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Descripción
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| INTRODUCTION Lactate response to resistance training has only been studied in isolated exercises without comparing same protocols at different intensities( 1). Individual variation in the cardiovascular response to the exercise due to genetic factors, such as the angiotensin-converting enzyme (ACE) gene polymorphism, are determinant with several fitness parameters(2, 3) and physical performance, especially endurance performance(4). However, only several studies without conclusive results(3, 5) have investigate the role of the ACE insertion/ deletion (I/D) polymorphisms with lactate metabolism. OBJETIVE: To describe lactate response to a circuit weight training on different intensities in relation with the ACE insertion/ deletion (I/D) polymorphisms. METHODS 10 male volunteers (mean +/- standard deviation, age 24+/-1.8 years, height 178.2+/-5.4 cm, weight 78.2+/-7.1) performed a circuit of 8 exercises at 6 different intensities (from 30% to 80% of 15RM) in 6 non-consecutive days. Capillary blood samples were analyzed at the end of each circuit, using the YSI 1500 SPORT Lactate Analyzer. The I/D polymorphism of ACE gene was determined by polymerase chain reaction. Subjects were divided in 2 groups: I (II homozygotes and ID heterozygotes) and D (DD homozygotes). RESULTS Lactate concentration was significantly correlated with the circuit intensity (Spearman correlation=0.815, p=0.01). Mann-Witney test showed significant differences between I group and D group (p=0.041) in maximal blood lactate during the strength circuit training, having lower concentration the I group. Percentage of genotypes: DD=70%, ID=20% and II=10%. DISCUSSION AND CONCLUSIONS Our results show that the increased energy requirement due to the increased intensity induces an elevated lactic metabolism. Thus, the needed energy to increase resistance training intensity it is not only due, as previously described, to a higher oxygen consumption(6), but also to an increased anaerobic metabolism. Furthermore, we found that individuals in I group reached lower lactate levels in strength training. These low levels might be caused by a worse oxygen delivery due to an impaired vasodilatation in the ACE DD homozygotes(3, 4). We conclude that in our cohort, lactate response to circuit weight training is very correlated with the intensity of this training, and that the subjects with DD genotype reach higher levels of blood lactate. Although our observation it is likely due to a different use of energetic substrates, further studies are needed in this research area. References. 1. Scott, CB. J Strength Cond Res (2006); 20: 404-11. 2. Kasikcioglu, E, et al. Heart Vessels (2004); 19: 287-93. 3. Rankinen, T, et al. J Appl Physiol (2000); 88: 1029-35. 4. Woods, DR, et al. Trends Endocrinol Metab (2000); 11: 416-20. 5. Liu, T and Sun, X. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi (2006); 23: 1045-7. 6. Robergs, RA, et al. J Strength Cond Res (2007); 21: 123-30. | |
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Internacional
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Si |
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Nombre congreso
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13th Annual Congress of the European College of Sport Science |
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Tipo de participación
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960 |
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Lugar del congreso
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Revisores
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No |
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ISBN o ISSN
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978-972-735-156-5 |
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DOI
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Fecha inicio congreso
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09/07/2008 |
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Fecha fin congreso
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12/07/2008 |
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Desde la página
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41 |
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Hasta la página
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42 |
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Título de las actas
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13th Annual Congress of the European College of Sport Science. Book of Abstracts. Digital version |