[show abstract][hide abstract] ABSTRACT: The objective of this study is to explore the effects of a moderate- to high-intensity physical activity program on fitness, cognitive functions, and ADHD-related behavior in children with ADHD.
Fitness level, motor skills, behaviors, and cognitive functions are assessed by standardized tests before and after a 10-week training or control period.
Findings show that participation in a physical activity program improves muscular capacities, motor skills, behavior reports by parents and teachers, and level of information processing.
A structured physical activity program may have clinical relevance in the functional adaptation of children with ADHD. This supports the need for further research in the area of physical activity with this population.
Journal of Attention Disorders 01/2012; 16(1):71-80. · 2.16 Impact Factor
[show abstract][hide abstract] ABSTRACT: The purpose of this study was to assess fitness and gross motor performance of children with ADHD, including users and nonusers of methylphenidate medication. Seventy boys took part in the study. Fitness level of children with ADHD using medication or not, including body composition, flexibility, and muscular endurance, was similar to that of a control group. The only difference was observed for body mass index, which was lower in children with ADHD using medication. Aerobic capacity was also similar when measured by a treadmill test. A lower performance was observed when aerobic capacity was estimated using a field shuttle test, however, suggesting that the methodology used is important. Finally, both groups of children with ADHD presented significantly lower scores for locomotion skills.
[show abstract][hide abstract] ABSTRACT: Developed for specialists who want to increase the physical activity (PA) level of type 2 diabetic and at-risk individuals, the 10-week DiabetAction program introduced participants to a wide variety of cardiovascular resistance, balance, and flexibility exercises. Thirty-three of 48 individuals completed the intervention in community-based settings, while 25 of 29 participants completed control group evaluations. A significant time effect (p < .05) was measured for leisure PA level, resting systolic and diastolic blood pressure, estimated aerobic capacity, and dynamic balance (nonsignificant group effect; p > .05). The physical functioning domain of quality of life improved in the experimental group, while the vitality domain improved in the control group (significant interactions; p < .05). Follow-ups of the experimental group revealed that they maintained postintervention parameters (leisure PA level, proportion of participants > or = 150 min of PA weekly, estimated aerobic capacity) or improved (mental component summary measure of quality of life). Ninety-four percent of the experimental group was "very" or "extremely" satisfied with the program, and participants perceived improvements in PA level, health, and tiredness postintervention. In conclusion, participants in community-based settings improved on many of the measured parameters and maintained PA practice up to 6 months postintervention. However, since control participants also saw improvements, further controlled studies will be needed.
Research quarterly for exercise and sport 09/2009; 80(3):583-92. · 1.11 Impact Factor
[show abstract][hide abstract] ABSTRACT: To study the changes in physical activity (PA) level, body composition, fitness, and health parameters after the DiabetAction program and evaluate if PA level was maintained during follow-up.
The design of this quasi-experimental study was 1-group pre-test and post-test.
The study was conducted at the sport center (CEPSUM) of the University of Montreal.
Out of the 39 subjects from different ethnic backgrounds with type 2 diabetes (T2D) or risk factors (obesity, insulin resistance, or familial history of T2D) who joined the program, 29 subjects took part in at least 50% of group sessions and performed post-intervention evaluations. Analyses were done using those 29 participants.
DiabetAction is a 10-week program designed for health and exercise professionals who want to introduce type 2 diabetic (T2D) and at-risk individuals to various modalities of exercise (cardiovascular, resistance, flexibility, and balance) in order to increase activity levels.
PA level, aerobic capacity, hand grip strength, dynamic balance, anthropometry, resting heart rate and blood pressure, fasting blood lipids and glucose, and metabolic syndrome prevalence.
A significant increase in PA practice was observed after the 10-week program, and more importantly was maintained during the 6-month follow-up. Significant increases in aerobic capacity, muscular strength at the hand, and high-density lipoprotein cholesterol were also observed post-intervention. After the program, significant reductions in body weight, waist circumference, skinfolds thickness, resting heart rate, and systolic blood pressure were reported. Overall, a reduction in the prevalence of metabolic syndrome was measured post-intervention.
Participants improved their fitness, cardiovascular risk factors, and PA level after their participation to the DiabetAction program, and those promising results justify further validation studies.
Clinical Journal of Sport Medicine 02/2008; 18(1):70-5. · 1.60 Impact Factor
[show abstract][hide abstract] ABSTRACT: The present study tested the hypothesis that the phosphorylation and regulation of metabolic proteins implicated in glucose homeostasis were impaired in the heart of the type 2 diabetic Zucker-diabetic-fatty (ZDF) rat model. The onset of hyperglycaemia in ZDF rats was not uniform, instead it either progressed rapidly (3-4 weeks) or was delayed (6-8 weeks). In both the early and late onset hyperglycaemic ZDF rats, AMPKalpha Thr172 phosphorylation in the heart was significantly decreased. In the early onset hyperglycaemic ZDF rats, PKB Ser473 phosphorylation was reduced, whereas Thr308 phosphorylation was significantly increased. In the late onset hyperglycaemic ZDF rats, PKB Ser473 phosphorylation was unchanged, but Thr308 phosphorylation remained elevated. Cardiac GLUT4 protein and mRNA expression were significantly reduced in the early onset hyperglycaemic ZDF rats, whereas increased protein expression was observed in the late onset hyperglycaemic ZDF rats. In conclusion, the present study has demonstrated that following a more rapid onset of hyperglycaemia, the type 2 diabetic heart is more prone to alterations in the signaling proteins implicated in glucose metabolism.
Canadian Journal of Physiology and Pharmacology 12/2006; 84(11):1205-13. · 1.56 Impact Factor
[show abstract][hide abstract] ABSTRACT: The signaling proteins extracellular signal-regulated kinase (ERK1/2) and protein kinase B (PKB) were implicated in the development of pathological cardiac hypertrophy. The present study examined whether the progression of physiological eccentric cardiac hypertrophy was associated with ERK1/2 and PKB recruitment.
Following 1 and 3 wk of voluntary exercise, female Sprague-Dawley rats ran a total distance of 55 +/- 10 and 195 +/- 19 km, respectively. Left ventricular hypertrophy was detected in 3-wk-exercised rats, albeit prepro-ANP protein expression was unchanged. ERK1/2 was not recruited in the left ventricle (LV) of either 1-wk-exercised rats or the hypertrophied LV of 3-wk-exercised rats. In 1-wk-exercised rats, PKB Thr308 and Ser473 phosphorylation were significantly reduced, whereas a selective increase of PKB Ser473 phosphorylation was observed in the hypertrophied LV of 3-wk-exercised rats. In both 1- and 3-wk-exercised rats, an upward electrophoretic mobility band shift of p70 ribosomal S6 kinase (p70 S6K) was detected. In 1-wk post-myocardial-infarcted (MI) female Sprague-Dawley rats, scar formation was associated with increased left ventricular end-diastolic pressure. In the hypertrophied noninfarcted left ventricle (NILV), ERK1/2, p70 S6K, PKB Ser473, and Thr308 phosphorylation were increased.
These data support the premise that ERK1/2 and PKB were differentially regulated during the development of eccentric physiological and pathological cardiac hypertrophy. It remains to be determined whether the chronic activation of either ERK1/2 and/or PKB in the NILV of post-MI rats may contribute in part to maladaptive cardiac remodelling.
Medicine & Science in Sports & Exercise 04/2006; 38(3):455-62. · 4.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: Exercise training could potentially exert beneficial effects on the signaling events associated with cardiac cell apoptosis. Spontaneously hypertensive rats (SHR) were trained 5 days/week on a treadmill (18 m/min for 120 min/day) between the ages of 4 weeks and 1 week, corresponding to the hypertensive accelerating phase. The effect of exercise training on the expression of anti-apoptotic proteins HSP-72, Bcl-2 and protein kinase B (PKB), and the apoptotic proteins Bax and glycogen synthase kinase-3 (GSK-3) was examined. Exercise had a significant acute lowering effect on blood pressure, but this decrease did not attenuate the progressive increase in blood pressure. In the left ventricles of exercised SHR, PKB phosphorylation of both Ser473 and Thr308 residues was significantly increased by 166% and 120%, respectively, compared to sedentary SHR. PKB phosphorylation significantly correlated with GSK-3beta phosphorylation. HSP-72 and Bcl-2 protein expression were increased in the left ventricle of exercised SHR, and associated with the concomitant increased expression of the protein Bax. Thus, the Bcl-2/Bax ratio was not changed by exercise training, suggesting that the anti-apoptotic mechanism was effective in compensating the increase in the expression of the pro-apoptotic protein Bax in the myocardium of the SHR.
Pflügers Archiv - European Journal of Physiology 11/2004; 449(1):26-32. · 4.87 Impact Factor
[show abstract][hide abstract] ABSTRACT: Cardiac dysfunction is a severe secondary effect of Type 2 diabetes. Recruitment of the protein kinase B/glycogen synthase kinase-3 pathway represents an integral event in glucose homeostasis, albeit its regulation in the diabetic heart remains undefined. Thus the following study tested the hypothesis that the regulation of protein kinase B/glycogen synthase kinase-3 was altered in the myocardium of the Zucker diabetic fatty rat. Second, exercise has been shown to improve glucose homeostasis, and, in this regard, the effect of swimming training on the regulation of protein kinase B/glycogen synthase kinase-3 in the diabetic rat heart was examined. In the sedentary Zucker diabetic fatty rats, glucose levels were elevated, and cardiac glycogen content increased, compared with wild type. A 13-wk swimming regimen significantly reduced plasma glucose levels and cardiac glycogen content and partially normalized protein kinase B-serine473, protein kinase B-threonine308, and glycogen synthase kinase-3alpha phosphorylation in Zucker diabetic fatty rats. In conclusion, hyperglycemia and increased cardiac glycogen content in the Zucker diabetic fatty rats were associated with dysregulation of protein kinase B/glycogen synthase kinase-3 phosphorylation. These anomalies in the Zucker diabetic fatty rat were partially normalized with swimming. These data support the premise that exercise training may protect the heart against the deleterious consequences of diabetes.
Journal of Applied Physiology 06/2004; 96(5):1606-12. · 3.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: Farnesylation represents an essential posttranslational modification of several well-defined proteins implicated in the homologous desensitization of the beta-adrenergic receptor (beta-ADR). The following study examined the effect of a novel farnesyltransferase inhibitor, BMS-191563, on agonist-mediated beta-ADR downregulation in skeletal muscle. Female Sprague-Dawley rats were treated for 12 days with the beta2-adrenergic agonist clenbuterol (4 mg/kg) with or without the concurrent administration of BMS-191563 (2 mg x kg(-1) x day(-1)). Clenbuterol promoted gastrocnemius muscle hypertrophy, whereas the soleus muscle was unaffected. Total beta-ADR density was decreased by 45 and 40% in the soleus and medial gastrocnemius (MG), respectively, after clenbuterol treatment. BMS-191563 treatment did not prevent clenbuterol-stimulated MG hypertrophy, but markedly attenuated beta-ADR downregulation in both muscle types. This latter effect in the soleus muscle was not associated with the inhibition of Ras farnesylation. Likewise, in rat cardiac fibroblasts, isoproterenol-mediated decrease of total beta-ADR density was abrogated by the prior treatment with BMS-191563. Collectively, these data demonstrate that the mechanism(s) implicated in agonist-mediated beta-ADR downregulation was sensitive to BMS-191563, thereby suggesting the involvement of farnesylated proteins.
[show abstract][hide abstract] ABSTRACT: The induction of transforming growth factor (TGF)-beta and prepro-atrial natriuretic peptide (ANP) mRNAs represent hallmark features of pathological cardiac hypertrophy. The present study examined whether this pattern of mRNA expression was conserved in a physiological model of cardiac hypertrophy. To address this thesis, female Sprague-Dawley rats were individually housed and permitted to run freely. Voluntary exercise for 3 and 6 wk resulted in biventricular hypertrophy and increased cytochrome c oxidase activity in the triceps muscle. In the hypertrophied left ventricle, the steady-state mRNA level of the cardiac fetal gene prepro-ANP and the extracellular matrix proteins preprocollagen-alpha(1) and fibronectin were similar in exercise-trained and sedentary rats. By contrast, an increased expression of TGF-beta(1) mRNA was observed, whereas TGF-beta(3) mRNA level was unchanged in the hypertrophied left ventricle of exercise-trained compared with sedentary rats. These data highlight a heterogeneity in the regulation of TGF-beta isoforms, and the increased expression of ventricular TGF-beta(1) mRNA in physiological cardiac hypertrophy may contribute to myocardial remodeling.
Journal of Applied Physiology 09/2001; 91(2):771-6. · 3.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: Preliminary study to investigate possible changes in skeletal muscle morphology and function, as well as hormonal and metabolic effects, after treatment with a selective beta2-adrenergic receptor agonist.
Double-blind, placebo-controlled trial.
Three individuals with spinal cord injury (SCI).
Two-week treatment with salbutamol (2mg) or placebo (ascorbic acid, 50mg) twice a day. Program of functional electronic stimulation (FES) cycling for 30 minutes twice a week.
Body weight, three measures of leg circumference (gluteal furrow, one third of subischial height up from tibial-femoral joint space, and minimum circumference above the knee), muscle fiber area, and total work output per session.
There were increases in body weight (2.30 +/- .70kg), leg circumferences (gluteal furrow 1.70 +/- .27cm, one third subischial height 1.53 +/- 1.65cm, minimum circumference above the knee .43 +/- .04cm), and muscle (vastus lateralis) cross-sectional area (1,374 +/- 493 to 2,446 +/- 1,177microm2) after salbutamol treatment, whereas quadriceps muscle contractile function was not modified. Total work output during FES cycling sessions was increased more during salbutamol treatment (64%) compared with training alone (27%). Salbutamol treatment was associated with a large decrease in skeletal muscle beta-adrenergic receptor density.
Although some side effects were noted, these results suggest that a short treatment with the beta2-adrenergic receptor agonist salbutamol during a training program with FES cycling could be beneficial in patients with SCI.
Archives of Physical Medicine and Rehabilitation 11/1999; 80(10):1264-7. · 2.36 Impact Factor
[show abstract][hide abstract] ABSTRACT: The mechanism(s) responsible for beta2-adrenergic receptor-mediated skeletal muscle and cardiac hypertrophy remains undefined. This study examined whether calcium influx through L-type calcium channels contributed to the development of cardiac and skeletal muscle (plantaris; gastrocnemius; soleus) hypertrophy during an 8-day treatment with the beta2-adrenergic receptor agonist clenbuterol. Concurrent blockade of L-type calcium channels with nifedipine did not reverse the hypertrophic action of clenbuterol. Moreover, nifedipine treatment alone resulted in both cardiac and soleus muscle hypertrophy (6% and 7%, respectively), and this effect was additive to the clenbuterol-mediated hypertrophy in the heart and soleus muscles. The hypertrophic effects of nifedipine were not associated with increases in total beta-adrenergic receptor density, nor did nifedipine reverse clenbuterol-mediated beta-adrenergic receptor downregulation in either the left ventricle or soleus muscle. Both nifedipine and clenbuterol-induced hypertrophy increased total protein content of the soleus and left ventricle, with no change in protein concentration. In conclusion, our results support the hypothesis that beta2-adrenergic receptor agonist-induced muscle hypertrophy is mediated by mechanisms other than calcium influx through L-type calcium channels.
Proceedings of The Society for Experimental Biology and Medicine 08/1999; 221(3):184-7.
[show abstract][hide abstract] ABSTRACT: The mechanism(s) responsible for β2-adrenergic receptor-mediated skeletal muscle and cardiac hypertrophy remains undefined. This study examined whether calcium influx through L-type calcium channels contributed to the development of cardiac and skeletal muscle (plantaris; gastrocnemius; soleus) hypertrophy during an 8-day treatment with the β2-adrenergic receptor agonist clenbuterol. Concurrent blockade of L-type calcium channels with nifedipine did not reverse the hypertrophic action of clenbuterol. Moreover, nifedipine treatment alone resulted in both cardiac and soleus muscle hypertrophy (6% and 7%, respectively), and this effect was additive to the clenbuterol-mediated hypertrophy in the heart and soleus muscles. The hypertrophic effects of nifedipine were not associated with increases in total β-adrenergic receptor density, nor did nifedipine reverse clenbuterol-mediated β-adrenergic receptor downregulation in either the left ventricle or soleus muscle. Both nifedipine and clenbuterol-induced hypertrophy increased total protein content of the soleus and left ventricle, with no change in protein concentration. In conclusion, our results support the hypothesis that β2-adrenergic receptor agonist-induced muscle hypertrophy is mediated by mechanisms other than calcium influx through L-type calcium channels.
Proceedings of The Society for Experimental Biology and Medicine 06/1999; 221(3):184 - 187.
[show abstract][hide abstract] ABSTRACT: The effects of a chronic 14-day administration of a selective beta2-adrenergic-receptor antagonist (ICI-118551) on skeletal muscle were evaluated in female Sprague-Dawley rats. Chronic ICI-118551 treatment did not modify muscle mass, oxidative potential, or protein concentration of the medial gastrocnemius muscle, suggesting that maintenance of these skeletal muscle characteristics is not dependent on beta2-adrenergic-receptor stimulation. However, the drug treatment increased beta-adrenergic-receptor density of the lateral gastrocnemius (42%) and caused an increase in specific (g/g) isometric in situ contractile forces of the medial gastrocnemius [twitch, 56%; tetanic (200 Hz), 28%]. The elevated contractile forces observed after a chronic treatment with ICI-118551 were completely abolished when the beta2-adrenergic antagonist was also administered acutely before measurement of contractile forces, suggesting that this response is beta2-adrenergic-receptor dependent. Possible mechanisms for the increased forces were studied. Caffeine administration potentiated twitch forces but had little effect on tetanic force in control animals. Administration of dibutyryl adenosine 3',5'-cyclic monophosphate in control animals also resulted in small increases of twitch force but did not modify tetanic forces. We conclude that increases in beta-adrenergic-receptor density and the stimulation of the receptors by endogenous catecholamines appear to be responsible for increased contractile forces but that the mechanism remains to be demonstrated.
Journal of Applied Physiology 09/1997; 83(2):459-65. · 3.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: The effects of clenbuterol, a selectiveβ
2-adrenergic agonist, and of exercise training on the properties of skeletal muscle were studied in the hindlimb of sedentary
and trained rats. A 2-week training programme, consisting of climbing on a grid with a load attached to the tail, did not
increase the muscle mass of the soleus, the plantaris and the gastrocnemius muscles or modify the isometricin situ contractile properties of the medial gastrocnemius muscle. The only change observed in a 12-week training regimen was a significant
increase in contractile forces (expressed in grams per gram of muscle) of the medial gastrocnemius muscle at sub-tetanic stimulating
frequencies (twitch 42%, 25Hz 45% and 50Hz 47%). Both training programmes significantly increased fatigue resistance of the
medial gastrocnemius muscle. A 2-week oral treatment with clenbuterol significantly increased the muscle mass of the soleus
(19.8%), plantaris (16.9%) and gastrocnemius (15.3%) muscles in all animals treated with the agonist. However, clenbuterol
had different effects in animals beginning their training programme than in animals that had been trained for the previous
10 weeks. Specifically, clenbuterol caused a significant increase in gastrocnemius muscle mass in the former group but not
in the latter. These results suggest that the responses to the combination of clenbuterol and training in previously trained
skeletal muscles are not as marked as those observed in untrained muscles.
European Journal of Applied Physiology and Occupational Physiology 73(3):304-310.