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Patrick J. O’Connor, Melanie S. Poudevigne, M. Elaine Cress, Robert W. Motl and James F. Clapp III

Objective:

Describe safety and efficacy of a supervised, low-to-moderate intensity strength training program adopted during pregnancy among women at increased risk for back pain.

Methods:

32 women adopted strength training twice per week for 12 weeks. Data on musculoskeletal injuries, symptoms, blood pressure, and the absolute external load used for 5 of 6 exercises were obtained during each session. A submaximal lumbar extension endurance exercise test was performed at weeks 5, 10, and 13.

Results:

The mean (± SD) exercise session attendance rate was 80.5% (± 11.3%). No musculoskeletal injuries occurred. Potentially adverse symptoms (eg, dizziness) were infrequent (2.1% of sessions). Repeated-measures ANOVA showed large increases in the external load across 12 weeks (all P values < .001) and the percentage increases in external load from weeks 1 to 12 were 36% for leg press, 39% for leg curl, 39% for lat pull down, 41% for lumbar extension and 56% for leg extension. Training was associated with a 14% increase in lumbar endurance. Blood pressure was unchanged following acute exercise sessions and after 12 weeks of exercise training.

Conclusion:

The adoption of a supervised, low-to-moderate intensity strength training program during pregnancy can be safe and efficacious for pregnant women.

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Désirée B. Maltais, Claire Gane, Sophie-Krystale Dufour, Dominik Wyss, Laurent J. Bouyer, Bradford J. McFadyen, Karl Zabjek, Jan Andrysek and Julien I.A. Voisin

Little is known about the effects of acute exercise on the cognitive functioning of children with cerebral palsy (CP). Selected cognitive functions were thus measured using a pediatric version of the Stroop test before and after maximal, locomotor based aerobic exercise in 16 independently ambulatory children (8 children with CP), 6–15 years old. Intense exercise had: 1) a significant, large, positive effect on reaction time (RT) for the CP group (preexercise: 892 ± 56.5 ms vs. postexercise: 798 ± 45.6 ms, p < .002, d = 1.87) with a trend for a similar but smaller response for the typically developing (TD) group (preexercise: 855 ± 56.5 ms vs. postexercise: 822 ± 45.6 ms, p < .08, d = 0.59), and 2) a significant, medium, negative effect on the interference effect for the CP group (preexercise: 4.5 ± 2.5%RT vs. postexercise: 13 ± 2.9%RT, p < .04, d = 0.77) with no significant effect for the TD group (preexercise: 7.2 ± 2.5%RT vs. postexercise: 6.9 ± 2.9%RT, p > .4, d = 0.03). Response accuracy was high in both groups pre- and postexercise (>96%). In conclusion, intense exercise impacts cognitive functioning in children with CP, both by increasing processing speed and decreasing executive function.

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Keith Tolfrey, Julia K. Zakrzewski-Fruer and James Smallcombe

Three publications were selected based on the strength of the research questions, but also because they represent different research designs that are used with varying degrees of frequency in the pediatric literature. The first, a prospective, longitudinal cohort observation study from 7 to 16 years with girls and boys reports an intrinsic reduction in absolute resting energy expenditure after adjustment for lean mass, fat mass, and biological maturity. The authors suggest this could be related to evolutionary energy conservation, but may be problematic now that food energy availability is so abundant. The second focuses on the effect of acute exercise on neutrophil reactive oxygen species production and inflammatory markers in independent groups of healthy boys and men. The authors suggested the boys experienced a “sensitized” neutrophil response stimulated by the exercise bout compared with the men; moreover, the findings provided information necessary to design future trials in this important field. In the final study, a dose-response design was used to examine titrated doses of high intensity interval training on cardiometabolic outcomes in adolescent boys. While the authors were unable to identify a recognizable dose-response relationship, there are several design strengths in this study, which was probably underpowered.

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Alex J. Wadley, Ida S. Svendsen and Michael Gleeson

Altitude exposure can exaggerate the transient increase in markers of oxidative stress observed following acute exercise. However, these responses have not been monitored in endurance-trained cyclists at altitudes typically experienced while training. Endurance trained males (n = 12; mean (± SD) age: 28 ± 4 years, V̇O2max 63.7 ± 5.3 ml/kg/min) undertook two 75-min exercise trials at 70% relative V̇O2max; once in normoxia and once in hypobaric hypoxia, equivalent to 2000m above sea level (hypoxia). Blood samples were collected before, immediately after and 2 h postexercise to assess plasma parameters of oxidative stress (protein carbonylation (PC), thiobarbituric acid reactive substances (TBARS), total antioxidant capacity (TAC) and catalase activity (CAT)). Participants cycled at 10.5% lower power output in hypoxia vs. normoxia, with no differences in heart rate, blood lactate or rating of perceived exertion observed. PC increased and decreased immediately after exercise in hypoxia and normoxia respectively (nmol/mg/protein: Normoxia—0.3 ± 0.1, Hypoxia + 0.4 ± 0.1; both p < .05). CAT increased immediately postexercise in both trials, with the magnitude of change greater in hypoxia (nmol/min/ml: Normoxia + 12.0 ± 5.0, Hypoxia + 27.7 ± 4.8; both p < .05). CAT was elevated above baseline values at 2 h postexercise in Hypoxia only (Normoxia + 0.2 ± 2.4, Hypoxia + 18.4 ± 5.2; p < .05). No differences were observed in the changes in TBARS and TAC between hypoxia and normoxia. Trained male cyclists demonstrated a differential pattern/ timecourse of changes in markers of oxidative stress following submaximal exercise under hypoxic vs. normoxic conditions.

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Romain Meeusen and Phil Watson

It is clear that the cause of fatigue is complex, infuenced by both events occurring in the periphery and the central nervous system (CNS). It has been suggested that exercise-induced changes in serotonin (5-HT), dopamine (DA), and noradrenaline (NA) concentrations contribute to the onset of fatigue during prolonged exercise. Serotonin has been linked to fatigue because of its documented role in sleep, feelings of lethargy and drowsiness, and loss of motivation, whereas increased DA and NA neurotransmission favors feelings of motivation, arousal, and reward. 5-HT has been shown to increase during acute exercise in running rats and to remain high at the point of fatigue. DA release is also elevated during exercise but appears to fall at exhaustion, a response that may be important in the fatigue process. The rates of 5-HT and DA/NA synthesis largely depend on the peripheral availability of the amino acids tryptophan (TRP) and tyrosine (TYR), with increased brain delivery increasing serotonergic and DA/NA activity, respectively. TRP, TYR, and the branched-chained amino acids (BCAAs) use the same transporter to pass through the blood-brain barrier, meaning that the plasma concentration ratio of these amino acids is thought to be a very important marker of neurotransmitter synthesis. Pharmacological manipulation of these neurotransmitter systems has provided support for an important role of the CNS in the development of fatigue. Work conducted over the last 20 y has focused on the possibility that manipulation of neurotransmitter precursors may delay the onset of fatigue. Although there is evidence that BCAA (to limit 5-HT synthesis) and TYR (to elevate brain DA/NA) ingestion can influence perceived exertion and some measures of mental performance, the results of several apparently well-controlled laboratory studies have yet to demonstrate a clear positive effect on exercise capacity or performance. There is good evidence that brain neurotransmitters can play a role in the development of fatigue during prolonged exercise, but nutritional manipulation of these systems through the provision of amino acids has proven largely unsuccessful.

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Dariush Sheikholeslami-Vatani, Slahadin Ahmadi and Hassan Faraji

sensitive tools for evaluating these physiological processes ( Kangas et al., 2017 ). Various types of cellular stress stimuli have been shown to trigger apoptosis. Strenuous acute exercise directly or indirectly can induce a stress response and apoptosis in working skeletal muscles ( Podhorska-Okołów et

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Blai Ferrer-Uris, Albert Busquets and Rosa Angulo-Barroso

associated with repeated bouts of acute exercise ( Griffin et al., 2011 ; Hopkins, Davis, Vantieghem, Whalen, & Bucci, 2012 ). In adults, acute exercise seems to transiently affect brain function through an increase in the concentration of certain neurochemicals, such as neurotransmitters (e

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Thomas Finkenzeller, Sabine Würth, Michael Doppelmayr and Günter Amesberger

, perceptual tasks, visual search tasks, memory tasks), exercise duration, exercise intensity, and fitness level. Furthermore, Lambourne and Tomporowski ( 2010 ) obtained different effect sizes depending on when the cognitive assessment was taken during acute exercise, indicating a decline in the initial 20

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Keishi Soga, Keita Kamijo and Hiroaki Masaki

studies have explored the effects of a single bout of acute exercise on memory functions. These studies have consistently indicated that retrieval performance improved when learning or when the encoding phase was performed after acute aerobic exercise ( Etnier, Labban, Piepmeier, Davis, & Henning, 2014

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Carolina Menezes Fiorelli, Emmanuel Gomes Ciolac, Lucas Simieli, Fabiana Araújo Silva, Bianca Fernandes, Gustavo Christofoletti and Fabio Augusto Barbieri

regulation of exercise-induced cognitive responses. However, the previous studies have analyzed the effects of acute exercise in neurologically healthy individuals. Therefore, an important lack in literature is about the effects of acute aerobic exercise in cognition impairments in PD. Therefore, 2 questions