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Articles by C Perret
Total Records ( 2 ) for C Perret
  V Goosey Tolfrey , E Foden , C Perret and H. Degens
  Background

There is considerable evidence that respiratory muscle training improves pulmonary function, quality of life and exercise performance in healthy athletic populations. The benefits for wheelchair athletes are less well understood. Therefore, in the present study, influence of inspiratory muscle training (IMT) on respiratory function and repetitive propulsive sprint performance in wheelchair basketball players was examined.

Methods

Using a placebo-controlled design, 16 wheelchair athletes were divided to an experimental (IMT; n=8) or placebo (sham-IMT; n=8) group based on selective grouping criteria. 30 dynamic breaths were performed by the IMT group twice daily at a resistance equivalent to 50% maximum inspiratory pressure (MIP), and 60 slow breaths were performed by the sham-IMT group once a day at 15% MIP for a period of 6 weeks.

Results

In the IMT group, both MIP and maximum expiratory pressure (17% and 23%, respectively; p≤0.03) were improved. Similar improvements were noted for the sham-IMT group with 23% and 33% from baseline for MIP and maximum expiratory pressure, respectively (p≤0.03). There were no significant changes in pulmonary function at rest and any of the performance parameters associated with the repetitive sprint test (sprint and recovery times, peak heart rate and peak blood lactate concentration). Reported experiences of using the IMT training device suggested "less breathlessness" and "less tightness in the chest during the training".

Conclusions

Although there was no improvement in sprint performance, an improved respiratory muscle function and quality of life were reported by participants in both the IMT and sham-IMT groups.

  R. B Schnabel , K. L Lunetta , M. G Larson , J Dupuis , I Lipinska , J Rong , M. H Chen , Z Zhao , J. F Yamamoto , J. B Meigs , V Nicaud , C Perret , T Zeller , S Blankenberg , L Tiret , J. F Keaney , R. S Vasan and E. J. Benjamin
 

Background— Environmental and genetic correlates of inflammatory marker variability are incompletely understood. In the family-based Framingham Heart Study, we investigated heritability and candidate gene associations of systemic inflammatory biomarkers.

Methods and Results— In offspring participants (n=3710), we examined 11 inflammatory biomarkers (CD40 ligand, C-reactive protein, intercellular adhesion molecule-1, interleukin-6, urinary isoprostanes, monocyte chemoattractant protein-1, myeloperoxidase, P-selectin, tumor necrosis factor-, tumor necrosis factor receptor II, fibrinogen). Heritability and bivariate genetic and environmental correlations were assessed by Sequential Oligogenic Linkage Analysis routines in 1012 family members. We examined 1943 tagging single-nucleotide polymorphisms in 233 inflammatory pathway genes with ≥5 minor allele carriers using a general genetic linear model. Clinical correlates explained 2.4% (CD40 ligand) to 28.5% (C-reactive protein) of the variability in inflammatory biomarkers. Estimated heritability ranged from 10.9% (isoprostanes) to 44.8% (P-selectin). Most correlations between biomarkers were weak although statistically significant. A total of 45 single-nucleotide polymorphism-biomarker associations met the q-value threshold of 0.25. Novel top single-nucleotide polymorphisms were observed in ICAM1 gene in relation to intercellular adhesion molecule-1 concentrations (rs1799969, P=1.32x10–8) and MPO in relation to myeloperoxidase (rs28730837, P=1.9x10–5). Lowest P values for trans-acting single-nucleotide polymorphisms were observed for APCS with monocyte chemoattractant protein-1 concentrations (rs1374486, P=1.01x10–7) and confirmed for IL6R with interleukin-6 concentrations (rs8192284, P=3.36x10–5). Novel potential candidates (APCS, MPO) need to be replicated.

Conclusions— Our community-based data support the relevance of clinical and genetic factors for explaining variation in inflammatory biomarker traits.

 
 
 
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