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Brain-derived neurotrophic factor (BDNF) is a mediator of exercise and nutrition-induced neural plasticity. In children with cerebral palsy (CP), neuromuscular deficits and mobility impairment have a negative impact on their physical activity level and nutritional status, but whether these children have reduced BDNF concentrations is unknown. Therefore, the aim of the present study was to investigate the plasma BDNF concentration, nutritional status, and physical activity level in children with mild to severe CP. Blood sampling, dietary registration, and questionnaires were completed for children with mild CP (gross motor function classification system (GMFCS) I⁻II, n = 31, age 10.6 ± 0.6 years), severe CP (GMFCS IV⁻V, n = 14, age 10.9 ± 1.1 years) and typically developed (TD) children ( n = 22, age 10.9 ± 0.6 years). Children with severe CP had ~40% lower plasma BDNF concentration than TD children ( p < 0.05). Furthermore, children with severe CP had lower daily physical activity level than TD children ( p < 0.01), and a daily intake of energy, n-3 fatty acids, and dietary fibers that was only ~50% of TD ( p > 0.001). Reduced plasma BDNF concentrations were observed in children with severe CP. This may be of significance for optimal neural growth and plasticity. This was observed together with low physical activity levels and a suboptimal intake of energy, n-3 fatty acids, and dietary fibers.

Individuals with cerebral palsy (CP) participate in reduced levels of physical activity and spend an increased amount of time in a sedentary state compared with healthy control subjects. Whether this in part can be explained by impaired muscle function is still unclear. The aim of the present study was to elucidate differences in muscle fibre recruitment during treadmill exercise between CP subjects and healthy age-, sex- and BMI-matched controls. This is a case-control study. Acoustic myography (AMG), a method recording fibre use and efficiency from contracting muscles, was applied during a period of treadmill exercise. The recorded AMG parameters revealed that the CP subjects had a significantly lower initial S-score (spatial summation) than the controls (P < 0.01). However, the T-score (temporal summation) and the E-score (efficiency) showed no significant differences between individuals with CP and the healthy control subjects. The present findings indicate that CP subjects use a higher degree of spatial summation (more fibres recruited) to keep up the same speed during treadmill exercise when compared to healthy matched control subjects. Our results suggest that individuals with CP have a tendency to recruit far more muscle fibres during bouts of exercise than healthy individuals. This may partly explain why CP subjects experience premature fatigue.

Muscle contractures are a common complication in patients with central nervous system (CNS) lesions which limit range of movement and cause joint deformities. Furthermore, it has previously been shown that muscles with contractures have a reduced number of capillaries, indicating decreased tissue vascularization. The aim of the present study was to investigate the microvascular volume (MV) at rest and after acute exercise in the muscle tissue of individuals with cerebral palsy (CP) and healthy control individuals. Contrast-enhanced ultrasound (CEUS) was used before and after 30 min of walking or running on a treadmill in 10 healthy control participants and 10 individuals with CP to detect MV of their skeletal muscle tissue. A significant increase in the MV was observed after exercise both in the adult CP group (21-53 yr) and in the control group (21-52 yr) (1.8 ± 0.8 ΔdB to 3.1 ± 0.9 ΔdB or 42.9% and 1.5 ± 0.6 ΔdB to 2.5 ± 0.9 ΔdB or 39.0%, respectively). Furthermore, a difference in the resting MV was observed between the most severe cases of CP [gross motor function classification scale (GMFCS) 3 and 4] (2.3 ± 0.5 ΔdB) and the less severe cases (GMFCS 1 and 2) (1.5 ± 0.2 ΔdB). When the CP group was walking (3.4 km/h), the lactate levels, Borg score, and heart rate matched the level of controls when they were running (9.8 km/h). In conclusion, individuals with CP become exhausted at much lower exercise intensities than healthy individuals. This is not explained by impaired microvascularization, since the MV of the individuals with CP respond normally to increased O 2 demand during acute exercise. NEW & NOTEWORTHY Cerebral palsy (CP) patients were less physically active compared with typically developed individuals. This may affect the microvascularization. We observed that the CP group became exhausted at much lower exercise intensities compared with healthy individuals. However, impaired microvascularization was not the reason for the decreased physical activity as the CP group responded normally to increased O 2 demand during acute exercise. These results indicate that walking may be recommended as an intervention to train and maintain skeletal muscle tissue in individuals with CP.

We have recently shown that a single bout of acute cardiovascular exercise improves motor skill learning through an optimization of long-term motor memory. Here we expand this previous finding, to explore potential exercise-related biomarkers and their association with measures of motor memory and skill acquisition. Thirty-two healthy young male subjects were randomly allocated into either an exercise or control group. Following either an intense bout of cycling or rest subjects practiced a visuomotor tracking task. Motor skill acquisition was assessed during practice and retention 1 h, 24 h and 7 days after practice. Plasma levels of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF-1), epinephrine, norepinephrine, dopamine and lactate were analyzed at baseline, immediately after exercise or rest and during motor practice. The exercise group showed significantly better skill retention 24h and 7 days after acquisition. The concentration of all blood compounds increased significantly immediately after exercise and remained significantly elevated for 15 min following exercise except for BDNF and VEGF. Higher concentrations of norepinephrine and lactate immediately after exercise were associated with better acquisition. Higher concentrations of BDNF correlated with better retention 1 h and 7 days after practice. Similarly, higher concentrations of norepinephrine were associated with better retention 7 days after practice whereas lactate correlated with better retention 1h as well as 24 h and 7 days after practice. Thus, improvements in motor skill acquisition and retention induced by acute cardiovascular exercise are associated with increased concentrations of biomarkers involved in memory and learning processes. More mechanistic studies are required to elucidate the specific role of each biomarker in the formation of motor memory., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Although histology data favour the view of a degenerative nature of tendinopathy, indirect support for inflammatory reactions to loading in affected tendons exists. The purpose of the present study was to elucidate whether inflammatory signalling responses after acute mechanical loading were more pronounced in tendinopathic versus healthy regions of human tendon and if treatment with non-steroidal anti-inflammatory medications (NSAID's) reduces this response. Twenty-seven tendinopathy patients (>6 months) were randomly assigned to a placebo (n = 14) or NSAID (Ibumetin NYCOMED GmbH Plant Oranienburg Germany (600 mg) × 3/day/1 week) group (n = 13) in a double-blinded-fashion. Tendon biopsies were taken from the painful and a healthy region of the same tendon 2 h after 1 h running. Gene-expression of several targets was analysed in the sampled Achilles tendon biopsies. The mRNA for TGF-β, collagen-I and collagen-III were significantly higher expressed, and decorin, CTGF, IL-6 and IL-10 were significantly lower expressed in the tendinopathic versus healthy tendon area. Only IL-10 was lower in expression in experiments with NSAID administration, while all other determined parameters were unaffected by NSAID. All ultrasonographic outcomes were unchanged in response to acute exercise and not influenced by NSAID. The signalling for collagen and TGF-beta was upregulated after acute loading in tendinopathic tendon. In contrast to the hypothesis, inflammatory signalling was not exaggerated in tendinopathic tendon 2 h after acute mechanical loading.

Background: Real-time harmonic contrast-enhanced ultrasound (CEU) is used in several diseases to visualize the microvascularization in various tissues, due to its high sensitivity., Aim: The aim of the present study was to investigate whether CEU could be used to detect an increase in the microvascular volume (MV) in healthy tendon tissue in response to exercise comprising a 1-h run., Methods: After a bolus injection of the ultrasound contrast SonoVue(®), CEU measurements of (MV) in the Achilles tendon were taken prior to exercise, immediately after a 1-h run, and 24 h after exercise in nine healthy young subjects (seven men and two women) mean age 31 ± 4 years. In addition, the effect of 15 min of arm cycling exercise on the flow within the Achilles tendon was tested in four athletes (mean age 33 ± 6 years) using the CEU method before and after exercise., Results: The present data show a significant increase in the (MV) of the Achilles tendon for all subjects following the run compared with before exercise. No significant change in (MV) was seen in the Achilles tendon after 15-min arm cycling exercise (P = 0·96). This indicates that the increase in microvascular blood volume within the Achilles tendon in response to running is a local response., Conclusion: The present data reveal that real-time harmonic CEU can be used to determine the MV of healthy Achilles tendons both at rest and after 1 h of running exercise., (© 2013 The Authors Clinical Physiology and Functional Imaging © 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine.)

Human connective tissue, e.g., tendon, responds dynamically to physical activity, with collagen synthesis being increased after both acute and prolonged exercise or training. Markers of collagen synthesis and degradation as well as concentration of several potential growth factors have been shown to increase markedly in the peritendinous tissue around the human Achilles tendon following exercise. Of these potential growth factors interleukin-6 (IL-6) showed the largest fold increase, suggesting that IL-6 may be involved in transforming mechanical loading into collagen synthesis in human tendon tissue. In the present study the tissue levels of type I collagen turnover markers [procollagen type I NH(2)-terminal propeptide (PINP) and C-OOH terminal telopeptide of type I collagen (ICTP)] were measured by the use of microdialysis in peritendinous tissue of the Achilles tendon in 14 male volunteers, who had recombinant human IL-6 (rhIL-6) infused into the peritendinous tissue of the Achilles' tendon in one leg, with the other leg serving as control. Subjects were randomly assigned to either a resting group or an exercise group performing a 1-h treadmill run (12 km/h, 2% uphill) before infusion. In addition to IL-6, serum concentrations of collagen turnover markers PINP, ICTP, and COOH-terminal telopeptide of type I collagen (ICTX) were measured. The peritendinous concentration of PINP rose markedly in response to rhIL-6 infusion in both the exercise and the rest group, demonstrating that infusion of IL-6 significantly stimulates collagen synthesis in the peritendinous tissue in humans. Exercise alone did not result in an increased collagen synthesis. This indicates that IL-6 is involved in the collagen synthesis and supports the hypothesis that IL-6 is an important growth factor of the connective tissue in healthy human tendons.

The article determines whether the microvascular volume (MV) of the Achilles tendon increases in patients with Achilles tendinopathy (AT) compared with healthy controls during pre-exercise rest, after acute exercise and 24 hours after exercise. The study used real-time harmonic contrast-enhanced ultrasound (CEU) measurements of the MV of the Achilles tendon taken in several volunteers. Results showed acute exercise increases MV of the Achilles tendon in healthy patients and patients with AT.

Through an unknown mechanism, the cyclooxygenase inhibitor and antipyretic acetaminophen (APAP) alters tendon mechanical properties in humans when consumed during exercise. Interleukin-6 (IL-6) is produced by tendon during exercise and is a potent stimulator of collagen synthesis. In nontendon tissue, IL-6 is upregulated in the presence of cyclooxygenase inhibitors and may contribute to alterations in extracellular matrix turnover, possibly due to inhibition of prostaglandin E2 (PGE2). We evaluated the effects of APAP on IL-6 and PGE2 in human Achilles peritendinous tissue after 1 h of treadmill exercise. Subjects were randomly assigned to a placebo (n = 8, 26 ± 1 yr) or APAP (n = 8, 25 ± 1 yr) group. Each subject completed a nonexercise and exercise experiment consisting of 6 h of microdialysis. Drug (APAP, 1,000 mg) or placebo was administered in a double-blind manner during both experiments. PGE2 and IL-6 were determined via enzyme immunoassay and APAP via high-performance liquid chromatography. In subjects given APAP, peritendinous APAP levels increased to 4.08 ± 0.65 μg/ml (P < 0.05). PGE2 did not increase with exercise in either group (P > 0.05), nor was PGE2 significantly reduced in the APAP group. IL-6 levels increased with exercise in both groups (P < 0.05), but this increase was greater in the APAP group (P < 0.05). Our findings suggest that APAP enhances tendon IL-6 production after exercise. Peak levels of APAP obtained in the peritendinous space were twofold lower than values reported in plasma or skeletal muscle. These findings provide insight into the effects of APAP on tendon and provide novel information on the kinetics of APAP in tendon tissue after oral APAP consumption. [ABSTRACT FROM AUTHOR]

Skeletal muscles fatigue after exercise, and reductions in maximal force appear. A difference in training status between the legs was introduced by unilateral immobilization of the calf muscles for 2 weeks in young men, who were randomly assigned to two groups, either a RUN group (n = 8) that was exposed to prolonged exercise (1-h running: individual pace) or a REST group (n = 12) that did no exercise after immobilization. Cross-sectional area (CSA) of the triceps-surae muscles was calculated by magnetic resonance imaging (MRI), and maximal voluntary contraction (MVC) force of the plantar flexors was measured before and after immobilization and after the running protocol. The CSA of triceps-surae muscles decreased significantly with a 7% reduction in both groups. A significant drop in the MVC of the triceps-surae muscle (10%; P < 0.05) was observed in response to immobilization. When subjected to running exercise immediately after immobilization, the muscle strength of the triceps-surae muscles dropped even further, but just in the immobilized leg (41%; P < 0.05). The present study highlights the importance of determining the muscle endurance when evaluating the effect of immobilization on muscle parameters. [ABSTRACT FROM AUTHOR]

When aerobic exercise is performed following skilled motor practice, it can enhance motor memory consolidation. Previous studies have suggested that dopamine may play a role in motor memory consolidation, but whether it is involved in the exercise effects on consolidation is unknown. Hence, we aimed to investigate the influence of dopaminergic pathways on the exercise-induced modulation of motor memory consolidation. We compared the effect of acute exercise on motor memory consolidation between the genotypes that are known to affect dopaminergic transmission and learning. By combining cluster analyses and fitting linear models with and without included polymorphisms, we provide preliminary evidence that exercise benefits the carriers of alleles that are associated with low synaptic dopamine content. In line with previous reports, our findings implicate dopamine as a modulator of the exercise-induced effects on motor memory consolidation, and suggest exercise as a potential clinical tool to counteract low endogenous dopamine bioavailability. Further experiments are needed to establish causal relations. [ABSTRACT FROM AUTHOR]