Introduction
The lactate threshold is a field in exercise physiology where several studies have already been conducted. A lactate threshold test is useful as it will lead to the discovery of specific applications of a person’s racing, training, and other exercise activities. The workload corresponding to the lactate threshold and onset of blood lactate accumulation has previously been quantified using lactate tests incorporating stage increments (McNaughton, 2002).
The anaerobic threshold is a submaximal index related to endurance exercise performance, which is usually determined by the measurement of blood lactate concentration during an incremental exercise test (lactate threshold). The lactate threshold, and thus the anaerobic threshold, can also be detected noninvasively in normal subjects by means of the gas exchange threshold (GET).
The concept that muscle contraction can occur for extended periods of time without sufficient oxygen supply may have been first suggested as early as 1871. As early as 1909, investigators surmised that lactate stimulated respiration during high-intensity exercise. Between 1910 and 1915, other investigators suggested that lactate was the “signal” that initiated muscle contraction, and the role of oxygen was to remove lactate once it was formed (it is now known, of course, that lactate is the product of, not the cause of, muscle contraction).
Shortly thereafter, several other laboratories in the United States and Europe independently reported that exercise intensity, lactate production, metabolic acidosis, and bicarbonate buffering appeared to be linked. The accumulation of lactate in the blood was thought to reflect a point during exercise in which oxygen supply was inadequate to meet the energy requirements of the working muscle. In the early 1960s, investigators linked lactate production in the blood to endurance performance among German athletes. In 1964, other investigators explicitly developed the concept that a critical threshold exists in which (1) the metabolic needs for oxygen in the muscle exceed the capacity of the cardiopulmonary system to supply them, (2) there is a sudden increase in anaerobic metabolism, and (3) lactate is formed in the muscle (Ashley, 1997).
There are limited data on the reproducibility of blood lactate variables, heart rates and ratings of perceived exertion (RPE) during sub-maximal exercise. The aim of this study was to determine the lactate threshold, at different blood lactate concentrations, heart rate (beats per minute) and RPE during a continuous, incremental training cycle. The hypothesis of this study is that there is a directly proportional relationship between heart rate and rate of perceived exertion to measures of blood lactate threshold.
Methods
The lactate threshold in this experiment was obtained by a progressive exercise test and by taking a blood sample at the end of each stage. The lactate content of each blood sample is then analyzed. Lactate profile is a form of testing that is very useful in monitoring changes in fitness and should be performed several times throughout the course of the training cycle.
Before starting the experiment, the conditions of the testing facility such as the room temperature, barometric pressure, and relative humidity are recorded on data sheets.
Informed consent is given to every participant of the study and each of them is also asked to complete the health questionnaire given to them. The body mass of the subject is then measured in terms of kilograms.
The heart rate transmitter was attached to the chest of the subject. RPE measurements were recorded every minute throughout the test. The appropriate lab safety and subject care protocol for obtaining a small blood sample were followed.
As is the same with some other studies that were conducted in the past, the sample blood is taken from the earlobe of the subject at rest and at the end of each stage. The Lactate Pro handheld lactate analyser was used to determine the blood lactate concentrations for the subject.
In this study conducted, the test started with 100 watts of power. This is increased steadily until exhaustion is reached by the subject. The duration of each stage is 4 minutes. Every 4 minutes, the resistance of the cycle ergometer is increased by 25 watts.
During the last 30 seconds of each stage, the physiological resistance of each stage is taken and recorded and the resistance is increased by 50 W.
The concentration of blood lactate, the ratings of perceived exertion, and the heart rate are all measured at the end of each 4 minute stage. The blood sample is taken during the last 30 seconds of each stage.
Results
Based on the above table and graph, the following interpretations can be made. At the start of the experiment, when the power is still at 0, the subject’s heart rate is 93 beats per minute, the lactate 1.3 mmol/l, and the RPE is not stated or lacking since this is measured at the start. At 100 watts, when the subject has a maximal heart rate of 121 beats per minute, the lactate is 3 mmol/l and the RPE is 7. At 130 watts, with a heart rate of 132 beats per minute, the lactate is 3.2 mmol/l and the RPE is still 7. At 160 watts, the heart rate is 149 beats per minute, the lactate 3.7 mmol/l and the RPE is 8. At 190 watts, the heart rate is 161 beats per minute, the lactate is 4.8 mmol/l, and the RPE is 10. At 220 watts with a heart rate of 173 beats per minute, the lactate is 7.6 mmol/l, and the RPE is 13. At 250 watts with a heart rate of 184 beats per minute, the lactate is 12.6 mmol/l, and the RPE is 15. Lastly, at 280 watts, the heart rate is 188 beats per minute, the lactate is 16.7 mmol/l, and the RPE is 19.
There is also a 2-minute post-exercise lactate which is 16.2 mmol/l and a 5-minute post-exercise lactate which is 15.2 mmol/l.
Critical Discussion
During exercise, such as sprinting type activities, when the rate of demand for energy is high, lactate is produced faster than the ability of the tissues to remove it and lactate concentration begins to rise. This is a beneficial process since the regeneration of NAD+ ensures that energy production is maintained and exercise can continue.
During exercise, the amount of oxygen entering the blood in the lungs is increased because the amount of oxygen to be added to each unit of blood and the pulmonary blood flow per minute are increased. The PO2 of blood flowing into the pulmonary capillaries falls from 40 to 25 mm Hg or less, so that the alveolar-capillary PO2 gradient is increased and more oxygen enters the blood (Ganong, 2001).
Blood flow per minute is increased from 5.5 L/min to as much as 20-35 L/min. The total amount of oxygen entering the blood therefore increases from 250 mL/min at rest to values as high as 4000 mL/min. The amount of carbon dioxide removed from each unit of blood is increased, and carbon dioxide excretion increases from 200 mL/min to as much as 8000 mL/min (Ganong, 2001).
The law of mass action states that as the end products of a chemical reaction build up in a reacting medium, the rate of the reaction approaches zero. The two end products of the glycolytic reactions are (1) pyruvic acid and (2) hydrogen atoms combined with NAD+ to form NADH and H+. The build-up of either or both of these would stop the glycolytic process and prevent further formation of adenosine triphosphate (ATP) (Guyton & Hall, 2000).
When their qualities begin to be excessive, these two end products react with each other to form lactic acid. Thus, under anaerobic conditions by far, the major portion of the pyruvic acid is converted into lactic acid, which diffuses readily out of the cells into the extracellular fluids and even into the intracellular fluids of other less active cells (Guyton & Hall, 2000).
The increase in oxygen uptake is proportionate to work load up to a maximum. Above this maximum, oxygen consumption levels off and the blood lactate level continues to rise. The lactate comes from muscles in which aerobic resynthesis of energy stores cannot keep pace with their utilization and an oxygen debt is being incurred (Ganong, 2001).
Contrary to popular belief, this increased concentration of lactate does not directly cause acidosis, nor is it responsible for muscle pain or “burning”. This is because lactate itself is not capable of releasing a proton, and secondly, the acidic form of lactate (lactic acid) cannot be formed under normal circumstances in human tissues. Analysis of the glycolytic pathway in human indicates that there are not enough hydrogen ions present in the glycolytic intermediates to produce lactic or any other acid.
The relationship between the increase in blood lactate and oxygen supply to the muscle has a long history. Studies performed early in this century closely linked exercise intensity, lactate appearance, metabolic acidosis, and bicarbonate buffering. These associations provided a convenient and logical explanation for lactate production during exercise.
Numerous studies have supported the link between oxygen supply and the magnitude of the increase in blood lactate, albeit without direct evidence of the cause and effect. For example, the extent to which lactate increases in the blood during exercise is reduced as fitness increases or with training increased in the presence of reduced cardiac output states or disease of the electron transport chain.
When oxygen supply is experimentally altered, blood lactate is profoundly affected. With an increase in inspired oxygen tension, either by increasing the oxygen content of the inspired air or by increasing the barometric pressure, the exercise-induced increase in lactate level is attenuated. Decreasing the fraction of inspired oxygen either experimentally or by exposure to altitude increases blood lactates. In normal subjects, reducing blood volume causes an increase in blood lactate level during exercise. In patients with chronic heart failure, increasing cardiac output with inotropic therapy attenuates the increase in blood lactate during exercise (Ashley, 1997).
The concept that a “threshold” exists, in which there is a sudden onset of anaerobic metabolism resulting in the accumulation of lactate in the blood has been challenged. Recently, this issue has generated some rather lively debate. Studies by some investigators raised questions about the subjective intraobserver and interobserver reliability and reproducibility of ventilatory and lactate thresholds. Concerns over the presence or absence of a discrete threshold point led investigators with the use of a log-log transformation (ie, plotting oxygen uptake, lactate, or [CO.sub.2] production on logarithmic axes). These investigators reported that lactate exhibited an abrupt transition from a slowly increasing phase to a rapidly accelerating phase, for which the findings are consistent with the historic interpretation of the anaerobic threshold (Ashley, 1997).
Despite of its wide adaption, however, such idea was unacceptable to many since among other things, a log transformation could “create” a visually apparent breakpoint where none existed before, by spreading out the early data points over the X-axis relative to the other later on (Ashley, 1997).
The lag in blood lactate concentration observed during the test is possibly related to vasoconstriction of the active muscle mass stemming from isometric contraction of the body during the exercise effort. More specifically, if a measurement of peak blood lactate concentration is required after an ergometry test, it is recommended that a capillary blood sample should be obtained 3-5 mins after exercise.
The fixed blood lactate concentration of 4.0 mmol * [l.sup.-1] has been used extensively to monitor and prescribe endurance exercise training programmes with adults in many studies. It is well recognized that the blood lactate response to exercise is different in young people than in adults. Therefore, a lower fixed blood lactate concentration has been proposed to use in children. The rationale for these single concentrations was that they represent the maximum exercise intensity at equilibrium between blood lactate accumulation and elimination occurs. This physiological parameter is believed to represent the highest intensity of exercise that can be supported almost exclusively by oxidative energy metabolism (Price, 2002).
Conclusion
The lactate threshold provides a clear picture of the subject’s current fitness level. The lactate threshold, along with the power output can determine a person’s specific heart-rate training zones. Knowing these zones and how to intersperse them enables everyone to ultimately improve performance.
At the start, concentrations of lactate rise slowly, but then suddenly, increase sharply at a clearly-defined point, which is termed as the lactate threshold. The lactate threshold corresponds to the shift in metabolism to anaerobic within the muscle cells after exercise has begun in the experiment. At this point, lactate is being produced faster than it can be metabolized and it accumulates, passing into the blood. Obtaining blood samples can determine the amount of lactate present in the blood.
The way to improve Lactate Threshold is to incorporate one or two Lactate Threshold training to run into the weekly plan. These are run at a comfortably hard, near race pace, with a steady, unvarying effort. After about five to 10 minutes of easy running, run for at least 20 minutes at Lactate Threshold pace. An individual should work hard but not have to slow down over the course. Considering this, they will be too fast and it won’t be as beneficial as maintaining a steady Lactate Threshold effort.
A person can measure their training zone by heart rate, pace, or perceived effort. But it is best if their course are on the average level and smooth so that they are able to maintain a regular tempo (hence the term tempo runs) rather than having to speed up or slow down to accommodate hills and rough terrain.
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