Michel Guinot | PubMed Health

PubMed2005

Maximal lactate steady state determination with a single incremental test exercise.

The aim of this study was to determine whether the power output associated with a maximal lactate steady state (MLSS) (.W(MLSS)) can be assessed using a single incremental cycling test. Eleven recreational sportsmen (age: 22+/-1 years, height: 175+/-6 cm, weight: 71+/-5 kg) volunteered to participate in the study. For each subject the first and second ventilatory thresholds (VT(1) and VT(2), respectively) and the power output corresponding to (respiratory exchange ratio) RER=1.00 were determined during an incremental test to exhaustion. Thereafter, each subject performed several 30-min constant load tests to determine MLSS. The workload used in the first constant test was set to the .W(RER=1.00) determined during the incremental test. .W(VT1) (175+/-24 W) and .W(VT2) (265+/-31 W) were significantly different from .W(MLSS )(220+/-36 W). Whereas, .W(RER=1.00) (224+/-33 W) was similar to .W(MLSS). HR, RER and .VE were significantly different between the 10th and the 30th minutes when exercising at .W(RER=1.00) and at .W(MLSS). In contrast, .VO(2) and .VCO(2) were stable over those 30-min constant tests. Power output at VT(1), RER=1.00 and VT(2) were all correlated to .W(MLSS) but the relationship was stronger between RER=1.00 and MLSS (R (2)=0.95). The present study shows that the power output associated with a RER value equal to 1.00 during an incremental test does not differ from that determined for MLSS. Hence, the MLSS can be estimated with a single exercise test.

Adult↗

PubMed2002

Increased body iron stores in elite road cyclists.

BACKGROUND: One third of French elite road cyclists were found to have hyperferritinemia on antidoping control tests performed during the Tour de France in 1998. PURPOSE: This study was undertaken to determine whether hyperferritinemia corresponded to elevated body iron stores or not and, affirmatively, what were its mechanism, its clinical consequences, and its spontaneous course. METHODS: 83 elite road male cyclists presenting with hyperferritinemia, defined as serum ferritin level greater than 300 microg.L-1, were studied with respect to consumption of iron and other drugs, serum iron tests, HFE mutations, and hepatic iron concentration (HIC; N < 35 micromol.g-1 dry weight). RESULTS: All cyclists were asymptomatic and had normal physical and cardiac examination. Their median (range) serum ferritin, serum iron, and transferrin saturation levels were 504 microg.L-1 (306-1671), 20 micromol.L-1 (8.5-36.3), and 39% (20-76), respectively. HIC was increased in 24/27 up to 187 micromol.g-1. Allelic frequency of the H63D mutation was increased in cyclists when compared to controls (P = 0.04). However, iron tests did not differ according to HFE genotypes. Most cyclists (89%) had been supplemented with iron. The median iron supplementation was 25.5 g (range: 1.4-336) and correlated well (P = 0.002) with serum ferritin. Evolution of serum ferritin levels did not differ whether cyclists had been continuing iron supplementation or not. CONCLUSION: Hyperferritinemia in elite road cyclists accounted for increased body iron stores caused by and persisting after cessation of excessive iron supplementation. Even when mild, iron excess may expose to long-term complications and should be removed, at least at the time when professional cyclists retire. To prevent iatrogenic iron overload, supplementation with iron must be done according to serum ferritin follow-up and not either blindly or on the basis of serum iron determination only.

Adult↗