OBJECTIVE Long before clinical complications of type 1 diabetes (T1D) develop, oxygen supply and use can be altered during activities of daily life. We examined in patients with uncomplicated T1D all steps of the oxygen pathway, from the lungs to the mitochondria, using an integrative ex vivo (muscle biopsies) and in vivo (during exercise) approach. RESEARCH DESIGN AND METHODS We compared 16 adults with T1D with 16 strictly matched healthy control subjects. We assessed lung diffusion capacity for carbon monoxide and nitric oxide, exercise-induced changes in arterial O2 content (SaO2, PaO2, hemoglobin), muscle blood volume, and O2 extraction (via near-infrared spectroscopy). We analyzed blood samples for metabolic and hormonal vasoactive moieties and factors that are able to shift the O2-hemoglobin dissociation curve. Mitochondrial oxidative capacities were assessed in permeabilized vastus lateralis muscle fibers. RESULTS Lung diffusion capacity and arterial O2 transport were normal in patients with T1D. However, those patients displayed blunted exercise-induced increases in muscle blood volume, despite higher serum insulin, and in O2 extraction, despite higher erythrocyte 2,3-diphosphoglycerate. Although complex I– and complex II–supported mitochondrial respirations were unaltered, complex IV capacity (relative to complex I capacity) was impaired in patients with T1D, and this was even more apparent in those with long-standing diabetes and high HbA1c. O2max was lower in patients with T1D than in the control subjects. CONCLUSIONS Early defects in microvascular delivery of blood to skeletal muscle and in complex IV capacity in the mitochondrial respiratory chain may negatively impact aerobic fitness. These findings are clinically relevant considering the main role of skeletal muscle oxidation in whole-body glucose disposal.

The purpose of the present study was to examine the effect of chronic exercise on the hypothalamus and hippocampus levels of the endocannabinoids (eCBs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) and of two AEA congeners and on the expression of genes coding for CB1, CB2 receptors (Cnr1 and Cnr2, respectively), and the enzymes responsible for eCB biosynthesis and degradation, in rats fed with a standard or high-fat diet. Male Wistar rats (n = 28) were placed on a 12-week high-fat (HFD) or standard diet period, followed by 12 weeks of exercise training for half of each group. Tissue levels of eCBs and related lipids were measured by liquid chromatography mass spectrometry, and expression of genes coding for CB1 and CB2 receptors and eCB metabolic enzymes was measured by quantitative real-time polymerase chain reaction (qPCR). HFD induced a significant increase in 2-AG (p < 0.01) in hypothalamus. High-fat diet paired with exercise training had no effect on AEA, 2-AG, and AEA congener levels in the hypothalamus and hippocampus. Cnr1 expression levels were significantly increased in the hippocampus in response to HFD, exercise, and the combination of both (p < 0.05). Our results indicate that eCB signaling in the CNS is sensitive to diet and/or exercise.

Aims/hypothesis Regular exercise is at the cornerstone of care in type 1 diabetes. However, relative hyperinsulinaemia and a blunted glucagon response to exercise promote hypoglycaemia. Recently, a selective antagonist of somatostatin receptor 2, PRL-2903, was shown to improve glucagon counterregulation to hypoglycaemia in resting streptozotocin-induced diabetic rats. The aim of this study was to test the efficacy of PRL-2903 in enhancing glucagon counterregulation during repeated hyperinsulinaemic exercise.Methods Diabetic rats performed daily exercise for 1 week and were then exposed to saline (154 mmol/l NaCl) or PRL-2903, 10 mg/kg, before hyperinsulinaemic exercise on two separate occasions spaced 1 day apart. In the following week, animals crossed over to the alternate treatment for a third hyperinsulinaemic exercise protocol.Results Liver glycogen content was lower in diabetic rats compared with control rats, despite daily insulin therapy (p < 0.05). Glucagon levels failed to increase during exercise with saline but increased three-to-six fold with PRL-2903 (all p < 0.05). Glucose concentrations tended to be higher during exercise and early recovery with PRL-2903 on both days of treatment; this difference did not achieve statistical significance (p > 0.05).Conclusions/interpretation PRL-2903 improves glucagon counterregulation during exercise. However, liver glycogen stores or other factors limit the prevention of exercise-induced hypoglycaemia in rats with streptozotocin-induced diabetes.

Type-1 diabetes mellitus (T1D) causes impairments within the skeletal muscle microvasculature. Both regular exercise and prazosin have been shown to improve skeletal muscle capillarization and metabolism in healthy rats through distinct angiogenic mechanisms. The aim of this study was to evaluate the independent and additive effects of voluntary exercise and prazosin treatment on capillary-to-fiber ratio (C:F) in streptozotocin (STZ)-treated diabetic rats. STZ (65 mg/kg) was intraperitoneally administered to male Sprague-Dawley rats (n = 36) to induce diabetes, with healthy, nondiabetic, sedentary rats (n = 10) as controls. The STZ-treated rats were then divided into sedentary (SED) or exercising (EX; 24-h access to running wheels) groups and then further subdivided into prazosin (Praz) or water (H2O) treatment groups: nondiabetic-SED-H2O, STZ-SED-H2O, STZ-EX-H2O, STZ-SED-Praz, and STZ-EX-Praz. After 3 wk, untreated diabetes significantly reduced the C:F in tibialis anterior (TA) and soleus muscles in the STZ-SED-H2O animals (both P < 0.05). Voluntary exercise and prazosin treatment independently resulted in a normalization of C:F within the TA (1.86 ± 0.12 and 2.04 ± 0.03 vs 1.71 ± 0.09, P < 0.05) and the soleus (2.36 ± 0.07 and 2.68 ± 0.14 vs 2.13 ± 0.12, P < 0.05). The combined STZ-EX-Praz group resulted in the highest C:F within the TA (2.26 ± 0.07, P < 0.05). Voluntary exercise volume was negatively correlated with fed blood glucose levels (r2 = -0.7015, P < 0.01) and, when combined with prazosin, caused further enhanced nonfasted glucose (P < 0.01). Exercise and prazosin reduced circulating nonesterified fatty acids more than either stimulus alone (P < 0.05). These results suggest that the distinct stimulation of angiogenesis, with both regular exercise and prazosin treatment, causes a cooperative improvement in the microvascular complications associated with T1D.NEW & NOTEWORTHY It is currently well established that poorly controlled diabetes reduces both skeletal muscle mass and muscle capillarization. These muscle-specific features of diabetes may, in turn, compromise insulin sensitivity and glucose control. Using a model of streptozotocin-induced diabetes, we show the vascular complications linked with disease and how chronic exposure to exercise and prazosin (an α1-adrenergic antagonist) can reduce these complications and improve glycemic control.

OBJECTIVE Cerebral vasoreactivity to pharmacologically induced hypercapnia is impaired in poorly controlled patients with type 1 diabetes but otherwise free from microangiopathy. However, whether this response is also compromised during exercise, a daily-life physiological condition challenging regional cerebral hemodynamics, is unknown. We aimed to investigate prefrontal cortex hemodynamics during incremental maximal exercise in patients with uncomplicated type 1 diabetes, taking into account long-term glycemic control as well as exercise- and diabetes-influenced vasoactive stimuli. RESEARCH DESIGN AND METHODS Two groups of patients (type 1 diabetes with adequate glycemic control [T1D-A], n = 8, HbA1c 6.8 ± 0.7% [51 ± 7.7 mmol/mol]; type 1 diabetes with inadequate glycemic control [T1D-I], n = 10, HbA1c 9.0 ± 0.7% [75 ± 7.7 mmol/mol]) were compared with 18 healthy control subjects (CON-A and CON-I) matched for physical activity and body composition. Throughout exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin (O2Hb), deoxyhemoglobin (HHb), and total hemoglobin (THb) in the prefrontal cortex. Venous and arterialized capillary blood was sampled during exercise to assess for factors that may alter prefrontal cortex hemodynamics and oxygenation. RESULTS No differences were observed between T1D-A and CON-A, but VO2max was impaired (P < 0.05) and cerebral blood volume (THb) increase blunted (P < 0.05) in T1D-I compared with CON-I. Nonetheless, O2Hb appeared unaltered in T1D-I probably partly due to blunting of simultaneous neuronal oxygen extraction (i.e., a lower HHb increase; P < 0.05). There were no intergroup differences in arterial oxygen content, Paco2, pH, [K+], and free insulin levels. CONCLUSIONS Maximal exercise highlights subtle disorders of both hemodynamics and neuronal oxygenation in the prefrontal cortex of poorly controlled patients with type 1 diabetes. These findings may warn clinicians of brain endothelial dysfunction occurring even before overt microangiopathy during exercise.

Grâce à des méthodes pharmacologiques induisant une hypercapnie, une altération de la vasoréactivité cérébrale altérée a été mise en évidence chez des patients diabétiques de type 1 (DT1) mal équilibrés et indemnes de complications microvasculaires. Notre hypothèse est que la vasoréactivité cérébrale pourrait être également compromise en réponse à des situations physiologiques stimulatrices de la perfusion régionale cérébrale, tel que l'exercice exhaustif. Des adultes DT1, indemnes de complications, divisés en deux groupes (HbA1c < 7 %, n = 8 et HbA1c > 8 %, n = 10), appariés à des témoins sains, ont réalisé un exercice progressif exhaustif avec mesure des variations d'oxyhémoglobine, de désoxyhémoglobine et d'hémoglobine totale, au niveau du cortex préfrontal gauche, par spectroscopie du proche infrarouge. Des prélèvements veineux et capillaires artérialisés au repos et à l'exercice maximal ont été réalisés afin de mesurer les variables qui sont connues par leurs actions sur l'hémodynamique cérébrale et qui peuvent être modifiées par le diabète et/ou l'exercice physique (PaCO2, pH et insuline libre). L'augmentation de l'hémoglobine totale (effets groupe p < 0,001 et interaction p < 0,05), reflétant la perfusion locale, ainsi que l'augmentation de HHb (effet interaction p < 0,05), reflétant l'extraction neuronale d'O2, sont significativement atténuées à l'exercice chez les patients mal équilibrés. Les variables capables d'influencer l'hémodynamique cérébrale étaient comparables entre les patients et leurs sujets contrôles. L'exercice physique maximal permet de mettre en exergue des altérations fonctionnelles de la microcirculation, au niveau du cortex préfrontal, avant même l'apparition de complications microvasculaires détectables par les tests cliniques habituels. Ces altérations fonctionnelles sont probablement la conséquence de l'effet délétère de l'hyperglycémie chronique sur la fonction endothéliale. Les auteurs déclarent ne pas avoir d'intérêt direct ou indirect (financier ou en nature) avec un organisme privé, industriel ou commercial en relation avec le sujet présenté.

Diabetes is rapidly induced in young male Sprague-Dawley rats following treatment with exogenous corticosterone (CORT) and a high-fat diet (HFD). Regular exercise alleviates insulin insensitivity and improves pancreatic β-cell function in insulin-resistant/diabetic rodents, but its effect in an animal model of elevated glucocorticoids is unknown. We examined the effect of voluntary exercise (EX) on diabetes development in CORT-HFD-treated male Sprague-Dawley rats (∼6 wk old). Animals were acclimatized to running wheels for 2 wk, then given a HFD, either wax (placebo) or CORT pellets, and split into 4 groups: placebo-sedentary (SED) or -EX and CORT-SED or -EX. After 2 wk of running combined with treatment, CORT-EX animals had reduced visceral adiposity, and increased skeletal muscle type IIb/x fiber area, oxidative capacity, capillary-to-fiber ratio and insulin sensitivity compared with CORT-SED animals (all P < 0.05). Although CORT-EX animals still had fasting hyperglycemia, these values were significantly improved compared with CORT-SED animals (14.3 ± 1.6 vs. 18.8 ± 0.9 mM). In addition, acute in vivo insulin response to an oral glucose challenge was enhanced ∼2-fold in CORT-EX vs. CORT-SED ( P < 0.05) which was further demonstrated ex vivo in isolated islets. We conclude that voluntary wheel running in rats improves, but does not fully normalize, the metabolic profile and skeletal muscle composition of animals administered CORT and HFD.

Purpose Aerobic fitness, as reflected by maximal oxygen (O-2) uptake (VO2max), is impaired in poorly controlled patients with type 1 diabetes. The mechanisms underlying this impairment remain to be explored. This study sought to investigate whether type 1 diabetes and high levels of glycated hemoglobin (HbA(1c)) influence O-2 supply including O-2 delivery and release to active muscles during maximal exercise.Methods Two groups of patients with uncomplicated type 1 diabetes (T1D-A, n = 11, with adequate glycemic control, HbA(1c) <7.0%; T1D-I, n = 12 with inadequate glycemic control, HbA(1c) >8%) were compared with healthy controls (CON-A, n = 11; CON-I, n = 12, respectively) matched for physical activity and body composition. Subjects performed exhaustive incremental exercise to determine VO2max. Throughout the exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin, deoxyhemoglobin, and total hemoglobin in the vastus lateralis. Venous and arterialized capillary blood was sampled during exercise to assess arterial O-2 transport and factors able to shift the oxyhemoglobin dissociation curve.Results Arterial O-2 content was comparable between groups. However, changes in total hemoglobin (i.e., muscle blood volume) was significantly lower in T1D-I compared with that in CON-I. T1D-I also had impaired changes in deoxyhemoglobin levels and increase during high-intensity exercise despite normal erythrocyte 2,3-diphosphoglycerate levels. Finally, VO2max was lower in T1D-I compared with that in CON-I. No differences were observed between T1D-A and CON-A.Conclusions Poorly controlled patients displayed lower VO2max and blunted muscle deoxyhemoglobin increase. The latter supports the hypotheses of increase in O-2 affinity induced by hemoglobin glycation and/or of a disturbed balance between nutritive and nonnutritive muscle blood flow. Furthermore, reduced exercise muscle blood volume in poorly controlled patients may warn clinicians of microvascular dysfunction occurring even before overt microangiopathy.

La consommation maximale d'oxygène (VO2max) est altérée chez les patients présentant un diabète de type 1 (DT1) mal équilibré. Notre objectif est d'étudier l'impact du DT1 et des niveaux d'hémoglobine glyquée (HbA1c) sur la cascade de l'O2, depuis sa diffusion alvéolo-capillaire, son transport artériel et sa libération au niveau musculaire, jusqu'à son utilisation mitochondriale. Des adultes DT1, indemnes de complications, divisés en deux groupes (HbA1c < 7 %, n = 11 et HbA1c > 8 %, n = 12), appariés à des témoins sains, ont effectué 1/ une double diffusion DLCO/DLNO (volume capillaire pulmonaire, conductance de la membrane alvéolo-capillaire) 2/ une épreuve d'effort progressive exhaustive incluant des mesures d'oxygénation et d'hémodynamique au niveau du vastus lateralis (spectroscopie du proche infrarouge), du contenu artériel en O2 et des variables influençant l'hémodynamique et/ou la dissociation de l'oxyhémoglobine (pH ; PaCO2 ; 2,3-DPG ; insuline ; glucose sur prélèvements veineux et capillaires artérialisés au repos et l'effort maximum). 3/ la respiration mitochondriale était mesurée (biopsie du vastus lateralis) chez 16 DT1 et leurs témoins. La VO2max est altérée chez les patients mal équilibrés (34,6 ± 7,2 vs 41,2 ± 7,2 ml.min-1.kg-1). La diffusion alvéolo-capillaire et le transport artériel de l'O2 ne diffèrent pas entre les groupes. Néanmoins, l'augmentation de l'hémodynamique locale (effet groupe, p < 0,01) et de l'extraction musculaire d'O2 (effet groupe, p < 0,0001 ; interaction, p < 0,01), induite par l'exercice, est atténuée chez les patients mal équilibrés. L'activité du complexe IV de la chaîne respiratoire tend à diminuer en cas d'HbA1c élevée (r = 0,47 ; p = 0,06 chez les 16 patients). Un niveau élevé d'HbA1c dans le DT1 pourrait modifier l'activité du complexe IV de la chaîne respiratoire et altérer l'extraction musculaire de l'O2 probablement en raison de l'affinité accrue de HbA1c pour O2. Une moindre perfusion musculaire à l'exercice chez les patients mal équilibrés peut être dépistée par spectroscopie du proche infrarouge et suggère l'existence d'altérations fonctionnelles de la microcirculation avant même l'apparition clinique de microangiopathie. Les auteurs déclarent ne pas avoir d'intérêt direct ou indirect (financier ou en nature) avec un organisme privé, industriel ou commercial en relation avec le sujet présenté.

1 School of Kinesiology and Health Science, Faculty of Health, Muscle Health Research Center and 5 Physical Activity and Chronic Disease Unit, York University, 4700 Keele St., Toronto, ON, Canada, M3J 6 1P3 7 *Co-AuthorsBoth identified authors contributed equally to this entire manuscript. 8 9 **Corresponding Author: Dr. Michael Riddell, School of Kinesiology and Health Science, Faculty of 10 Health, Muscle Health Research Center and Physical Activity and Chronic Disease Unit, York University, 11 4700 Keele St., Toronto, ON, Canada. Tel: 416-736-2100 Fax: 416-736-5774. Email: mriddell@yorku.ca 12

AimTo analyze breathing pattern and mechanical ventilatory constraints during incremental exercise in healthy and cystic fibrosis (CF) children.MethodsThirteen healthy children and 6 children with cystic fibrosis volunteered to perform an incremental test on a treadmill. Exercise tidal flow/volume loops were plotted every minute within a maximal flow/volume loop (MFVL). Expiratory flow limitation (expFL expressed in %Vt) was evaluated and end-expiratory and end-inspiratory lung volumes (EELV and EILV) were estimated from expiratory reserve volume relative to vital capacity (ERV/FVC) and from inspiratory reserve volume relative to vital capacity (IRV/FVC).ResultsDuring the incremental exercise, expFL was first observed at 40% of maximal aerobic speed in both groups. At maximal exercise, 46% of healthy children and 83% of CF children presented expFL, without significant effect of cystic fibrosis on the severity of expFL. According to the two-way ANOVA results, both groups adopted similar breathing pattern and breathing strategies as no significant effect of CF has been revealed. But, according to one-way ANOVA results, a significant increase of ERV/FVC associated with a significant decrease of IRV/FVC from resting value shave been observed in healthy children at maximal exercise, but not in CF children.DiscussionThe hypothesis of this study was based on the assumption that mild cystic fibrosis could induce more frequent and more severe mechanical ventilatory constraints due to pulmonary impairment and breathing pattern disturbances. But, this study did not succeed to highlight an effect of mild cystic fibrosis on the mechanical ventilatory constraints (expFL and dynamic hyperinflation) that occur during an incremental exercise. This absence of effect could be due to the absence of an impact of the disease on spirometric data, breathing pattern regulation during exercise and breathing strategy. Pediatr Pulmonol. 2014; 49:221-229. (c) 2013 Wiley Periodicals, Inc.

This study aimed to examine if the faster pulmonary oxygen uptake ( VO 2p ) phase 2 in children could be explained by increased O 2 availability or extraction at the muscle level. For that purpose, O 2 availability and extraction were assessed using deoxyhemoglobin ( HHb ) estimated by near‐infrared spectroscopy during moderate‐intensity constant load cycling exercise in children and young adults. Eleven prepubertal boys and 12 men volunteered to participate in the study. They performed one maximal graded exercise to determine the power associated with the gas exchange threshold ( GET ) and four constant load exercises at 90% of GET . VO 2p and HHb were continuously monitored. VO 2p , HHb , and estimated capillary blood flow ( ) kinetics were modelled after a time delay and characterized by the time to achieve 63% of the amplitude (τ) and by mean response time ( MRT : time delay + τ), respectively. Mean values of τ for VO 2p ( P < 0.001), of MRT for HHb ( P < 0.01) and of MRT for ( P < 0.001) were significantly shorter in children. Faster VO 2p kinetics have been shown in children; these appear due to both faster O 2 extraction and delivery kinetics as indicated by faster HHb and kinetics, respectively.

The diagnosis of type 1 diabetes (T1D) often occurs in childhood; age and maturation of that patient come with elevated risk of developing microvacular complications and cardiac disease. Insulin treatment, diet control and physical activity are incorporated in T1D treatment, and childhood should be a time at which good diabetes control habits should be developed. Exercise clearly offers many health and psychological benefits, improves body composition, insulin sensitivity, glycemic control and quality of life. Unfortunately, T1D adolescents often do not achieve the recommended physical activity level and are sometimes less active than healthy adolescents. A clear statement about expected beneficial effects is required in order to encourage and to provide opportunities for engaging in physical activity since childhood fosters the maintenance of an active lifestyle in adulthood. This review highlights the beneficial effects of physical activity in T1D children and adolescents and provides some guidance on how physical activity should be managed in this patient population.

The Wingate cycle test (WAnT) is a 30-s test commonly used to estimate anaerobic work capacity (AWC). However, the test may be too short to fully deplete anaerobic energy reserves. We hypothesized that a 90-s all-out isokinetic test (ISO_90) would be valid to assess both aerobic and anaerobic capacities in young females. Eight girls (11.9 ± 0.5 y) performed an exhaustive incremental test, a WAnT and an ISO_90. Peak VO 2 attained during the ISO_90 was significantly greater than VO 2 peak. Mean power, end power, fatigue index, total work done and AWC were not significantly different between the WAnT and after 30 s of the 90-s test (i.e., ISO_30). However, 95% limits of agreement showed large variations between the two tests when comparing all anaerobic parameters. It is concluded that an ISO-90 may be a useful test to assess aerobic capacity in young girls. However, since the anaerobic parameters derived from the ISO_30 did not agree with those derived from a traditional WAnT, the validity of using an ISO_90 to assess anaerobic performance and capacity within this population group remains unconfirmed.

Background: The aim of this study was to evaluate the occurrence and severity of mechanical ventilatory constraints in healthy prepubescent children during continuous and intermittent exercise. Methods: Twelve prepubescent children (7-11 years old) performed 7 exercises on a treadmill: one graded test for the determination of maximal aerobic speed (MAS), three continuous exercises (CE) at 60, 70, and 80% of MAS and three intermittent exercises (IE), alternating 15 sec of exercise with 15 sec of passive recovery, at 90, 100, and 110% of MAS. During each CE and IE, tidal flow/volume loops were plotted within a maximal flow/volume loop (MFVL) measured at rest before each exercise. Expiratory flow limitation (expFL expressed in %Vt) was defined as the part of exercise tidal volume (Vt) meeting the boundary of MFVL. Breathing strategy was estimated by measuring inspiratory capacity relative to forced vital capacity and tidal volume relative to inspiratory capacity. Other breathing pattern parameters (ventilation VE, Vt, respiratory frequency f) were continuously recorded during exercise. Results: An "intensity" effect was found for (V) over dotE during CE (P < 0.001) but not during IE (P = 0.08). The increase in (V) over dotE was predominantly assumed by an increase in f for both exercise modalities. During each exercise, several children heterogeneously experienced expFL ranging between 10 and 90%Vt. For all exercises, Vt was predominantly regulated by an increase in Vt/IC with no change in IC/FVC from rest to exercise. Finally, no significant "modality" effect was found for mechanical ventilatory constraint parameters (expFL, Vt/IC, and IC/FVC). Discussion: We could conclude that neither of the modalities studied induced more mechanical ventilatory constraints than the other, but that exercise intensities specific to each modality might be greater sources of exacerbation for mechanical ventilatory constraints. Pediatr Pulmonol. 2011; 46:785-794. (C) 2011 Wiley-Liss, Inc.

The endocannabinoid system is known to have positive effects on depression partly through its actions on neurotrophins, such as Brain-Derived Neurotrophic Factor (BDNF). As BDNF is also considered the major candidate molecule for exercise-induced brain plasticity, we hypothesized that the endocannabinoid system represents a crucial signaling system mediating the beneficial antidepressant effects of exercise. Here we investigated, in 11 healthy trained male cyclists, the effects of an intense exercise (60 min at 55% followed by 30 min at 75% Wmax) on plasma levels of endocannabinoids (anandamide, AEA and 2-arachidonoylglycerol, 2-AG) and their possible link with serum BDNF. AEA levels increased during exercise and the 15 min recovery (P < 0.001), whereas 2-AG concentrations remained stable. BDNF levels increased significantly during exercise and then decreased during the 15 min of recovery (P < 0.01). Noteworthy, AEA and BDNF concentrations were positively correlated at the end of exercise and after the 15 min recovery (r > 0.66, P < 0.05), suggesting that AEA increment during exercise might be one of the factors involved in exercise-induced increase in peripheral BDNF levels and that AEA high levels during recovery might delay the return of BDNF to basal levels. AEA production during exercise might be triggered by cortisol since we found positive correlations between these two compounds and because corticosteroids are known to stimulate endocannabinoid biosynthesis. These findings provide evidence in humans that acute exercise represents a physiological stressor able to increase peripheral levels of AEA and that BDNF might be a mechanism by which AEA influences the neuroplastic and antidepressant effects of exercise.

Leclair, E, Mucci, P, Borel, B, Baquet, G, Carter, H, Berthoin, S. Time to exhaustion and time spent at a high percentage of (V) over dotO2max in severe intensity domain in children and adults. J Strength Cond Res 25(4): 1151-1158, 2011-The aim of the study was to compare time spent at a high percentage of (V) over dotO2max (>90% of (V) over dotO2max) (ts90%), time to achieve 90% of (V) over dotO2max (ta90%), and time to exhaustion (TTE) for exercise in the severe intensity domain in children and adults. Fifteen prepubertal boys (10.3 +/- 0.9 years) and 15 men (23.5 +/- 3.6 years) performed a maximal graded exercise to determine (V) over dotO2max, maximal aerobic power (MAP) and power at ventilatory threshold (PVTh). Then, they performed 4 constant load exercises in a random order at PVTh plus 50 and 75% of the difference between MAP and PVTh (P Delta 50 and P Delta 75) and 100 and 110% of MAP (P100 and P110). (V) over dotO2max was continuously monitored. The P110 test was used to determine maximal accumulated oxygen deficit (MAOD). No significant difference was found in ta90% between children and adults. ts90% and TTE were not significantly different between children and adults for the exercises at PD50 and PD75. However, ts90% and TTE during P100 (p < 0.05 and p < 0.01, respectively) and P110 (p < 0.001) exercises were significantly shorter in children. Children had a significantly lower MAOD than adults (34.3 +/- 9.4 ml.kg-1 vs. 53.6 +/- 11.1 ml.kg-1). A positive relationship (p < 0.05) was obtained between MAOD and TTE values during the P100 test in children. This study showed that only for intensities at, or higher than MAP, lower ts90% in children was linked to a reduced TTE, compared to adults. Shorter TTE in children can partly be explained by a lower anaerobic capacity (MAOD). These results give precious information about exercise intensity ranges that could be used in children's training sessions. Moreover, they highlight the implication of both aerobic and