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117
result(s) for
"Bourdon, P C"
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Monitoring changes in physical performance with heart rate measures in young soccer players
2012
The aim of the present study was to verify the validity of using exercise heart rate (HRex), HR recovery (HRR) and post-exercise HR variability (HRV) during and after a submaximal running test to predict changes in physical performance over an entire competitive season in highly trained young soccer players. Sixty-five complete data sets were analyzed comparing two consecutive testing sessions (3–4 months apart) collected on 46 players (age 15.1 ± 1.5 years). Physical performance tests included a 5-min run at 9 km h
−1
followed by a seated 5-min recovery period to measure HRex, HRR and HRV, a counter movement jump, acceleration and maximal sprinting speed obtained during a 40-m sprint with 10-m splits, repeated-sprint performance and an incremental running test to estimate maximal cardiorespiratory function (end test velocity
V
Vam-Eval
). Possible changes in physical performance were examined for the players presenting a substantial change in HR measures over two consecutive testing sessions (greater than 3, 13 and 10% for HRex, HRR and HRV, respectively). A decrease in HRex or increase in HRV was associated with likely improvements in
V
Vam-Eval
; opposite changes led to unclear changes in
V
Vam-Eval
. Moderate relationships were also found between individual changes in HRR and sprint [
r
= 0.39, 90% CL (0.07;0.64)] and repeated-sprint performance [
r
= −0.38 (−0.05;−0.64)]. To conclude, while monitoring HRex and HRV was effective in tracking improvements in
V
Vam-Eval
, changes in HRR were moderately associated with changes in (repeated-)sprint performance. The present data also question the use of HRex and HRV as systematic markers of physical performance decrements in youth soccer players.
Journal Article
Adding heat to the live-high train-low altitude model: a practical insight from professional football
by
Coutts, A J
,
Bilsborough, J
,
Mendez-Villanueva, A
in
Acclimatization - physiology
,
Aerobic fitness/Vo2 Max
,
Altitude
2013
Objectives To examine with a parallel group study design the performance and physiological responses to a 14-day off-season ‘live high-train low in the heat’ training camp in elite football players. Methods Seventeen professional Australian Rules Football players participated in outdoor football-specific skills (32±1°C, 11.5 h) and indoor strength (23±1°C, 9.3 h) sessions and slept (12 nights) and cycled indoors (4.3 h) in either normal air (NORM, n=8) or normobaric hypoxia (14±1 h/day, FiO2 15.2–14.3%, corresponding to a simulated altitude of 2500–3000 m, hypoxic (HYP), n=9). They completed the Yo-Yo Intermittent Recovery level 2 (Yo-YoIR2) in temperate conditions (23±1°C, normal air) precamp (Pre) and postcamp (Post). Plasma volume (PV) and haemoglobin mass (Hbmass) were measured at similar times and 4 weeks postcamp (4WPost). Sweat sodium concentration ((Na+)sweat) was measured Pre and Post during a heat-response test (44°C). Results Both groups showed very large improvements in Yo-YoIR2 at Post (+44%; 90% CL 38, 50), with no between-group differences in the changes (−1%; −9, 9). Postcamp, large changes in PV (+5.6%; −1.8, 5.6) and (Na+)sweat (−29%; −37, −19) were observed in both groups, while Hbmass only moderately increased in HYP (+2.6%; 0.5, 4.5). At 4WPost, there was a likely slightly greater increase in Hbmass (+4.6%; 0.0, 9.3) and PV (+6%; −5, 18, unclear) in HYP than in NORM. Conclusions The combination of heat and hypoxic exposure during sleep/training might offer a promising ‘conditioning cocktail’ in team sports.
Journal Article
The effect of cumulative endurance exercise on leptin and adiponectin and their role as markers to monitor training load
2016
Leptin and adiponectin play an essential role in energy metabolism. Leptin has also been proposed as a marker for monitoring training load. So far, no studies have investigated the variability of these hormones in athletes and how they are regulated during cumulative exercise. This study monitored leptin and adiponectin in 15 endurance athletes twice daily in the days before, during and after a 9-day simulated cycling stage race. Adiponectin significantly increased during the race (p = 0.001) and recovery periods (p = 0.002) when compared to the baseline, while leptin decreased significantly during the race (p < 0.0001) and returned to baseline levels during the recovery period. Intra-individual variability was substantially lower than inter-individual variability for both hormones (leptin 34.1 vs. 53.5%, adiponectin 19% vs. 37.2%). With regards to exercise, this study demonstrated that with sufficient, sustained energy expenditure, leptin concentrations can decrease within the first 24 hours. Under the investigated conditions there also appears to be an optimal leptin concentration which ensures stable energy homeostasis, as there was no significant decrease over the subsequent race days. In healthy endurance athletes the recovery of leptin takes 48-72 hours and may even show a supercompensation-like effect. For adiponectin, significant increases were observed within 5 days of commencing racing, with these elevated values failing to return to baseline levels after 3 days of recovery. Additionally, when using leptin and adiponectin to monitor training loads, establishing individual threshold values improves their sensitivity.
Journal Article
The effect of acute simulated moderate altitude on power, performance and pacing strategies in well-trained cyclists
2007
Athletes regularly compete at 2,000-3,000 m altitude where peak oxygen consumption (VO2peak) declines approximately 10-20%. Factors other than VO2peak including gross efficiency (GE), power output, and pacing are all important for cycling performance. It is therefore imperative to understand how all these factors and not just VO2peak are affected by acute hypobaric hypoxia to select athletes who can compete successfully at these altitudes. Ten well-trained, non-altitude-acclimatised male cyclists and triathletes completed cycling tests at four simulated altitudes (200, 1,200, 2,200, 3,200 m) in a randomised, counter-balanced order. The exercise protocol comprised 5 x 5-min submaximal efforts (50, 100, 150, 200 and 250 W) to determine submaximal VO2 and GE and, after 10-min rest, a 5-min maximal time-trial (5-minTT) to determine VO2peak and mean power output (5-minTT(power)). VO2peak declined 8.2 +/- 2.0, 13.9 +/- 2.9 and 22.5 +/- 3.8% at 1,200, 2,200 and 3,200 m compared with 200 m, respectively, P < 0.05. The corresponding decreases in 5-minTT(power) were 5.8 +/- 2.9, 10.3 +/- 4.3 and 19.8 +/- 3.5% (P < 0.05). GE during the 5-minTT was not different across the four altitudes. There was no change in submaximal VO2 at any of the simulated altitudes, however, submaximal efficiency decreased at 3,200 m compared with both 200 and 1,200 m. Despite substantially reduced power at simulated altitude, there was no difference in pacing at the four altitudes for athletes whose first trial was at 200 or 1,200 m; whereas athletes whose first trial was at 2,200 or 3,200 m tended to mis-pace that effort. In conclusion, during the 5-minTT there was a dose-response effect of hypoxia on both VO2peak and 5-minTT(power) but no effect on GE.
Journal Article
Monitoring fitness, fatigue and running performance during a pre-season training camp in elite football players
2013
To examine the usefulness of selected physiological and perceptual measures to monitor fitness, fatigue and running performance during a pre-season, 2-week training camp in eighteen professional Australian Rules Football players (21.9±2.0 years).
Observational.
Training load, perceived ratings of wellness (e.g. fatigue, sleep quality) and salivary cortisol were collected daily. Submaximal exercise heart rate (HRex) and a vagal-related heart rate variability index (LnSD1) were also collected at the start of each training session. Yo-Yo Intermittent Recovery level 2 test (Yo-YoIR2, assessed pre-, mid- and post-camp, temperate conditions) and high-speed running distance during standardized drills (HSR, >14.4kmh−1, 4 times throughout, outdoor) were used as performance measures.
There were significant (P<0.001 for all) day-to-day variations in training load (coefficient of variation, CV: 66%), wellness measures (6–18%), HRex (3.3%), LnSD1 (19.0%), but not cortisol (20.0%, P=0.60). While the overall wellness (+0.06, 90% CL (−0.14; 0.02)AUday−1) did not change substantially throughout the camp, HRex decreased (−0.51 (−0.58; −0.45)%day−1), and cortisol (+0.31 (0.06; 0.57)nmolL−1day−1), LnSD1 (+0.1 (0.04; 0.06)msday−1), Yo-YoIR2 performance (+23.7 (20.8; 26.6)mday−1, P<0.001), and HSR (+4.1 (1.5; 6.6)mday−1, P<0.001) increased. Day-to-day ΔHRex (r=0.80, 90% CL (0.75; 0.85)), ΔLnSD1 (0.51 (r=0.40; 0.62)) and all wellness measures (0.28 (−0.39; −0.17)
Journal Article
Spirometric Standards for Healthy Male Lifetime Nonsmokers
1989
The FVC, FEV1,0, FEF25-75%, and FEV1,0/FVC (%) were measured in 162 males aged 18.9-78.6 yr using a Stead-Wells spirometer. Multiple regression equations were generated to predict these lung parameters from the best weighted combination (p < 0.05) of age, standing height, sitting height, biacromial breadth, and chest expansion (FVC: R = 0.843, SEE = 513 ml BTPS; FEV1,0: R = 0.850, SEE = 436 ml BTPS; FEF25-75%,: R = 0.665, SEE = 997 ml/s BTPS; FEV1.0/FVC: R = 0.537, SEE = 4.95%). The lower limit of normality was defined as the predicted value minus the 95% confidence interval (one-tailed test). Cross-validation of other FVC, FEV1.0,, and FEF25-75%, equations in the literature indicate that all the FVC and FEV1.0 ones are unsuitable for the sample and instrumentation used in this investigation.
Journal Article
Biological functions of p53 isoforms through evolution: lessons from animal and cellular models
by
Dichtel-Danjoy, M-L
,
Hainaut, P
,
Sagne, C
in
631/136/334
,
631/45/612/1244
,
Amino Acid Sequence
2011
The
TP53
tumour-suppressor gene is expressed as several protein isoforms generated by different mechanisms, including use of alternative promoters, splicing sites and translational initiation sites, that are conserved through evolution and within the
TP53
homologues,
TP63
and
TP73
. Although first described in the eighties, the importance of p53 isoforms in regulating the suppressive functions of p53 has only become evident in the last 10 years, by analogy with observations that p63 and p73 isoforms appeared indispensable to fully understand the biological functions of
TP63
and
TP73
. This review summarizes recent advances in the field of ‘p53 isoforms’, including new data on p63 and p73 isoforms. Details of the alternative mechanisms that produce p53 isoforms and
cis-
and
trans
-regulators identified are provided. The main focus is on their biological functions (apoptosis, cell cycle, aging and so on) in cellular and animal models, including mouse, zebrafish and
Drosophila
. Finally, the deregulation of p53 isoform expression in human cancers is reviewed. Based on these latest results, several developments are expected in the future: the identification of drugs modulating p53 isoform expression; the generation of animal models and the evaluation of the use of p53 isoform as biomarkers in human cancers.
Journal Article
The p53 isoform, Δ133p53α, stimulates angiogenesis and tumour progression
2013
The tumour suppressor p53, involved in DNA repair, cell cycle arrest and apoptosis, also inhibits blood vessel formation, that is, angiogenesis, a process strongly contributing to tumour development. The
p53
gene expresses 12 different proteins (isoforms), including TAp53 (p53 (or p53α), p53β and p53γ) and Δ133p53 isoforms (Δ133p53α, Δ133p53β and Δ133p53γ). The Δ133p53α isoform was shown to modulate p53 transcriptional activity and is overexpressed in various human tumours. However, its role in tumour progression is still unexplored. In the present study, we examined the involvement of Δ133p53 isoforms in tumoural angiogenesis and tumour growth in the highly angiogenic human glioblastoma U87. Our data show that conditioned media from U87 cells depleted for Δ133p53 isoforms block endothelial cell migration and tubulogenesis without affecting endothelial cell proliferation
in vitro
. The Δ133p53 depletion in U2OS osteosarcoma cells resulted in a similar angiogenesis blockade. Furthermore, using conditioned media from U87 cells ectopically expressing each Δ133p53 isoform, we determined that Δ133p53α and Δ133p53γ but not Δ133p53β, stimulate angiogenesis. Our
in vivo
data using the chicken chorio-allantoic membrane and mice xenografts establish that angiogenesis and growth of glioblastoma U87 tumours are inhibited upon depletion of Δ133p53 isoforms. By TaqMan low-density array, we show that alteration of expression ratio of Δ133p53 and TAp53 isoforms differentially regulates angiogenic gene expression with Δ133p53 isoforms inducing pro-angiogenic gene expression and repressing anti-angiogenic gene expression.
Journal Article
Micronutrient supplements can promote disruptive protozoan and fungal communities in the developing infant gut
2021
Supplementation with micronutrients, including vitamins, iron and zinc, is a key strategy to alleviate child malnutrition. However, association of gastrointestinal disorders with iron has led to ongoing debate over their administration. To better understand their impact on gut microbiota, we analyse the bacterial, protozoal, fungal and helminth communities of stool samples collected from a subset of 80 children at 12 and 24 months of age, previously enrolled into a large cluster randomized controlled trial of micronutrient supplementation in Pakistan (ClinicalTrials.gov identifier NCT00705445). We show that while bacterial diversity is reduced in supplemented children, vitamins and iron (as well as residence in a rural setting) may promote colonization with distinct protozoa and mucormycetes, whereas the addition of zinc appears to ameliorate this effect. We suggest that the risks and benefits of micronutrient interventions may depend on eukaryotic communities, potentially exacerbated by exposure to a rural setting. Larger studies are needed to evaluate the clinical significance of these findings and their impact on health outcomes.
Micronutrient supplements are key to global efforts to address child malnutrition. Here, in a cohort of children, previously enrolled into a large cluster randomized controlled trial of micronutrient supplementation in Pakistan, Popovic
et al
. find that vitamins and iron increase carriage of protozoa and fungi in the gut, potentially disrupting the bacterial microbiome.
Journal Article
p53/p63/p73 isoforms: an orchestra of isoforms to harmonise cell differentiation and response to stress
2006
p63, p73 and p53 compose a family of transcription factors involved in cell response to stress and development. p53 is the most frequently mutated gene in cancer (50%) and loss of p53 activity is considered to be ubiquitous to all cancers. Recent publications may have a profound impact on our understanding of p53 tumour suppressor activity.
p63
,
p73
and
p53
genes have a dual gene structure conserved in drosophila, zebrafish and man. They encode for multiple p63, p73 or p53 proteins containing different protein domains (isoforms) due to multiple splicing, alternative promoter and alternative initiation of translation. In this review, we describe the different isoforms of p63, p73, p53 and their roles in development and cancer. The changes in the interactions between p53, p63 and p73 isoforms are likely to be fundamental to our understanding in the transition between normal cell cycling and the onset of tumour formation.
Journal Article
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