|Optimize Endurance Training
By Lance C. Dalleck, M.S. & Len Kravitz, Ph.D.
One of your clients, a recreational runner, informs you he/she has just registered for a 10-k road race and would appreciate your input in designing a training program. Wanting to optimize his/her endurance training, you begin some background research and quickly discover that the lactate threshold is the best predictor of endurance performance. However, as you continue your reading, ventilatory threshold, anaerobic threshold, and other terminology are also frequently referred to as the same physiological event as the lactate threshold. Interested but confused, you wonder what does it all mean?
If this scenario sounds familiar, youre not alone deciphering the inconsistent terminology regarding the most essential component of endurance performance can be tricky. The purpose this article will be to clearly describe the physiological mechanisms behind the lactate, ventilatory, and anaerobic thresholds, as well as discuss the heart rate threshold. This knowledge will be used to outline training principles for the improvement of lactate threshold values in your clientele.
Lactate Threshold and Endurance Performance
Traditionally, maximal oxygen uptake (VO2max) has been viewed as the key component to success in prolonged exercise activities (Bassett & Howley 2000). However, more recently researchers have proposed that the lactate threshold is the best and most consistent predictor of performance in endurance events. Research studies have repeatedly found high correlations between performance in endurance events such as running, cycling, and race-walking and the maximal steady-state workload at the lactate threshold (McKardle, Katch, & Katch 1996).
What is the Lactate Threshold?
At rest and under steady-state exercise conditions, there is a balance between blood lactate production and blood lactate removal (Brooks 2000). The lactate threshold refers to the intensity of exercise at which there is an abrupt increase in blood lactate levels (Roberts & Robergs 1997). Although the exact physiological factors of the lactate threshold are still being resolved, it is thought to involve the following key mechanisms (Roberts & Robergs 1997):
1) Decreased lactate removal
2) Increased fast-twitch motor unit recruitment
3) Imbalance between glycolysis and mitochondrial respiration
4) Ischemia (low blood flow) or hypoxia (low oxygen content in blood)
Before discussing the key mechanisms of the lactate threshold, a brief overview of the metabolic pathways of energy production is necessary.
Metabolic Pathways Overview
All energy transformations that occur in the body are referred to as metabolism. Thus a metabolic pathway is a series of chemical reactions that will result in the formation of ATP and waste products (such as carbon dioxide). The three energy systems of the body are the ATP-PC (often referred to as phosphagen) system, glycolysis (break down of sugar), and mitochondrial respiration (cellular production of ATP in the mithochondrion).
ATP-PC is the simplest energy system of the body with the shortest capacity (up to 15 seconds) to maintain ATP production. During intense exercise, such as in sprinting, the ATP-PC is the most rapid and available source of ATP.
During submaximal endurance exercise, the energy for muscle contraction comes from ATP regenerated almost exclusively through mitochondrial respiration, which initially has the same pathway as glycolysis. It is a misconception to think that the bodys energy systems work independently. In fact, the three energy systems work together cooperatively to produce ATP. Through glycolysis, blood glucose or muscle glycogen is converted to pyruvate, which once produced will either enter the mitochondria or be converted to lactate depending on the intensity of exercise. Pyruvate enters the mitochondria at exercise intensity levels below the lactate threshold, while at exercise intensity levels above the lactate threshold the capacity for mitochondrial respiration is exceeded and pyruvate is converted to lactate. It is at this point that high-intensity exercise is compromised, because the glycolytic and phosphagen energy systems that are sustaining the continued muscle contraction above the lactate threshold can produce ATP at a high rate, yet are only capable of doing so for short durations of time (Bassett & Howley 2000).
So, the energy for exercise activities requires a blend of all the energy systems. However, the determinants of the involvement of the particular energy system are highly dependent on the intensity of the exercise. Let us now continue the discussion of the mechanisms contributing to the lactate threshold.
1) Lactate Removal
Although once viewed as a negative metabolic event (see Side Bar I), increased lactate production occurring exclusively during high-intensity exercise is natural (Roberts & Robergs 1997). Even at rest a small degree of lactate production takes place, which indicates there must also exist lactate removal or else there would be lactate accumulation occurring at rest. The primary means of lactate removal include its uptake by the heart, liver, and kidneys as a metabolic fuel (Brooks 1985). Within the liver, lactate functions as a chemical building block for glucose production (known as gluconeogenesis), which is then released back into the blood stream to be used as fuel (or substrate) elsewhere. Additionally, non-exercising or less active muscles are capable of lactate uptake and consumption. At exercise intensities above the lactate threshold, there is a mismatch between production and uptake, with the rate of lactate removal apparently lagging behind the rate of lactate production (Katz & Sahlin 1988).
2) Increased Fast-Twitch Motor Unit Recruitment
At low levels of intensity, primarily slow-twitch muscles are recruited to support the exercise workload. Slow-twitch muscle is characterized by a high aerobic endurance capacity that enhances the energy metabolism of the mitochondrial respiration energy system. Conversely, with increasing exercise intensity there is a shift towards the recruitment of fast-twitch muscles, which have metabolic characteristics that are geared towards glycolysis. The recruitment of these muscles will shift energy metabolism from mitochondrial respiration towards glycolysis, which will eventually lead to increased lactate production (Anderson & Rhodes 1989).
3) Imbalance between Glycolysis and Mitochondrial Respiration
At increasing exercise intensities, there is an increased reliance on the rate in the transfer of glucose to pyruvate through the reactions of glycolysis. This is referred to as glycolytic flux. As described earlier, the pyruvate produced at the end of glycolysis can either enter the mitochondria or be converted to lactate. There are some researchers who believe that at high rates of glycolysis, pyruvate is produced faster than it can enter into the mitochondria for mitochondrial respiration (Wasserman, Beaver, & Whipp 1986). Pyruvate that cannot enter the mitochondria will be converted to lactate, which can then be used as fuel elsewhere in the body (such as the liver or other muscles).
4) Ischemia and Hypoxia
For years, one of the primary causes of lactate production was thought to include low levels of blood flow (ischemia) or low levels of blood oxygen content (hypoxia) to exercising muscles (Roberts & Robergs 1997). This led to the term anaerobic threshold, which will be discussed in more detail shortly. However, there is no experimental data indicating ischemia or hypoxia in exercising muscles, even at very intense bouts of exercise (Brooks 1985).
Unfortunately and confusing, the lactate threshold has been described with different terminology by researchers, including maximal steady-state, anaerobic threshold, aerobic threshold, individual anaerobic threshold, lactate breaking point, and onset of blood lactate accumulation (Weltman 1995). Whenever reading on the topic of lactate threshold it is important to realize that these differing terms are essentially describing the same physiological event (Weltman 1995).
What is the Ventilatory Threshold?
As exercise intensity progressively increases in intensity, the air into and out of your respiratory tract (called ventilation) increases linearly or similarly. As the intensity of exercise continues to increase, there becomes a point at which ventilation starts to increase in a non-linear fashion. This point where ventilation deviates from the progressive linear increase is called the ventilatory threshold. The ventilatory threshold corresponds (but is not identical) with the development of muscle and blood acidosis (Brook 1985). Blood buffers, which are compounds that help to neutralize acidosis, work to reduce the muscle fibers acidosis. This leads to an increase in carbon dioxide, which the body attempts to eliminate with the increase in ventilation (Neary et al 1985).
Because increased ventilation occurs with increasing blood lactate values and acidosis, scientists originally believed this was an indication that the ventilatory and lactate threshold occur at similar exercise intensities. This interpretation is appealing because measuring the ventilatory threshold is non-invasive compared to the lactate threshold. And while numerous studies have shown a close correlation between the thresholds, separate studies have demonstrated that different conditions, including training status and carbohydrate nutritional supplementation, can cause thresholds in the same individual to differ substantially (Neary et al 1985).
What is the Anaerobic Threshold?
The term anaerobic threshold was introduced in the 1960s based on the concept that at high-intensity levels of exercise, low levels of oxygen (or hypoxia) exists in the muscles (Roberts & Robergs 1997). At this point, for exercise to continue, energy supply needed to shift from the aerobic energy system (mitochondrial respiration) to anaerobic energy systems (glycolysis and the phosphagen system).
However, there are many researchers who strongly object to the use of the term anaerobic threshold, believing it is misleading. The main argument against using the term anaerobic threshold is that it suggests oxygen supply to muscles is limited at specific exercise intensities. However, as previously mentioned, there is no evidence that indicates muscles become deprived of oxygen - even at maximal exercise intensities (Brooks 1985). The second main argument against using anaerobic threshold is that it suggests at this point in exercise intensity, metabolism shifts completely from aerobic to anaerobic energy systems. This interpretation is an overly simplistic view of the regulation of energy metabolism, as anaerobic energy systems (glycolysis and the phosphagen system) do not take over the task of ATP regeneration completely at higher intensities of exercise, but rather augment the energy supply provided from mitochondrial respiration (Roberts & Robergs 1997).
What is the Heart Rate Threshold
In the early 1980s, Conconi and fellow Italian researchers developed the methodology to detect the lactate threshold through a running test by determining the heart rate deflection point (Conconi 1982). This easy and non-invasive approach to indirect lactate threshold measurement has been utilized extensively for training program design and exercise intensity recommendations (Hofmann et al 1994, Janssen 2001). However, some research has shown that the heart rate deflection point is only visible in about half of all individuals and commonly over-estimates lactate threshold (Vachon, Bassett, & Clarke 1999). Because of these findings, and the grave errors associated with its use, personal trainers and fitness professionals are discouraged from recommending the heart rate threshold method when designing endurance training programs for clients.
Summary of Anaerobic, Ventilatory, Lactate and Heart Rate Thresholds
In summary, ventilatory and lactate thresholds, although very similar, should not be viewed as occurring at precisely the same exercise workloads. The use of the term anaerobic threshold in the lay community and with exercise professionals has led to much confusion and oversimplification of the function of the bodys energy systems. So much error presently exists with the heart rate threshold technique that further research is needed to be able to confidently utilize this technique. Therefore, the focus of designing a successful endurance training program will be based upon the physiological understanding of the lactate threshold.
Training and the Lactate Threshold
While it has been suggested that training intensity should be based upon the velocity (mph) or workload (cycling speed) that corresponds to the lactate threshold, a leading researcher on the topic, Arthur Weltman, acknowledges that more research is needed to identify the minimal or optimal training intensity for improving lactate threshold (Weltman 1995). Despite this, it is well known that following endurance training, the lactate threshold will occur at a higher relative percentage of an individuals maximal oxygen uptake (VO2max) than prior to training. This physiological training adaptation allows for an individual to maintain higher steady-state running velocities or cycling workloads, while maintaining a balance between lactate production and removal. Endurance training influences both the rate of lactate production and the capability for lactate removal.
The reduced lactate production, at the same given workload, following endurance training can be attributed to increased mitochondria size, mitochondrial numbers, and mitochondrial enzymes (Holloszy & Coyle 1984; Honig, Connett, & Gayeski 1992). The combined result of these training adaptations is an enhanced ability to generate energy through mitochondrial respiration, thus lowering the amount of lactate production at a given workload.
In addition, endurance training appears to cause an increase in lactate utilization by muscles, leading to a greater capacity for lactate removal from circulation (Gladden 2000). Consequently, despite the heightened lactate production rates occurring at high levels of exercise intensity, blood lactate levels will be lower. It should be noted that endurance training may also improve capillary density around the muscles, especially the slow-twitch muscles. This adaptation improves blood flow to and from exercising muscles, which will enhance the clearance of lactate and acidosis (Roberts & Robergs 1997).
Lactate Threshold Training Programs and Workouts
Although the optimal training for lactate threshold improvement has yet to be fully identified by researchers, there are still some excellent guidelines you can follow in generating training programs and workouts in order to enhance the lactate threshold levels of clients. Research has indicated that training programs that are a combination of high volume, interval and steady-state workouts have the most pronounced effect on lactate threshold improvement (Roberts & Robergs 1997, Weltman 1995).
Initially, the best way to improve the lactate threshold levels of your clients is to simply increase their training volume, whether their endurance activity is cycling, running, or swimming. Increased training volume should be gradual and in the order of approximately 10-20% per week (Bompa 1999). For example, if an individual is currently running 20 miles per week, the increase in training volume should be 2-4 miles per week. While this approach may appear conservative, it will help to prevent over training and injuries. Additionally, intensity during this phase of training, when volume is being steadily increased, should be low. The maximum training volume an individual attains is dependant on numerous factors and can be best gauged by determining the overall physical capacity and motivation of your client. Factors such as training status, age, body weight, and training time will all determine the training volume your client is realistically capable of achieving. The premier benefit of increased training volume is an increased capacity for mitochondrial respiration, which, as explained earlier, is imperative to improvements in lactate threshold.
Interval and Steady-State Training
Following an adequate build-up in training volume, the next aspect that should be addressed is interval and steady-state training. Correct training intensity during this phase, which will be focused around an individuals lactate threshold, is key to the continued success of your clients training program. The methods used for monitoring interval and steady-state training must ensure that intensity is not being under-estimated or over-estimated.
Most individuals will not have access to scientific laboratories, where the lactate threshold can be accurately determined from blood sampled during an incremental VO2max test. Consequently, alternative methods have been recommended for the non-invasive, estimation of lactate threshold, including relative percentage of heart rate reserve (HRR) and rating of perceived exertion (RPE) scale. Research has shown that the lactate threshold occurs at 80-90% HRR in trained individuals and at 50-60% HRR in untrained individuals (Weltman 1995). The RPE scale may be the most accurate way to determine training intensity during steady-state and interval training. Research has shown that RPE is strongly related to the blood lactate response to exercise regardless of gender, training status, type of exercise being performed, or the intensity of training (Weltman 1995). Findings from studies have indicated that the lactate threshold occurs between 13 and 15 on the RPE scale, which corresponds to feelings of somewhat hard and hard (Weltman 1995).
Steady-state workout sessions should be performed as close as possible to the lactate threshold. The length of these bouts can vary depending on training status, type of endurance-activity being performed, and distance of endurance-activity. The novice runner, training for 5-k road races, performing their first steady-state run may only do a workout 10 minutes in duration. A semi-professional cyclist, training for multiple-days of racing 80 to 100 miles distances, may complete a steady-state workout of an hour in duration.
Interval training workouts are high-intensity training sessions performed for short durations of time at velocities or workloads above the lactate threshold. Similar to steady-state workouts, interval workout times and distances are dependant on training status, type of endurance-activity being performed, and distance of endurance-activity. The novice runner, training for 5-k road races, may complete three, 1-mile intervals at or faster than race pace, with adequate recovery time between each repeat. The semi-professional cyclist, training for multiple-days of 80 to 100 mile distances, may perform several 5 to 10 mile intervals at, or in excess of, their race pace with appropriate recovery bouts between repeats.
The key to successful steady-state and interval workouts is careful monitoring of training intensity. While it is necessary to perform these training sessions at an elevated intensity, trainers should ensure their clients avoid the pitfalls of racing these workouts, as it will eventually result in over-training. Furthermore, it has been suggested that steady-state and interval workouts should not exceed approximately 10-20% of total weekly training volume (Foran 2001).
The Bottom Line on the Lactate, Ventilatory, Anaerobic and Heart Rate Thresholds
Hopefully, you now feel much more comfortable with much of the terminology, physiological mechanisms, and understanding of the lactate, ventilatory, anaerobic, and heart rate thresholds. The task of designing the optimal endurance-training program for your client in preparation for his/her 10-k road race should now be less formidable. Clearly, the lactate threshold is the most important determinant of success in endurance-related activities and events, and the main goal of endurance training programs should be the improvement of this parameter. This can be accomplished by first focusing on developing training volume, and then the incorporation of steady-state sessions (at the lactate threshold) and interval workouts (above the lactate threshold). Finally, remember that correct training intensity is essential to the success of any endurance-training program. Utilization of both the relative percentage of heart rate reserve (HRR) and the rating of perceived exertion (RPE) scale are proven methods for monitoring the training intensity of your clients during their workouts.
Table 1. Terms Related to Article
Acidosis: The decrease in pH
Anaerobic threshold: Original concept describing increased lactate production during conditions of low blood flow and oxygen
Gluconeogenesis: Synthesis of glucose from non-carbohydrate sources
Glycolysis: Series of steps that breaks down glucose to pyruvate
Gycolytic flux: An increased rate in the transfer of glucose to pyruvate through the reactions of glycolysis
Hypoxia: Low levels of blood oxygen content
Ischemia: Low levels of blood flow
Lactate: This compound is manufactured from pyruvate during higher intensity exercise
Lactate threshold: Intensity of exercise at which there is an abrupt increase in blood lactate levels
Metabolic pathway: Chemical reactions causing the formation of ATP and waste products
Metabolism: Sum of all energy transformations in the body
Mitochondrial respiratio: Reactions within the mitochondrion that ultimately lead to the production of ATP and consumption of oxygen
Phosphagen system: Production of energy from coupled reactions of ATP and PC
Pyruvate: Compound derived from metabolism of carbohydrates
Substrate: Substance acted upon and changed by an enzyme, such as a foodstuff
Ventilatory threshold: Occurrence in progressive increase in intensity of exercise at which there is a non-linear increase in ventilation
Side Bar I. Lactate is not the Cause of Fatigue
The classical explanation for the cause of fatigue, denoted by sensations of pain and the muscle burn experienced during intense exercise, is lactic acid build-up. Coaches, athletes, personal trainers, and scientists alike have traditionally linked lactic acidosis with an inability to continue exercise at a given intensity. Although the lactate threshold indicates that conditions within the muscle cell have shifted to a state favorable for the development of acidosis, lactate production itself does not directly contribute to the fatigue experienced at high intensities of exercise. It is the proton (H+) accumulation, coinciding with but not caused by lactate production, that results in decreased cellular pH (metabolic acidosis), impairing muscle contraction, and ultimately leading to fatigue (Robergs, 2001). The increased proton accumulation occurs from a few different biochemical reactions during intense physical exercise, most notably in the splitting of ATP at the muscle myofilaments for sustained muscle contraction.
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