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Use of Ventilatory and Blood Lactate Threshold - Essay Example

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From the paper "Use of Ventilatory and Blood Lactate Threshold" it is clear that there are exercises and protocols that are specifically designed to improve the ability of one athlete to perform in the anaerobic threshold which is very important in crucial moments during a match, a race, running…
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Use of Ventilatory and Blood Lactate Threshold
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Critical discussion of the use of ventilatory (VT1, VT2) and blood lactate threshold (LTP) in the evaluation or predicted performance and training prescriptions and practicality The usage of the knowledge of the modern medicine in sports today is widely accepted practice. Methods for evaluating the fitness and physical condition and predisposition in one athlete are important in order to design the best model of training and exercise for optimal results. In order to assess the level of physical endurance and general shape of the athlete sports medicine developed several techniques that is believed that are the best indicators for the shape of the athlete. For a long time it was believed that peak oxygen uptake or power (VO2 max) is the best indicator of the shape and physical condition. The level of peak oxygen uptake is a measure of the ability of the organism to transport and use oxygen. It is calculated in absolute levels liters per minute (l/min) or a relative measurement of usage of oxygen per kilogram per minute (ml/kg/min) (Bassett and Howley 2000). Nevertheless some new studies have suggested that the so called anaerobic threshold is much more reliable method for evaluating the physical endurance and fitness (McArdle, Katch and Katch 1996). In order to understand this we must first talk about the metabolism that is involved during physical exercise. The main systems of energy production during exercise are ATP system, anaerobic system or glycolisis and aerobic system or mitochondrial respiration. However we must understand that they are not separate but are simply all part of one chain of events that eventually leads to production of ATP, which is the main source of energy in human organism. During the low level exercises which doesn’t require much energy muscle fibers almost exclusively use aerobic mitochondrial production of energy. This is much slower source of energy compared to anaerobic glycolisis but much more effective because from one molecule of glucose produces 29 to 30 molecules of ATP, instead glycolisis produces only 2 molecules of ATP from 1 molecule of glucose. It is estimated that mitochondrial respiration is 19 times more efficient than glycolisis. This is why during low level exercise our body tends to use mitochondrial respiration as a source of energy. However in the metabolism of glycosis - the main energy source used by muscles is conducted through both aerobic and anaerobic metabolism. In the anaerobic metabolism glycosis is converted to pyruvate. This molecule is then further metabolized to oxalate and eventually to CO2 and water in the mitochondrial aerobic metabolism. In a case of sub-maximal endurance physical involvement muscles almost exclusively use mitochondrial aerobic metabolism and pyruvate is almost completely metabolized. This is why at rest and low level exercises blood levels of lactate are normal. But in a case of extensive exercise there is a demand for more energy and therefore more glucose is metabolized to pyruvate. There is a point where the mitochondria are no longer able to metabolize all the pyruvate that is produced and some of it is converted to lactate which enters the blood and muscles. This lactate is than utilized by the liver (and converted to glucose) or heart or kidneys. The point at which at physical exercise the blood concentrations of lactate start to rise is called lactate threshold point (Bassett and Howley 2000). Actually some authors differentiate two distinct lactate thresholds or aerobic and anaerobic lactate threshold. The first, aerobic threshold is the point in the intensity of the physical exercise when the blood lactate levels start to rise. The second, or anaerobic lactate threshold is the point when the concentration of lactate reaches the maximal steady state of concentration (MSSL), when the concentrations of lactate in the blood and muscles reaches maximal stabile values (that can be maintained for some time without further incensement) and it is estimated that in different people ranges between 3.1 and 5.54 mmol.1-1, and normally is accepted that appears on concentrations of 4 mmol.1-1 concentration on average. At this stage the concentration of lactate in the muscle is maximal, and the process of eliminating and producing lactate is at equilibrium. Any further increase in the physical exercise will lead to increase of lactate concentrations and eventually muscle shutdown and weakness (Bassett and Howley 2000). Rising concentrations of lactate in the organism results in blood acidosis, or increasing of the acidity of the blood. Since our organism is a very precise and extremely controlled “machine” it tries to stabilize the acidity of the blood. This is done by the puffer systems of the blood, predominantly bicarbonate puffers. Incensement of the blood acidity is a result of release of positive (+) protons, which are than neutralized and the end product is CO2. This CO2 is than eliminated from the body with respiration. Based on this discussion we can conclude that lactic threshold is associated with changes in the respiration also. This is why other method of measuring of anabolic threshold or physical endurance is the so called ventilatory threshold (Robergs 2001). What is ventilatory threshold? Normally during a physical exercise the respiratory rate increases at a steady rate that can be drawn on a table. At the point when the respiration starts to increase at non-linear way this point is called ventilator threshold (Neary et al. 1985). Actually there are two distinct ventilator thresholds VT1 and VT2. The first ventilator threshold of VT1 is estimated that coincide with the aerobic lactate threshold, when the concentration of lactate start’s to rise in the blood, and we measured it at the point where the respiration start to increase at non-linear way. The second ventilator threshold is believed to coincide with the second, or anaerobic lactate threshold, and it is a level of physical activity that cannot be sustained for a long periods of time due to accumulation of lactate (Riley and Cooper 2002) As we can see lactic and ventilator thresholds are in some degree connected, but the question arises are they identical? This is important because ventilatory threshold is much easier to measure, using only noninvasive techniques (talk test for example), where the lactic threshold requires blood to be conducted. Even though ventilator and lactic threshold have some level of correspondence, ventilator threshold is not identical with elevation of the lactate in the blood and muscles. This is because the puffer systems of the blood reduce the muscle and blood acidity, before the respiratory compensatory mechanisms activate (Brooks 2000). There are many studies that try to explore the correlation between ventilator and lactate threshold. In a study made by Plato et al. 2008 they tried to find if noninvasive ventilator measurements can be used to lactate threshold. They found a 45% correlation between ventilatory and lactate threshold in 19 cyclists. However they found that the accuracy can be significantly improved if the heart rate, body weight, gender and other factors are taken into account also. In another old study made by Neary et al. 1985 it was found that there is no direct causative effect between the blood lactate levels and the appearance of ventilatory threshold. Other studies also find that other factors like training status, carbon-hydrate intake and other factors can significantly influence the correlation between ventilatory and lactate threshold ( Neary et al 1985). The mechanisms behind this discoordination were first recognized in patients with the McArde disease. It is a condition where the enzyme that is responsible for breakdown of glycogen into lactate called phosphorylase is absent. Even though these patients are incapable of producing lactic acid they still manifest signs of ventilatory threshold during extensive, high intensity exercises. Based on these facts it is long known fact that blood lactate levels are not directly correlated with the appearance of ventilatory threshold. (Hagberg 1981). More interestingly there are some new studies that actually suggest that lactate has actually beneficial effect on the ability of the muscle to perform. The main reason for the drop of PH and blood acidity during exercise are the positive (+) protons that are released into the blood and muscles (mostly from ATP), and lactate production and accumulation in the muscles is suggested that has neutralizing effect on the acidity and actually improves the muscle performance (Robergs, Ghiasvand, Parker 2004). In another study made by Meyer et al 2004 they delayed the decrease in acidity in the blood by intravenously adding bicarbonate. This way they directly tested the correlation between blood acidity and drop of PH and it’s correlation with the appearance of ventilatory threshold. In the conclusion of this study is stated that nevertheless that blood acidity has significance in appearance of respiratory compensation and ventilatory threshold, other factors like mechano-receptors found in the muscles, perception of the pain and neuronal impulses from this pain or from other origin, serum potassium levels and other have great importance also. It is important that this study also shows that metabolic acidosis is actually one of the major factors that contribute to respiratory compensation and ventilatory threshold. We can conclude that ventilatory threshold is not identical to lactate threshold, but nevertheless there is significant correlation, that can be further improved by taking in account additional aspects that can be measured by noninvasive methods – like heart rate, weight, age etc. There are studies that found that this correlation is significant and recommend the usage of noninvasive ventilatory threshold. In a study made on cyclists it was found that lactate threshold and ventilatory threshold give similar values for the peak oxygen power (VO2 max) and heart rate values, and based by their findings ventilatory threshold is accurate method for evaluating the anaerobic threshold in cyclists (Alexandre et al 2006). Other studies also conclude that ventilatory threshold along with other parameters is effective method for measurement of maximal lactate steady state (MLSS) or the lactate threshold (Palmer et al 1999). Lactate and ventilatory threshold and other similar methods are used to recognize the so called anaerobic threshold. It is found that anerobic threshold is extremely powerful and precise tool to examinate the performance and physical condition of the athletes for aerobic exercises. Measurement and monitoring of the anaerobic threshold is excellent predictor for the capability of the athlete to conduct some exercise or a predictor for the maximal performance of one athlete. Because anaerobic threshold is dynamic condition, that can be improved with exercise and with selectively chosen exercises it is excellent tool for guidance and improvement of the physical condition, strength and endurance of the athletes. There are exercises and protocols that are specifically designed to improve the ability of one athlete to perform in the anaerobic threshold which is very important in crucial moments during a match, a race, running etc. One way is to increase the volume of the exercise, that should be gradual and over prolonged periods of time to reduce the negative effects. Increasement of the volume should be gradual and no more that 10-20 % increasement a week (Bompa 1999). Other method is training and exercise at lactate threshold point. It is found that in trained athletes lactate threshold appears at 80 to 90 % of the heart rate reserve (maximal heart rate during exercise), and in 50 to 60% in untrained individuals. This can be improved even more with training at the lactate threshold point (Weltman 1995). Interval training is another method for improving the ability of the athlete to perform in the phase of lactate or anaerobic threshold. It is a method of short, high intensity workouts and exercises above the lactate threshold levels. This is why non invasive methods of monitoring the lactate threshold point are so important. It reduces the need for invasive vain catheters and complications that may arise from it, it is available in less equipped laboratories or even at the training site (talk test for example) which eventually will lead to a training that is effective and will give results. References: Bassett, D.R., Jr., & Howley, E.T. 2000. Limiting factors for maximum oxygen uptake and determinants of endurance performance. Medicine and Science in Sport and Exercise, 32 (1), 70-84. McArdle, W.D., Katch, F.I., & Katch, V.L. 1996. Exercise Physiology: Energy, Nutrition, and Human Performance. Baltimore, MD: Williams & Wilkins. Brooks, G.A. 2000. Intra- and extra-cellular lactate shuttles. Medicine and Science in Sport and Exercise, 32 (4), 790-799. Plato PA, McNulty M, Crunk SM, Tug Ergun A (2008), Predicting lactate threshold using ventilatory threshold, Int J Sports Med. 2008 Sep;29(9):732-7. Epub 2008 Jan 23, Department of Kinesiology, San Jose State University, San Jose, California 95192-0054, United States.  Neary, P.J., MacDougall, J.D., Bachus, R., & Wenger, H.A. 1985. The relationship between lactate and ventilatory thresholds: coincidental or cause and effect? European Journal of Applied Physiology, 54 (1), 104-108 Hagberg J M (1981), Ventilatory threshold without increasing blood lactic acid levels in McArdle disease patients. Med Sci Sports Exerc 1981;13:115-8. P. J. Neary, J. D. MacDougall, R. Bachus and H. A. Wenger (1985), The relationship between lactate and ventilatory thresholds: coincidental or cause and effect?, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, Volume 54, Number 1, 1985, 104-108, DOI: 10.1007/BF00426308 T Meyer, O Faude, J Scharhag, A Urhausen, W Kinderman (2004), Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point?, Br J Sports Med 2004;38:622–625. doi: 10.1136/bjsm.2003.007815 Alexandre Hideki Okano, Leandro Ricardo Altimari, Herbert Gustavo Simões, Antonio Carlos de Moraes, Fábio Yuzo Nakamura, Edilson Serpeloni Cyrino and Roberto Carlos Burini (2006), Comparison between anaerobic threshold determined by ventilatory variables and blood lactate response in cyclists, Department of Sport Science, Av. Érico Veríssimo, 701, Caixa Postal 6134 – 13083-851 – Campinas, SP, Brazil, Rev Bras Med Esporte, Vol. 12, Nº 1 – Jan/Fev, 2006 Palmer AS, Potteiger JA, Nau KL, Tong RJ (1999), A 1-day maximal lactate steady-state assessment protocol for trained runners, Medicine and Science in Sports and Exercise [1999, 31(9):1336-41], (PMID:10487377, DOI: 10.1097/00005768-199909000-00016 Robergs, R. A., Ghiasvand, F., Parker, D. (2004). Biochemsitry of exercise-induced metabolic acidosis. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 287: R502-R516. Bompa, T.O. 1999. Periodization: Theory and Methodology of Training, 2nd Ed., Champaign, IL: Human Kinetics. Weltman A (1995): The Blood Lactate Response to Exercise. Current Issues in Exercise Science. Monograph Number Four. Champaign: Human Kinetics, pp49-97. Robergs, R. A. 2001. Exercise-Induced Metabolic Acidosis: Where do the Protons come from? Sportscience 5 (2), sportsci.org/jour/0102/rar.htm. Riley, M. S. and C. B. Cooper (2002), Ventilatory and gas exchange responses during heavy constant work-rate exercise. Med. Sci. Sports Exerc. 34:98–104, 2002. Read More
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