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      Effect of self-paced active recovery and passive recovery on blood lactate removal following a 200 m freestyle swimming trial

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          Abstract

          Purpose

          The aim of this study was to investigate the effect of self-paced active recovery (AR) and passive recovery (PR) on blood lactate removal following a 200 m freestyle swimming trial.

          Patients and methods

          Fourteen young swimmers (with a training frequency of 6–8 sessions per week) performed two maximal 200 m freestyle trials followed by 15 minutes of different recovery methods, on separate days. Recovery was performed with 15 minutes of passive rest or 5 minutes of passive rest and 10 minutes of self-paced AR. Performance variables (trial velocity and time), recovery variables (distance covered and AR velocity), and physiological variables (blood lactate production, blood lactate removal, and removal velocity) were assessed and compared.

          Results

          There was no difference between trial times in both conditions (PR: 125.86±7.92 s; AR: 125.71±8.21 s; p=0.752). AR velocity was 69.10±3.02% of 200 m freestyle trial velocity in AR. Blood lactate production was not different between conditions (PR: 8.82±2.47 mmol L −1; AR: 7.85±2.05 mmol L −1; p=0.069). However, blood lactate removal was higher in AR (PR: 1.76±1.70 mmol L −1; AR: 4.30±1.74 mmol L −1; p<0.001). The velocity of blood lactate removal was significantly higher in AR (PR: 0.18±0.17 mmol L −1 min −1; AR: 0.43±0.17 mmol L −1 min −1; p<0.001).

          Conclusion

          Self-paced AR shows a higher velocity of blood lactate removal than PR. These data suggest that athletes may be able to choose the best recovery intensity themselves.

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          Most cited references27

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          Lactate physiology in health and disease

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            Blood lactate measurements and analysis during exercise: a guide for clinicians.

            Blood lactate concentration ([La(-)](b)) is one of the most often measured parameters during clinical exercise testing as well as during performance testing of athletes. While an elevated [La(-)](b) may be indicative of ischemia or hypoxemia, it may also be a "normal" physiological response to exertion. In response to "all-out" maximal exertion lasting 30-120 seconds, peak [La(-)](b) values of approximately 15-25 mM may be observed 3-8 minutes postexercise. In response to progressive, incremental exercise, [La(-)](b) increases gradually at first and then more rapidly as the exercise becomes more intense. The work rate beyond which [La(-)](b) increases exponentially [the lactate threshold (LT)] is a better predictor of performance than V O2max and is a better indicator of exercise intensity than heart rate; thus LT (and other valid methods of describing this curvilinear [La(-)](b) response with a single point) is useful in prescribing exercise intensities for most diseased and nondiseased patients alike. H(+)-monocarboxylate cotransporters provide the primary of three routes by which La(-) transport proceeds across the sarcolemma and red blood cell membrane. At rest and during most exercise conditions, whole blood [La(-)] values are on average 70% of the corresponding plasma [La(-)] values; thus when analyzing [La(-)](b'), care should be taken to both (1) validate the [La(-)](b)-measuring instrument with the criterion/reference enzymatic method and (2) interpret the results correctly based on what is being measured (plasma or whole blood). Overall, it is advantageous for clinicians to have a thorough understanding of [La(-)](b) responses, blood La(-) transport and distribution, and [La(-)](b) analysis.
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              Muscle fatigue: lactic acid or inorganic phosphate the major cause?

              Intracellular acidosis due mainly to lactic acid accumulation has been regarded as the most important cause of skeletal muscle fatigue. Recent studies on mammalian muscle, however, show little direct effect of acidosis on muscle function at physiological temperatures. Instead, inorganic phosphate, which increases during fatigue due to breakdown of creatine phosphate, appears to be a major cause of muscle fatigue.
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                Author and article information

                Journal
                Open Access J Sports Med
                Open Access J Sports Med
                Open Access Journal of Sports Medicine
                Open Access Journal of Sports Medicine
                Dove Medical Press
                1179-1543
                2017
                28 June 2017
                : 8
                : 155-160
                Affiliations
                [1 ]College of Education and Health Sciences, University Center of Brasília – UniCEUB, Brasília
                [2 ]College of Physical Education, UniEVANGÉLICA, Anápolis, Goiás
                [3 ]College of Physical Education, Universidade Estadual de Goiás -UEG, Quirinópolis, Goiás
                [4 ]College of Physical Education, University of Brasília – UnB, Brasília, Brazil
                Author notes
                Correspondence: Márcio Rabelo Mota, University Center of Brasília, SEPN, s/n -Asa Norte, DF, 70790-075, Brazil, Tel +55 61 981 115 759, Email marciormota@ 123456gmail.com
                Article
                oajsm-8-155
                10.2147/OAJSM.S127948
                5499938
                6bd47f60-ed9a-4c45-80ac-838c9976266f
                © 2017 Mota et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

                athletic performance,fatigue,acidosis,anaerobic,metabolic response,sports

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