Exercise prior to a freely requested meal modifies pre and postprandial glucose profile, substrate oxidation and sympathovagal balance

<p>Abstract</p> <p>Background</p> <p>The effects of exercise on glucose and metabolic events preceding and following a freely initiated meal have never been assessed. Moreover, the relationship between these events and sympathovagal balance is not known. The objective of this study was to determine whether exercise prior to a freely requested meal modifies the pre- and postprandial glucose profile, substrate oxidation and sympathovagal balance.</p> <p>Methods</p> <p>Nine young active male subjects consumed a standard breakfast (2298 ± 357 kJ). After 120 min, they either performed 75 min of exercise on a cycle ergometer (EX - 70% VO_2max) or rested (RT). Lunch was freely requested but eaten <it>ad libitum </it>only during the 1^stsession, and then energy intake was fixed across conditions. Glucose and sympathovagal balance were assessed continuously using a subcutaneous glucose monitoring system and analysis of heart rate variability, respectively. Every 5 min, a mean value was calculated for both glucose and sympathovagal balance. Substrate oxidation was determined by calculating the gas exchange ratio when lunch was requested and 180 min after the onset of eating.</p> <p>Results</p> <p>Preprandial glucose profiles were found in 72% of the sessions and with a similar frequency under both conditions. Meals were requested after a similar delay (40 ± 12 and 54 ± 10 min in EX and RT respectively; ns). At meal request, sympathovagal balance was not different between conditions but CHO oxidation was lower and fat oxidation higher in EX than in RT (-46% and +63%, respectively; both p < 0.05). Glucose responses to the meal were higher in incremental (+ 48%) but not in absolute value in EX than in RT, with a higher fat oxidation (+ 46%, p < 0.05), and a greater vagal withdrawal (+ 15%, p < 0.05).</p> <p>Conclusions</p> <p>These results show that exercise does not impair preprandial glucose declines at the following meal freely requested, but leads to an increased postprandial glucose response and an elevated fat oxidation, an effect that vagal withdrawal may contribute to explain.</p

Appropriateness of indirect markers of muscle damage following lower limbs eccentric-biased exercises: A systematic review with meta-analysis

Purpose The aim of this review was to (1) characterize the time-course of markers of exercise-induced muscle damage (EIMD) based on the level of maximal voluntary contraction torque loss at 24-48h post-exercise (MVCloss24-48h), (2) identify factors (e.g., exercise and population characteristics) affecting the level of MVCloss24-48h, and (3) evaluate the appropriateness of EIMD markers as indicators of MVCloss24-48h. Methods Magnitude of change of each EIMD markers was normalized using the standardized mean differences method to compare the results from different studies. Time-course of EIMD markers were characterized according to three levels of MVCloss24-48h based on a clustering analysis of the 141 studies included. Association between MVCloss24-48h levels and participant´s characteristics or exercise type/modalities were assessed. Meta-regressions were performed to investigate the associations between MVCloss24-48h and EIMD markers changes at \u3c6h, 24h, 48h, 72h and \u3e 96h after exercise. Results Time-course of EIMD markers recovery differs between levels of MVCloss24-48h. Training status and exercise type/modality were associated with MVCloss24-48h level (p \u3c 0.05). MVCloss24-48h was correlated to changes in myoglobin concentration ( \u3c 6h), jump height (24h) and range of motion (48h) (p \u3c 0.001). Conclusion As the exercise could differently affect markers as function of the EIMD severity (i.e., MVCloss24-48h levels), different markers should be used as function of the timing of measurement. Mb concentration should be used during the first hours after the exercise ( \u3c 6h), whereas jump height (24h) and range of motion (48h) could be used as surrogate for maximal voluntary contraction later. Moreover, training status and exercise type/modality could influence the magnitude of MVCloss24-48

Resting Muscle Shear Modulus Measured With Ultrasound Shear-Wave Elastography as an Alternative Tool to Assess Muscle Fatigue in Humans

The aim of this study was to investigate the time course of the resting vastus lateralis (VL) muscle shear elastic modulus (μ) measured with ultrasound shear-wave elastography during repetition of isometric maximal voluntary contractions (MVCs) of the knee extensors (KE). Fifteen well-trained young males repeated 60 5-s isometric MVCs. Evoked electrical stimulations and the VLμ were measured every ten MVCs at rest. The resting VLμ significantly decreased (−34.7 ± 6.7%; P &lt; 0.001) by the end of the fatigue protocol. There was also a 38.4 ± 12.6 % decrease in MVC after exercise (P &lt; 0.001). The potentiated doublet and single twitch torque amplitudes and properties were significantly modified by the end of exercise (P &lt; 0.001). This study shows the time course of the resting VLμ during the repetition of maximal voluntary fatiguing exercise of the KE muscles. The decrease of the resting VLμ could directly affect the force transmission capabilities accounting for peripheral fatigue

Impacts physiologiques de la fragmentation de la prise alimentaire

International audienceAucu

Notre appétit est-il modifié par une exposition au froid ou au chaud ?

International audienceAucu

Influence of Hot and Cold Environments on the Regulation of Energy Balance Following a Single Exercise Session: A Mini-Review

Understanding the regulation of human food intake in response to an acute exercise session is of importance for interventions with athletes and soldiers, as well as overweight individuals. However, the influence of hot and cold environments on this crucial function for the regulation of body mass and motor performance has not been summarized. The purpose of this review was to exhaustively search the literature on the effect of ambient temperature during an exercise session on the subsequent subjective feeling of appetite, energy intake (EI) and its regulation. In the absence of stress due to environmental temperature, exercise-induced energy expenditure is not compensated by EI during an ad libitum meal following the session, probably due to decreased acylated ghrelin and increased peptide tyrosine tyrosine (PYY), glucagon-like peptide 1 (GLP-1), and pancreatic polypeptide (PP) levels. No systematic analysis has been yet made for major alterations of relative EI in cold and hot environments. However, observed eating behaviors are altered (proportion of solid/liquid food, carbohydrate/fat) and physiological regulation appears also to be altered. Anorexigenic signals, particularly PYY, appear to further increase in hot environments than in those that are thermoneutral. Ghrelin and leptin may be involved in the observed increase in EI after exercise in the cold, in parallel with increased energy expenditure. The potential influence of ambient thermal environment on eating behaviors after an exercise session should not be neglected

Negative energy balance during military training: The role of contextual limitations

International audienc

Effets des expositions aiguës et chroniques à des températures extrêmes sur les déterminants de la prise alimentaire

International audienceAucu

Energy compensation after an aerobic exercise session in high-fat/low-fit and low-fat/high-fit young male subjects

International audienceThere is general agreement that exercise-induced energy expenditure is not entirely compensated for at the next meal or over the following 24 h, but inter-individual variability is high. The role of ‘fatness and fitness’ in this variability has never been assessed. Therefore, eighteen non-obese male subjects aged 22·2 ( sd 2·0) years were selected and separated into a ‘high-fatness and low-fitness’ (Hfat/Lfit, n 9) and a ‘low-fatness and high-fitness’ (Lfat/Hfit, n 9) group, according to three criteria: maximal oxygen uptake; weekly hours of physical activity; fat mass index. At 1 h before lunch, they were subjected to 60 min of exercise on a cycle ergometer (70 % V O2max ), or stayed at rest. Then, they self-reported food intake in diaries until the next breakfast. Intake at lunch was not different between conditions, but was higher after exercise than after rest over the 24 h, leading to a significant but partial mean level of compensation of 49·8 ( sem 16·5) and 37·8 ( sem 24·6) % for the Hfat/Lfit and Lfat/Hfit groups, respectively. Energy compensation at lunch and over the 24 h were strongly correlated ( r 0·76, P < 0·001). Both groups consumed more fat and protein after exercise than after rest over the 24 h, but the percentage of energy derived from fat increased only in the Hfat/Lfit group (2·1 ( sem 0·6) %, P = 0·026). Thus, the energy cost of an aerobic exercise session was partially compensated over the next 24 h independently of the ‘fatness and fitness’ status, but ‘high-fat and low-fit’ individuals compensated more specifically on fats

Physiology of energy homeostasis: Models, actors, challenges and the glucoadipostatic loop

International audienceThe aim of this review is to discuss the physiology of energy homeostasis (EH), which is a debated concept. Thus, we will see that the set-point theory is highly challenged and that other models integrating an anticipative component, such as energy allostasis, seem more relevant to experimental reports and life preservation. Moreover, the current obesity epidemic suggests that EH is poorly efficient in the modern human dietary environment. Non-homeostatic phenomena linked to hedonism and reward seem to profoundly impair EH. In this review, the apparent failed homeostatic responses to energy challenges such as exercise, cafeteria diet, overfeeding and diet-induced weight loss, as well as their putative determinants, are analyzed to highlight the mechanisms of EH. Then, the hormonal, neuronal, and metabolic factors of energy intake or energy expenditure are briefly presented. Last, this review focuses on the contributions of two of the most pivotal and often overlooked determinants of EH: the availability of endogenous energy and the pattern of energy intake. A glucoadipostatic loop model is finally proposed to link energy stored in adipose tissue to EH through changes in eating behavior via leptin and sympathetic nervous system activity