56
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Sodium bicarbonate intake improves high-intensity intermittent exercise performance in trained young men

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Sodium bicarbonate intake has been shown to improve exercise tolerance, but the effects on high-intensity intermittent exercise are less clear. Thus, the aim of the present study was to determine the effect of sodium bicarbonate intake on Yo-Yo intermittent recovery test level 2 performance in trained young men.

          Method

          Thirteen men aged 23 ± 1 year (height: 180 ± 2 cm, weight: 78 ± 3 kg; VO 2max: 61.3 ± 3.3 mlO 2 · kg −1 · min −1; means ± SEM) performed the Yo-Yo intermittent recovery test level 2 (Yo-Yo IR2) on two separate occasions in randomized order with (SBC) and without (CON) prior intake of sodium bicarbonate (0.4 g · kg −1 body weight). Heart rate and rating of perceived exertion (RPE) were measured during the test and venous blood samples were taken frequently.

          Results

          Yo-Yo IR2 performance was 14 % higher (P = 0.04) in SBC than in CON (735 ± 61 vs 646 ± 46 m, respectively). Blood pH and bicarbonate were similar between trials at baseline, but higher (P = 0.003) immediately prior to the Yo-Yo IR2 test in SBC than in CON (7.44 ± 0.01 vs 7.32 ± 0.01 and 33.7 ± 3.2 vs 27.3 ± 0.6 mmol · l −1, respectively). Blood lactate was 0.9 ± 0.1 and 0.8 ± 0.1 mmol · l −1 at baseline and increased to 11.3 ± 1.4 and 9.4 ± 0.8 mmol · l −1 at exhaustion in SBC and CON, respectively, being higher (P = 0.03) in SBC. Additionally, peak blood lactate was higher (P = 0.02) in SBC than in CON (11.7 ± 1.2 vs 10.2 ± 0.7 mmol · l −1). Blood glucose, plasma K + and Na + were not different between trials. Peak heart rate reached at exhaustion was 197 ± 3 and 195 ± 3 bpm in SBC and CON, respectively, with no difference between conditions. RPE was 7 % lower (P = 0.003) in SBC than in CON after 440 m, but similar at exhaustion (19.3 ± 0.2 and 19.5 ± 0.2).

          Conclusion

          In conclusion, high-intensity intermittent exercise performance is improved by prior intake of sodium bicarbonate in trained young men, with concomitant elevations in blood alkalosis and peak blood lactate levels, as well as lowered rating of perceived exertion.

          Related collections

          Most cited references34

          • Record: found
          • Abstract: found
          • Article: not found

          Muscle and blood metabolites during a soccer game: implications for sprint performance.

          To examine muscle and blood metabolites during soccer match play and relate it to possible changes in sprint performance. Thirty-one Danish fourth division players took part in three friendly games. Blood samples were collected frequently during the game, and muscle biopsies were taken before and after the game as well as immediately after an intense period in each half. The players performed five 30-m sprints interspersed by 25-s recovery periods before the game and immediately after each half (N=11) or after an intense exercise period in each half (N=20). Muscle lactate was 15.9+/-1.9 and 16.9+/-2.3 mmol.kg d.w. during the first and second halves, respectively, with blood lactate being 6.0+/-0.4 and 5.0+/-0.4 mM, respectively. Muscle lactate was not correlated with blood lactate (r=0.06-0.25, P>0.05). Muscle glycogen decreased (P<0.05) from 449+/-23 to 255+/-22 mmol.kg d.w. during the game, with 47+/-7% of the muscle fibers being completely or almost empty of glycogen after the game. Blood glucose remained elevated during the game, whereas plasma FFA increased (P<0.05) from 0.45+/-0.05 to 1.37+/-0.23 mM. Mean sprint time was unaltered after the first half, but longer (P<0.05) after the game (2.8+/-0.7%) as well as after intense periods in the first (1.6+/-0.6%) and second halves (3.6+/-0.5%). The decline in sprint performance during the game was not correlated with muscle lactate, muscle pH, or total glycogen content. Sprint performance is reduced both temporarily during a game and at the end of a soccer game. The latter finding may be explained by low glycogen levels in individual muscle fibers. Blood lactate is a poor indicator of muscle lactate during soccer match play.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Cellular mechanisms of muscle fatigue.

            R Fitts (1993)
            Fatigue, defined as the failure to maintain the required or expected power output, is a complex problem, since multiple factors are clearly involved, with the relative importance of each dependent on the fiber type composition of the contracting muscles(s), and the intensity, type, and duration of the contractile activity. The primary sites of fatigue appear to be within the muscle cell itself and for the most part do not involve the central nervous system or the neuromuscular junction. The major hypotheses of fatigue center on disturbances in the surface membrane, E-C coupling, or metabolic events. The cell sites most frequently linked to the etiology of skeletal muscle fatigue are shown in Figure 1. Skeletal muscles are composed of at least four distinct fiber types (3 fast twitch and 1 slow twitch), with the slow type I and fast type IIa fibers containing the highest mitochondrial content and fatigue resistance. Despite fiber type differences in the degree of fatigability, the contractile properties undergo characteristic changes with the development of fatigue that can be observed in whole muscles, single motor units, and single fibers. The Po declines, and the contraction and relaxation times are prolonged. Additionally, there is a decrease in the peak rate of tension development and decline and a reduced Vo. Changes in Vo are more resistant to fatigue than Po and are not observed until Po has declined by at least 10% of its initial prefatigued value. However, the reduced peak power by which fatigue is defined results from both a reduction in Vo and Po. In the absence of muscle fiber damage, the prolonged relaxation time associated with fatigue causes the force-frequency curve to shift to the left, such that peak tensions are obtained at lower frequencies of stimulation. In a mechanism not clearly understood, the central nervous system senses this condition and reduces the alpha-motor nerve activation frequency as fatigue develops. In some cases, selective LFF develops that displaces the force-frequency curve to the right. Although not proven, it appears likely that this condition is associated with and likely caused by muscle injury, such that the SR releases less Ca2+ at low frequencies of activation. Alternatively, LFF could result from a reduced membrane excitability, such that the sarcolemma action potential frequency is considerably less than the stimulation frequency.(ABSTRACT TRUNCATED AT 400 WORDS)
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Na+-K+ pump regulation and skeletal muscle contractility.

              In skeletal muscle, excitation may cause loss of K+, increased extracellular K+ ([K+]o), intracellular Na+ ([Na+]i), and depolarization. Since these events interfere with excitability, the processes of excitation can be self-limiting. During work, therefore, the impending loss of excitability has to be counterbalanced by prompt restoration of Na+-K+ gradients. Since this is the major function of the Na+-K+ pumps, it is crucial that their activity and capacity are adequate. This is achieved in two ways: 1) by acute activation of the Na+-K+ pumps and 2) by long-term regulation of Na+-K+ pump content or capacity. 1) Depending on frequency of stimulation, excitation may activate up to all of the Na+-K+ pumps available within 10 s, causing up to 22-fold increase in Na+ efflux. Activation of the Na+-K+ pumps by hormones is slower and less pronounced. When muscles are inhibited by high [K+]o or low [Na+]o, acute hormone- or excitation-induced activation of the Na+-K+ pumps can restore excitability and contractile force in 10-20 min. Conversely, inhibition of the Na+-K+ pumps by ouabain leads to progressive loss of contractility and endurance. 2) Na+-K+ pump content is upregulated by training, thyroid hormones, insulin, glucocorticoids, and K+ overload. Downregulation is seen during immobilization, K+ deficiency, hypoxia, heart failure, hypothyroidism, starvation, diabetes, alcoholism, myotonic dystrophy, and McArdle disease. Reduced Na+-K+ pump content leads to loss of contractility and endurance, possibly contributing to the fatigue associated with several of these conditions. Increasing excitation-induced Na+ influx by augmenting the open-time or the content of Na+ channels reduces contractile endurance. Excitability and contractility depend on the ratio between passive Na+-K+ leaks and Na+-K+ pump activity, the passive leaks often playing a dominant role. The Na+-K+ pump is a central target for regulation of Na+-K+ distribution and excitability, essential for second-to-second ongoing maintenance of excitability during work.
                Bookmark

                Author and article information

                Contributors
                pkrustrup@nexs.ku.dk , P.Krustrup@exeter.ac.uk
                germidis@phyed.duth.gr
                +298 292270 , magnim@setur.fo
                Journal
                J Int Soc Sports Nutr
                J Int Soc Sports Nutr
                Journal of the International Society of Sports Nutrition
                BioMed Central (London )
                1550-2783
                4 June 2015
                4 June 2015
                2015
                : 12
                : 25
                Affiliations
                [ ]Department of Nutrition, Exercise and Sports, Section of Human Physiology, Copenhagen Centre for Team Sport and Health, University of Copenhagen, Copenhagen, Denmark
                [ ]Sport and Health Sciences, College of Life and Environmental Sciences, St. Luke’s Campus, University of Exeter, Exeter, UK
                [ ]Democrite University of Thrace, Komotini, 69100 Greece
                [ ]Faculty of Natural and Health Sciences, University of the Faroe Islands, Jónas Broncks gøta 25. 3rd floor, Tórshavn, Faroe Islands
                [ ]Department of Food and Nutrition, and Sport Science, Center of Health and Human Performance, University of Gothenburg, Gothenburg, Sweden
                Article
                87
                10.1186/s12970-015-0087-6
                4475610
                26097440
                948f7003-e5cc-4a66-9a11-4b4052eb522c
                © Krustrup et al. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 16 February 2015
                : 22 May 2015
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2015

                Sports medicine
                fatigue,yo-yo ir2 performance,blood ph and lactate,plasma potassium,buffer capacity

                Comments

                Comment on this article