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      The Measurement of Maximal (Anaerobic) Power Output on a Cycle Ergometer: A Critical Review

      review-article
      1 , * , 2
      BioMed Research International
      Hindawi Publishing Corporation

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          Abstract

          The interests and limits of the different methods and protocols of maximal (anaerobic) power ( P max) assessment are reviewed: single all-out tests versus force-velocity tests, isokinetic ergometers versus friction-loaded ergometers, measure of P max during the acceleration phase or at peak velocity. The effects of training, athletic practice, diet and pharmacological substances upon the production of maximal mechanical power are not discussed in this review mainly focused on the technical (ergometer, crank length, toe clips), methodological (protocols) and biological factors (muscle volume, muscle fiber type, age, gender, growth, temperature, chronobiology and fatigue) limiting P max in cycling. Although the validity of the Wingate test is questionable, a large part of the review is dedicated to this test which is currently the all-out cycling test the most often used. The biomechanical characteristics specific of maximal and high speed cycling, the bioenergetics of the all-out cycling exercises and the influence of biochemical factors (acidosis and alkalosis, phosphate ions…) are recalled at the beginning of the paper. The basic knowledge concerning the consequences of the force-velocity relationship upon power output, the biomechanics of sub-maximal cycling exercises and the study on the force-velocity relationship in cycling by Dickinson in 1928 are presented in Appendices.

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          Human muscle metabolism during intermittent maximal exercise.

          Eight male subjects volunteered to take part in this study. The exercise protocol consisted of ten 6-s maximal sprints with 30 s of recovery between each sprint on a cycle ergometer. Needle biopsy samples were taken from the vastus lateralis muscle before and after the first sprint and 10 s before and immediately after the tenth sprint. The energy required to sustain the high mean power output (MPO) that was generated over the first 6-s sprint (870.0 +/- 159.2 W) was provided by an equal contribution from phosphocreatine (PCr) degradation and anaerobic glycolysis. Indeed, within the first 6-s bout of maximal exercise PCr concentration had fallen by 57% and muscle lactate concentration had increased to 28.6 mmol/kg dry wt, confirming significant glycolytic activity. However, in the tenth sprint there was no change in muscle lactate concentration even though MPO was reduced only to 73% of that generated in the first sprint. This reduced glycogenolysis occurred despite the high plasma epinephrine concentration of 5.1 +/- 1.5 nmol/l after sprint 9. In face of a considerable reduction in the contribution of anaerobic glycogenolysis to ATP production, it was suggested that, during the last sprint, power output was supported by energy that was mainly derived from PCr degradation and an increased aerobic metabolism.
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            What is the cause of the ageing atrophy?

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              Repeated-sprint ability - part II: recommendations for training.

              Short-duration sprints, interspersed with brief recoveries, are common during most team sports. The ability to produce the best possible average sprint performance over a series of sprints (≤10 seconds), separated by short (≤60 seconds) recovery periods has been termed repeated-sprint ability (RSA). RSA is therefore an important fitness requirement of team-sport athletes, and it is important to better understand training strategies that can improve this fitness component. Surprisingly, however, there has been little research about the best training methods to improve RSA. In the absence of strong scientific evidence, two principal training theories have emerged. One is based on the concept of training specificity and maintains that the best way to train RSA is to perform repeated sprints. The second proposes that training interventions that target the main factors limiting RSA may be a more effective approach. The aim of this review (Part II) is to critically analyse training strategies to improve both RSA and the underlying factors responsible for fatigue during repeated sprints (see Part I of the preceding companion article). This review has highlighted that there is not one type of training that can be recommended to best improve RSA and all of the factors believed to be responsible for performance decrements during repeated-sprint tasks. This is not surprising, as RSA is a complex fitness component that depends on both metabolic (e.g. oxidative capacity, phosphocreatine recovery and H+ buffering) and neural factors (e.g. muscle activation and recruitment strategies) among others. While different training strategies can be used in order to improve each of these potential limiting factors, and in turn RSA, two key recommendations emerge from this review; it is important to include (i) some training to improve single-sprint performance (e.g. 'traditional' sprint training and strength/power training); and (ii) some high-intensity (80-90% maximal oxygen consumption) interval training to best improve the ability to recover between sprints. Further research is required to establish whether it is best to develop these qualities separately, or whether they can be developed concurrently (without interference effects). While research has identified a correlation between RSA and total sprint distance during soccer, future studies need to address whether training-induced changes in RSA also produce changes in match physical performance.
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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi Publishing Corporation
                2314-6133
                2314-6141
                2013
                29 August 2013
                : 2013
                : 589361
                Affiliations
                1CeRSM, E.A. 2931, Equipe de Physiologie et de Biomécanique du Mouvement, UFR STAPS, Université Paris Ouest Nanterre—La Défense, 200 avenue de la République, 92000 Nanterre, France
                2Laboratoire de Physiologie, UFR de Santé, Médecine et Biologie Humaine, Université Paris XIII, Rue Marcel Cachin, 93017 Bobigny Cedex, France
                Author notes

                Academic Editor: José M. Vilar

                Article
                10.1155/2013/589361
                3773392
                24073413
                ea7b253a-ea03-41d7-bbe1-90a9c789cb59
                Copyright © 2013 T. Driss and H. Vandewalle.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 November 2012
                : 22 June 2013
                Categories
                Review Article

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