palmitique alimentaires semblent avoir une absorption, un acheminement et une captation par les tissus périphériques similaires, l'inactivité physique altèrerait la répartition des acides gras saturés au profit d'un stockage au niveau musculaire. Cette hypothèse semble étayée par la relation négative obtenue entre la réduction d'oxydation du palmitate et la quantité de lipides au niveau musculaire. Ce résultat est d'autant plus intéressant lorsque l'on considère la relation établie entre l'insulino-résistance et les triglycérides intramusculaires. Ainsi, l'inactivité physique, indépendamment des changements de la balance énergétique, induit chez des individus sains des caractéristiques physiologiques proches de celles que l'on observe chez des sujets obèses. Ces observations soutiennent notre hypothèse selon laquelle la sédentarité serait une des causes majeures de l'étiologie de l'obésité. De plus amples études sur les mécanismes impliqués dans le stockage préférentiel des acides gras saturés dans les triglycérides intramusculaires et l'impact sur la réponse à l'insuline en conditions d'inactivité physique sont cependant requises afin d'étendre notre compréhension sur l'interaction entre régime alimentaire et activité physique dans le développement de l'obésité et du diabète. En testant l'efficacité de deux protocoles d'entraînement d'exercice physique (résistif versus résistif et aérobic) pour contrer les effets délétères de l'inactivité physique, nos résultats ont mis en avant le rôle clef de la dépense énergétique dans la régulation de l'oxydation lipidique totale. Toutefois, nous pensons que l'inefficacité de l'entraînement physique observée sur le maintien de l'oxydation des acides gras exogènes serait plutôt due à une faible activité de type spontanée (tout type de mouvement) qu à une dépense énergétique insuffisante induite par l'exercice physique. Ainsi, l'activité physique de type structurée ou spontanée influencerait différemment le métabolisme lipidique. Ceci ne représente qu une hypothèse à ce jour et des études supplémentaires sur la physiologie de l'exercice, de l'activité physique non structurée mais aussi de l'inactivité physique sont clairement requises. Le modèle de l'alitement prolongé semble approprié pour de telles investigations.Obesity is a fat storage disease and its aetiology is classically viewed as the result of an incapacity to use fat as fuel. However, the recent observation of the tight relationship between energy and lipid balances strongly suggests that the physical activity level, which represents the main variable component of the total energy expenditure, may play a key role in the dietary lipid fate. The direct corollary of this observation is that the incapacity to use fat as fuel observed in both obese and post-obese individuals may be secondary to the generalised adoption of sedentary behaviours in the general population. Nevertheless, our current knowledge on the physical inactivity physiology is very poor. The main aim of this present thesis was to determine in normal-weight men and women whether the physical inactivity impairs the regulation of both energy and lipid balances, both involved in the body weight regulation and to delineate the related mechanisms. To do so, we used the long-term bed rest model to submit healthy lean women and men without any genetic predisposition to obesity to 2 and 3 months of physical inactivity, respectively. We showed that during long periods of physical inactivity, energy intake is spontaneously decreased under the control of satietogenic signals (i.e. leptin) and matches the reduced energy expenditure. Energy balance can thus be maintained on the long-term. However, physical inactivity alters the macronutrients homeostasis. Indeed, it induces a preferential channelling of lipids towards storage associated with a reduced fat oxidation and a development of an insulin resistance. This decrease in total lipid oxidation is likely due, at least in part, to a reduced transport of fatty acids into myocyte and mitochondria. Physical inactivity also induces an increase in intestinal absorption and/or a drop in the plasmatic clearance of exogenous fatty acids, which results in a hypertriglyceridemia and an elevated spill-over of the fre fatty acids released by the hydrolysis of the triglyceride-rich lipoproteins by the lipoprotein lipase. Interestingly, physical inactivity decreases the oxidation of the dietary saturated fatty acids (palmitate) but not that of the dietary monounsaturated fatty acids (oleate). Since saturated and monounsaturated fatty acids have a similar absorption rate, trafficking and uptake by the peripheral tissues, physical inactivity seems to impact the partitioning of saturated fatty acids towards storage versus oxidation likely via a preferential accumulation of palmitate in muscle fat. This hypothesis is supported by a negative relationship between the physical inactivity-induced reduced palmitate oxidation and the muscle lipid content. This result is of particular interest when considering the clear relationship observed between intra-muscular triglycerides and the development of insulin resistance. Therefore, physical inactivity, independent of energy balance changes, triggers the development of metabolic features close to what is observed in both obese and diabetic individuals. These observations support our hypothesis, which places sedentary behaviours as one of the major causes responsible for the aetiology of obesity. Further studies on the mechanisms involved in the preferential storage of saturated fatty acids towards intra-muscular triglycerides and on the related insulin response under physical inactivity conditions are, however, required in order to gain a better understanding on the interaction between diet and physical activity in the development of both obesity and diabetes. The second aim of this thesis was to test the efficiency of two physical exercise training programs (resistive vs. resistive and aerobic) to counteract the deleterious effects induced by physical inactivity. Our results highlighted the key role of the total energy expenditure in the regulation of total lipid oxidation. Nevertheless, we think that the inefficacy of the exercise trainings to maintain the exogenous fatty acid oxidation would be rather due to a low spontaneous physical activity (any bodily movement) than to an insufficient exercise-induced energy expenditure. Thus, structured and spontaneous physical activity may differently affect the lipid metabolism. This only represents a hypothesis and further studies on the physiology of exercise, of non-structured physical activity but also of physical inactivity are clearly required. The model of the long-term bed rest seems to be highly relevant for such nvestigations

Écologie de la santé : la transition globale de l'activité physique

Écologie-éthologi