23 Mar 2015
In sport disciplines that rely on speed endurance or strength endurance, anaerobic glycolysis provides the primary energy source for muscular contractions (Zajac et al., 2009)
During high intensity exercise there is an increase of hydrogen (H+) ions in the mitochondria (Pilegaard et al., 1999). The metabolic demands of high-intensity exercise are met primarily by glycolysis, which is the non-oxidative breakdown of glucose (Gosselink et al.,1995). This is caused when the demand for energy exceeds oxygen supply or utilisation rate. As a result the cell mitochondria cannot process all hydrogen ions joined to its carrier NADH. The hydrogen ions begin to accumulate in the cells which decrease the pH of exercising muscles and cellular acidosis occurs (Brooks 1985). To maintain availability of NAD+, and to prevent acidosis, excess Hydrogen ions are temporarily bound with pyruvate to form lactic acid.
Rupp et al., (1983) states that at rest arterial blood pH is ~7.4, while venous blood pH is normally slightly lower (~7.3-7.35) and muscle pH is ~6.9. It is also suggested Exhaustive exercise decreases pH ~0.4 pH units in both blood and muscle, and is highly correlated to increased blood lactate concentration. Similarly, blood and muscle bicarbonate ion concentration decreases linearly as a function of increasing lactate ion concentration.
This increase in hydrogen ion concentration interferes with anaerobic metabolism by disrupting the activities of key enzymes; it is also associated with reduction in ATP production, lipolysis, and muscle tension (Monedero & Donne. 2000).
Harrison and Thompson (2005) state that the increase in acidity ultimately inhibits energy transfer and the ability of the muscles to contract; forcing the athlete to decrease the intensity of exercise. Gollnick et al., (1986) suggests that this is because hydrogen ions displace calcium from troponin, which causes interference in muscle contraction. It is the production of these hydrogen ions and the decrease in pH that causes the effects associated with fatigue (Robergs, 2004)
Acidemia also has an effect on the cardiovascular system, by reducing or stops the responses of the heart to stimulation of sympathetic nerves and slows the heart rate due to vagal stimulation (Hainsworth 1986)
CO2 levels and the pH of the blood perfusing the cephalic circulation has an effect on efferent signal activity (Soladoye et al., 1985)
The body's first line of defence to prevent acidemia are naturally occurring chemical buffers such as a weak carbonic acid and sodium bicarbonates (Zajac et al., 2009)
A buffer is a solution containing substances which have the ability to minimise changes in pH when an acid or base is added to it (worthley 1977)
The intracellular buffering system, includes amino acids, proteins, Pi, HCO3, creatine phosphate (CrP) hydrolysis, and lactate production, binds or consumes H_ to protect the cell against intracellular proton accumulation (Robergs et al., 2004)
In the bicarbonate buffer (HCO3) system the chemical equilibrium between carbonic acid and bicarbonate act as a ph regulator. Buffering results in H+ ions being drawn out from the muscle cells into the blood due to a concentration gradient. This process reduces the acidity within in the muscle cells (Lambert et al., 1993). If the [H+] in blood begins to drop then the pH raises, more carbonic acid dissociates, replenishing hydrogen ions. When [H+] rises, the bicarbonate ion acts as a base and removes the excess hydrogen ions lowering the pH (Mcnaughton et al., 2008)
During buffering NaHCO3 in plasma exerts a strong buffering action on lactic acid to form sodium lactate and carbonic acid. An additional increase in [H+] from carbonic acid dissociation causes the dissociation reaction to move in the opposite direction to release carbon dioxide into plasma. (McArdle et al., 2007)
Hydrogen ions, carbon dioxide, and oxygen are detected by specialized chemoreceptors in the brain. Inside cells, carbon dioxide (CO2) combines with water (H2O) to form carbonic acid (H2CO3). The carbonic acid breaks down rapidly into hydrogen ions and bicarbonate ions. Therefore, an increase in carbon dioxide results in an increase in hydrogen ions, while a decrease in carbon dioxide brings about a decrease in hydrogen ions (West 1995)
chemoreceptors in the medulla detect the raised level of carbon dioxide and hydrogen ions. They send afferent signals the inspiratory center, which immidately stimulates veltilation to eliminate excess carbondioxide (McArdle et al., 2007)
Hawthorn (1986) states that in the short term the most important buffer in the body is haemoglobin as it produces the smallest change in pH per given amount of acid, showing that it is most effective in retaining equilibrium. In the long term the most important buffer during exercise is the ventilatory buffer system in combination with bicarbonate. As the lungs remove excess CO2, reduced plasma CO2 levels accelerate the recombination of H+ and HCO3, lowering free [H+]s in plasma (McArdle et al., 2007)
When the buffering capacity within the cell is exceeded, lactate and hydrogen ions diffuse outside the cells (McNaughton, 1992) thus reducing [H+] in muscle cell, this however leads to a higher H+ gradient in the blood (Robergs et al., 2004) resulting in an increased acidic environment. The ability to tolerate high-intensity exercise is limited by the body's ability to counteract decreases in intracellular (muscle) and extracellular (blood) pH through its intrinsic buffering systems (Gosselink et al.,1995)
Lambert et al., (1993) states that Sodium bicarbonate is an alkalising agent that reduces the acidity of the blood by the process of buffering. Sodium bicarbonatebuffers the acidity from lactic acid that is created by anaerobic metabolism. This allows prolonged maintenance of force or power (Montgomery and Beaudin 1982)
Sodium is an electrolyte that helps increase or maintain blood volume, creating a larger buffering space for muscles to excrete the extra acidity created by high-intensity activity. Benardot (2006) has suggested that the sodium in the sodium bicarbonate may actually be more useful than the bi carbonate. Potteiger et al. (1996) tested the effect of sodium citrate on 30-km cycling performance. Performance times averaged almost 3% faster than those in the placebo condition, showing the effectiveness of sodium and its effect on performance.
Bicarbonate serves a crucial biochemical role in the pHbuffering system by accepting hydrogen ions from solutions when they are in excess and donating hydrogen ions to the solution when they are depleted, keeping a constant state of homeostasis. (Robergs et al., 2004) This process reduces the acidity within in the muscle cells. The process of buffering could therefore result in delayed fatigue and increased muscle force production. (Lambert et al., 1993)
Despite an increase in extracellular bicarbonate, studies show that the sarcolemma is not permeable to bicarbonate (Mainwood &Cechetto 1980). This suggests that H+ ions are not buffered inside muscle cells. Extracellular bicarbonate concentration results in greater H+ efflux to the blood (Mainwood & Worsley-Brown. 1975)
Thus it has been reasoned by physiologists that by increasing bicarbonate reserves, the body's extracellular buffering capacity will allow hydrogen ions to diffuse from the muscles at a faster rate. The benefit from sodium bicarbonate supplementation would therefore be a delayed onset of fatigue during anaerobic exercise (Cairns, 2006)
In the early 1980s it was suggested that ingestion of NaCO3 could be effective in improving short-term exercise performance. Wilkes et al., (1983)compared the effects of NaCO3 and a placebo in six competitive 800-m runners. The bicarbonate was givenover a two-hour period at a dose equivalent to 21 gm for a 70-kg person (0.3 g per kg of body weight).The athletes completed a competitive 800-m race. Average performance was 2% faster in the bicarbonate condition than in the control or placebo conditions.
In a similar study, but using a higher dose of sodium bicarbonate (0.4 g/kg, or 28 gm for a 70-kg person),Goldfinch et al. (l988)investigated the 400-m race performance of six trained runners.Athletes competed in pairs to simulate real competition. The performance of the bicarbonate group was 2% better than the control and placebo, which were not different from each other. The time difference was equivalent to a 10-m distance at the finish.
Muscle biopsy's on athletes have shown that after bicarbonate loading, the less acidic your blood pH and also less acidic your muscle pH. (Bouissou et al., 1988)
Lactate production acts as both a buffering system, by consuming H+, and a proton remover, by transporting H+ across the sarcolemma, to protect the cell against metabolic acidosis. (Robergs et al., 2004)
Katz and Sahlin (1988) states that rapid the increase in the production of lactic acid and the free H+ can be buffered by bicarbonate causing the nonmetabolic production of carbon dioxide (CO2). Consecutively the raised blood CO2 content stimulate an increased rate of ventilation causing the temporal relationship between the lactate and ventilatory thresholds (Stringer et al., 1992). Thomas et al., (2005) state that Lactate concentrations increase post exercise after NaHCO3 ingestion. This is common amongst studies testing the effects of NaHCO3.
Raymer et al. (2004) suggests that at the point of fatigue, muscle [H+] does not decrease with sodium-bicarbonate ingestion. However the acidosis threshold increases, meaning that during induced alkalosis, muscle acidosis is lower at the same muscle workload. This is congruent with Cairns (2006) who stated that NaHCO3 delays onset of fatigue during anaerobic exercise.
However there are potential negative side effects from taking sodium bicarbonate include severe gastrointestinal distress and nausea; this should give athletes reason to be careful before taking this potential ergogenic aid (Applegate 1999). These risks can be reduced through appropriate dosing and timing
RPE and anticipation, if RPE is reduced then you should go faster
How bicarb affects perceived exersion
How other mechanism so regulating ph and mayb central gonenor afferent and efferent pacing algorithm
However it has been suggested that NaHCO3 ingestion alone may not increase performance and other mechanisms may regulate performance for example the Central Governor model.
The central governor model suggests that the brain is contently monitoring biochemical changes in the body through afferent and efferent signals and regulates them accordingly. This safety mechanism is in place to regulate and possibly stop exertion to prevent damage to the cells. This would suggest that the reason athletes are able to exert for longer is that the afferent signals such as pH levels in the muscle allow the brain to exert more without the risk of damage.
Studies giving evidence for this argument include studies by Kostka & Cafarelli (1982) have suggested that RPE during exercise maybe influenced through manipulation of acid-base status, suggesting that shifts in [H+] are linked to sensory processes (Renfree 2009)
Ingestion of NaHCO3has been demonstrated to reduce RPE during supra lactate threshold (>LT) intensity exercise (Robertson et al 1986). This is congruent with finding from Renfree (2009) who found that Power output was higher (P<0.05)following NaHCO3 ingestion than following CaCO3ingestion at all times above the subjects lactate threshold.
Robbertson et al 1986
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