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![点击此处可从《British journal of sports medicine》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Objective: To determine the prevalence and discuss potential clinical implications of mutations of HFE (the gene responsible for hereditary haemochromatosis) in endurance athletes.
Methods: Basal concentrations of iron, ferritin, and transferrin and transferrin saturation were determined in the period before competition in 65 highly trained athletes. Possible mutations in the HFE gene were evaluated in each subject by extracting genomic DNA from peripheral blood. The restriction enzymes SnaBI and BclI were used to detect the mutations 845G→A (C282Y) and 187C→G (H63D).
Results: Our findings indicate a high prevalence of HFE gene mutations in this population (49.2%) compared with sedentary controls (33.5%). No association was detected in the athletes between mutations and blood iron markers.
Conclusions: The findings support the need to assess regularly iron stores in elite endurance athletes.
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Objective: To examine the relation between quantifiable levels of exertion (TRIMPS) and resting heart rate (HR) and resting supine heart rate variability (HRV) in professional cyclists during a three week stage race.
Method: Eight professional male cyclists (mean (SEM) age 27 (1) years, body mass 65.5 (2.3) kg, and maximum rate of oxygen consumption (V·O2MAX) 75.6 (2.2) ml/kg/min) riding in the 2001 Vuelta a España were examined for resting HR and HRV on the mornings of day 0 (baseline), day 10 (first rest day), and day 17 (second rest day). The rest days followed stages 1–9 and 10–15 respectively. HR was recorded during each race stage, and total HR time was categorised into a modified, three phase TRIMPS schema. These phases were based on standardised physiological laboratory values obtained during previous V·O2MAX testing, where HR time in each phase (phase I = light intensity and less than ventilatory threshold (VT; ~70% V·O2MAX); phase II = moderate intensity between VT and respiratory compensation point (RCP; ~90% V·O2MAX); phase III = high intensity (>RCP)) was multiplied by exertional factors of 1, 2, and 3 respectively.
Results: Multivariate analysis of variance showed that total TRIMPS for race stages 1–9 (2466 (90)) were greater than for stages 10–15 (2055 (65)) (p<0.0002). However, TRIMPS/day were less for stages 1–9 (274 (10)) than for stages 10–15 (343 (11)) (p<0.01). Despite a trend to decline, no difference in supine resting HR was found between day 0 (53.2 (1.8) beats/min), day 10 (49.0 (2.8) beats/min), and day 17 (48.0 (2.6) beats/min) (p = 0.21). Whereas no significant group mean changes in HR or HRV indices were noted during the course of the race, significant inverse Pearson product-moment correlations were observed between all HRV indices relative to total TRIMPS and TRIMPS/day accumulated in race stages 10–15. Total TRIMPS correlated with square root of mean squared differences of successive RR intervals (r = –0.93; p<0.001), standard deviation of the RR intervals (r = –0.94; p<0.001), log normalised total power (r = –0.97; p<0.001), log normalised low frequency power (r = –0.79; p<0.02), and log normalised high frequency power (r = –0.94; p<0.001).
Conclusion: HRV may be strongly affected by chronic exposure to heavy exertion. Training volume and intensity are necessary to delineate the degree of these alterations.
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