A thorough understanding of the components that limit performance in endurance exercise is crucial to designing effective programs for your clients.
What are the physiological limitations of the human body? How much are your clients capable of doing? The attempt to answer these questions led to a plethora of research on the subject of human potential. The factors limiting muscular strength are just now being discovered, but we have a pretty clear picture of what limits the body's capacity for endurance exercise. Hence, endurance exercise will be the focus of this article. Whether your clients are world-class athletes, recreational runners or recovering couch potatoes, they face similar physiological limitations to their capacity for endurance exercise training and performance.
Endurance exercise can be defined as cardiovascular exercise–such as running, cross-country skiing, cycling, aerobic exercise or swimming–that is performed for an extended period of time (Rogers & Roberts 1997). Endurance exercise involves complex integration of multiple physiological functions, but despite its multifaceted nature, this type of exercise is characterized by one simple requirement–the ability to sustain repeated muscle contraction. This criterion is fulfilled primarily through two basic functions:
- oxygen consumption
- adequate fuel provision In addition, two other physiological factors play a critical role:
This article will examine how these four physiological mechanisms effect your clients' capacity for endurance exercise training and performance.
Oxygen consumption is key to sustaining the repeated muscle contraction required for endurance exercise. Let’s take a look at the metabolic machinery involved in this process. An individual’s capacity for oxygen consumption depends on three major physiological parameters: (1) maximal oxygen uptake, (2) exercise economy and (3) lactate threshold.
Maximal oxygen uptake, or VO2max, refers to the highest rate at which the body can take up and consume oxygen during intense exercise (Bassett & Howley 2000). Traditionally, the magnitude of an individual’s VO2max has been viewed as one of the most important predictors of endurance exercise performance. A classic study conducted in the 1970s at Ball State University confirmed the importance of VO2max to endurance exercise performance, with findings indicating a strong correlation between VO2max and 10-mile run times (Costill 1970).
Prolonged exercise requires sustained energy to maintain muscle contraction. This energy is provided by the continual production of ATP (adenosine triphosphate), the universal energy molecule. ATP is produced when a fuel is broken down to release energy. This is accomplished through three metabolic pathways: the phosphagen system, glycolysis and mitochondrial respiration. The first two pathways can produce energy only for short periods; consequently, ATP regeneration for extended exercise is accomplished predominantly through mitochondrial respiration, or aerobic metabolism within the mitochondria of the cells.
For proper functioning, the biochemical reactions involved in mitochondrial respiration depend on continuous oxygen availability. Enhanced oxygen delivery and utilization during exercise will improve mitochondrial respiration and subsequently the capacity for endurance exercise. Both central physiological functions involving the cardiorespiratory system (heart, lungs and blood vessels) and peripheral physiological functions (such as the tissue extraction of oxygen) can limit VO2max. For decades, exercise physiologists have researched and debated the relative importance of each function in limiting the capacity to perform endurance exercise.
CENTRAL PHYSIOLOGICAL FUNCTIONS LIMITING THE VO2 MAX
The ability of the cardiorespiratory system to transport oxygen to the exercising muscles is considered the central component of VO2max (Robergs & Roberts 1997). The role of this component is to transport oxygen from the atmosphere and deliver it to the muscles, where it is used during mitochondrial respiration to produce ATP. The central factors limiting oxygen delivery are maximal cardiac output, pulmonary diffusion and blood volume and flow (Bassett & Howley 2000).
Cardiac output (the product of heart rate and stroke volume) is commonly identified as one of the main limiting factors (Bassett & Howley 2000). In fact, some researchers have concluded that 70 to 85 percent of the limitation in VO2max can be attributed to maximal cardiac output (Cerretelli & DiPrampero 1987). On the one hand, a person’s maximal heart rate is quite stable, remaining unchanged with endurance training. (Maximal heart rate is much more dependent on a person’s age, decreasing as one ages.) On the other hand, stroke volume, or the amount of blood pumped per heartbeat, can be substantially increased through endurance training. Much of this improvement is the result of an increase in the chamber size and wall thickness of the left ventricle (the heart’s hardest-working chamber, which pumps blood throughout the body). Endurance training enables both the left and right ventricles to pump a greater volume of blood per heartbeat. As a result, more blood returns to the heart during exercise. In addition, the heart, being a muscle with the properties of extensibility and contractility, is stretched by the increased blood volume, resulting in increased stroke volume and a more forceful delivery of blood to the body tissues.
The variation in maximal stroke volume explains most of the range observed in VO2max in trained and untrained individuals. During incremental exercise that gradually increases to maximal, untrained individuals experience a plateau in stroke volume at an intensity of approximately 50 percent of VO2max. In highly trained endurance athletes performing the same type of exercise, stroke volume continues to increase right up to VO2max (Robergs & Roberts 2000). This increased stroke volume allows for further increases in cardiac output and improvements in endurance exercise capacity.
Pulmonary diffusion may be another factor limiting oxygen delivery for endurance exercise, though this factor is thought to play a minor role. The primary function of the lungs is to transfer oxygen from the atmosphere to the blood and remove carbon dioxide from the body. Pulmonary ventilation, or breathing, is the movement of air into and out of the lungs. Pulmonary diffusion is the exchange of oxygen and carbon dioxide between the lungs and the blood. In normal individuals, pulmonary diffusion is not a factor limiting VO2max. However, in highly trained endurance athletes with much higher cardiac outputs, pulmonary diffusion may become a limiting factor. A very high cardiac output shortens the time during which the blood can pick up oxygen in the lungs, possibly leading to lower blood oxygen saturation levels (Robergs & Roberts 1997).
The final link in the oxygen delivery chain is blood volume and flow. Working muscles demand considerably more oxygen and nutrients than resting muscles. To meet the increased needs, more blood must be allocated to the muscles during endurance exercise. In the blood, oxygen is bound to a molecule called hemoglobin, located within the red blood cells. Regular, intense endurance training increases blood volume via two mechanisms: (1) An increase in hormones (antidiuretic hormone and aldosterone) causes the kidneys to retain water, thereby increasing blood plasma (the fluid portion of blood); and (2) a boost in plasma protein production also leads to more blood plasma (Wilmore & Costill 1999). This increase in plasma, or fluid, reduces the blood’s viscosity. Reduced viscosity may improve blood flow through the blood vessels, especially the smallest vessels, thereby enhancing oxygen delivery to the working muscles (Wilmore & Costill 1999).
Endurance training may also lead to an increase in red blood cell volume (an adaptation that varies among individuals), which can result in an additional increase in the blood’s oxygen-carrying capacity. Research has shown that increasing the number of red blood cells in the body through blood infusion concurrently increases VO2max values by 5 to 10 percent (Bassett & Howley 2000; Gledhill 1982; Spriet et al. 1986). It is important to add that during intense endurance exercise, the body redistributes blood flow to the metabolically active skeletal muscles, readying the tissues for extraction of the needed oxygen.
Research suggests that during endurance exercise, oxygen delivery to the working muscles is limited, not only by central physiological functions, but also by peripheral physiological functions.
PERIPHERAL PHYSIOLOGICAL FUNCTIONS LIMITING THE VO2 MAX
The peripheral component of VO2max involves the exercising muscles’ ability to extract and use the oxygen that the cardiorespiratory system has transported (Robergs & Roberts 1997). Peripheral factors that may limit VO2max include muscle diffusion capacity, mitochondrial enzyme levels and capillary density (Bassett & Howley 2000).
In regard to muscle diffusion capacity, a pressure gradient, or difference, that exists between the blood and muscle cells allows for the transportation of oxygen from the red blood cells into the mitochondria. Oxygen utilization and continued mitochondrial respiration rely on the maintenance of this gradient.
Mitochondrial enzyme levels may also play a role. Certain enzymes facilitate ATP production in the mitochondria, thereby allowing the working muscles to use more oxygen. Endurance training increases these mitochondrial enzyme levels twofold, resulting in a higher VO2max. According to some researchers, these findings indicate that this adaptation is a peripheral limitation to VO2max (Honig, Connett & Gayeski 1992).
Finally, capillary density can be a peripheral limiting factor, since oxygen exchange between the blood and muscles takes place in the capillaries. A 20 percent increase in capillary density has been reported with endurance training, signifying improved distribution and extraction of blood within the muscle (Robergs & Roberts 2000).
WHICH IS MORE CRUCIAL: THE CENTRAL OR PERIPHERAL COMPONENT?
Although the average increase in VO2max with endurance training is 15 to 20 percent in a person sedentary prior to training, it is intriguing to note that increases of up to 93 percent have been reported (Wilmore & Costill 1999). Although most current research supports the central component as the main limitation to VO2max (Wilmore & Costill 1999), the importance of the peripheral component should not be minimized. However, due to the logistical constraints of studying oxygen consumption at the cellular level during highly intense endurance exercise, the entire picture of oxygen utilization is still developing (Robergs 2001).
A second parameter involved in oxygen consumption is exercise economy. This term refers to the oxygen consumption required to perform a given exercise workload during endurance activity (Daniels 1985). Differences in oxygen consumption between exercisers performing similar workloads illustrate variation in exercise economy. Depending on their economy of movement, exercisers with similar VO2max values can have very different endurance performances (as measured by running time). In fact, in highly trained runners with comparable VO2max values, exercise economy has been found to account for a significant amount of the variation in 10-kilometer run performance (Conley & Krahenbuhl 1980). Individual exercise economy is enhanced with endurance training, possibly due to improvements in biomechanical techniques for performing the specific physical activity (Robergs & Roberts 1997).
The final factor to consider with regard to oxygen consumption is the lactate threshold, or the exercise intensity at which blood lactate levels abruptly increase (Robergs & Roberts 1997). Many scientists consider the lactate threshold to be a primary indicator of endurance exercise performance (Wilmore & Costill 1999). Additionally, compared to VO2max and exercise economy, the lactate threshold appears to be the physiological parameter most responsive to endurance training (McArdle, Katch & Katch 1996).
In untrained individuals, the lactate threshold occurs at approximately 50 to 60 percent of VO2max. Following endurance training, individuals generally improve their lactate threshold to 75 percent of VO2max, with values of 80 to 90 percent reported in elite, world-class endurance athletes (McArdle, Katch & Katch 1996). The performance benefit of this training adaptation is that it enables an individual to maintain a higher steady-state exercise intensity (below the lactate threshold) during endurance exercise, thereby improving performance. In fact, research has consistently reported high correlations between lactate threshold and performance in a variety of endurance events, including running, cycling and race walking (McArdle, Katch & Katch 1996). Some researchers have proposed that the best predictor of endurance exercise performance is the maximal steady-state workload achieved near VO2max (Weltman 1995).
The physiological explanations for lactate threshold improvements with endurance training are related to the increased size, number and enzyme levels of the mitochondria. Following endurance training, the size and number of mitochondria have increased by 50 to 100 percent, thus increasing mitochondrial respiration capacity (Holloszy & Coyle 1984). Additionally, the previously mentioned twofold increase in mitochondrial enzyme levels produced by endurance training also enhances mitochondrial respiration capacity. The result of these adaptations is a delayed time to lactate threshold and a greater capacity for endurance exercise performance.
According to the physiological parameters we have examined so far, endurance exercise potential is limited by the complex interaction of VO2max, exercise economy and lactate threshold. Potential is improved by maximizing physiological capacities in each of these components. In an effort to investigate the endurance exercise potential of humans, researchers have input VO2max, exercise economy and lactate threshold levels into theoretical models to predict the ideal performance for a marathon (Joyner 1991). These models suggest an endurance runner with a VO2max of 85 milliliters per kilogram per minute, a lactate threshold of 85 percent of VO2max and an ideal running economy could maintain a marathon pace of 13.33 miles, or 21.46 kilometers, per hour. These optimal performances in all physiological components would result in an amazing time of one hour, 57 minutes and 58 seconds, which is more than eight minutes faster than the current world record.
Thus far, we have focused on the metabolic machinery necessary for endurance exercise performance. However, the ability to exercise for extended periods requires not only adequate metabolic machinery but also fuel. The human body is dependent on fats (lipids) and carbohydrates (blood glucose and muscle glycogen) to support ATP regeneration for sustained muscle contraction (Robergs & Roberts 1997). The availability and utilization of these substrates significantly affect endurance exercise capacity.
The intensity of the endurance exercise regulates the substrate used to provide energy. During low-intensity endurance exercise (< 60% of VO2max), fats and carbohydrates are used to support metabolism. With increasing exercise intensity, there is a shift toward more carbohydrate metabolism to support continuous exercise (Robergs & Roberts 1997). After approximately two hours of intense steady-state exercise, muscle glycogen stores become significantly depleted, resulting in fatigue, regardless of the presence of an adequate oxygen supply. When muscle glycogen stores are exhausted, individuals experience fatigue and muscular pain. In marathon running, this physiological event is commonly referred to as “hitting the wall.” Research has demonstrated that ingesting carbohydrates during exercise can prolong the duration of exercise beyond the time supplied by muscle glycogen stores (Coggan & Coyle 1991).
Whereas carbohydrate substrate supply is limited, fat supply in most individuals is unlimited. One of the most noted physiological adaptations to endurance training is increased reliance on fats, or lipids, at a workload of the same relative intensity. This carbohydrate-sparing modification increases an individual’s potential for endurance activity and performance at exercise intensities of less than 60 percent of VO2max. However, regardless of training status, at exercise intensities nearing lactate threshold, there is a greater predominance of carbohydrate use for substrate supply because carbohydrate metabolism (which results in the formation of ATP) is more efficient with regard to oxygen consumption (Robergs & Roberts 1997).
Most endurance competitions are performed at intensities near the lactate threshold; at these intensities, substrate utilization relies almost entirely on blood glucose and muscle glycogen. Long-term training in many endurance sports—including cycling, running and swimming—has been shown to increase muscle glycogen levels (Robergs & Roberts 1997). This training adaptation extends the duration and intensity of endurance exercise prior to muscle glycogen depletion and, as a result, prolongs the time to fatigue.
Since the 1960s, research has indicated that a modified diet strategy known as glycogen supercompensation (commonly referred to as carbohydrate loading), used in the week preceding endurance events, can enhance muscle glycogen stores. This approach calls for the individual to train intensely while maintaining a low-carbohydrate diet early in the week, thus depleting muscle glycogen stores. Later in the week, the individual decreases training intensity and consumes a high-carbohydrate diet, which enhances muscle glycogen stores. Unfortunately, this practice, though effective, is also mentally and physically demanding for the individual. More recent research has determined that simply following a diet with a higher-than-normal percentage of carbohydrate (> 70%) the entire week prior to competition sufficiently increases muscle glycogen stores (Robergs & Roberts 1997).
In ultra-endurance events—such as 50-mile runs and the increasingly popular “eco-challenge” events—in which the exercise intensity is far below the lactate threshold, the primary substrate used becomes fats that are circulating in the blood (free fatty acids) or are stored within the muscles (intramuscular lipids). During these events, the energy supply provided by lipids is virtually inexhaustible in most individuals. Consequently, the limitation to performance in these longer, lower-intensity events is the result of physiological mechanisms other than substrate supply and oxygen availability, and may be the product of muscle damage.
Sweating is a normal physiological response to prolonged exercise and is required for the dissipation of heat produced during energy metabolism. Unfortunately, this naturally occurring response can also result in substantial fluid loss and impaired endurance performance. Inadequate fluid balance throughout prolonged bouts of exercise or training sessions results in several deleterious physiological effects, including increased heart rate and temperature. Research has suggested that rising body core temperature may cause fatigue in the muscles (by impairing mitochondrial respiration) and in the central nervous system (Fitts 1994). Dehydration also results in higher heart rate values for the same submaximal intensity, due to decreased stroke volume resulting from the lower volume of blood plasma (which is 90% water). During severe dehydration, it is possible for heart rate values to approach maximal levels despite the submaximal nature of endurance exercise (Robergs & Roberts 1997).
Adequate hydration practices both before and during endurance exercise can counter dehydration to a certain degree. Currently, endurance exercise enthusiasts use many different products for hydration; these include solutions consisting of water, salt, simple carbohydrates, electrolytes and glycerol.
All the physiological factors limiting endurance exercise performance may be influenced by another factor—genetics. Various researchers have reported a genetically regulated upper limit to individual VO2max values (Bouchard et al. 1999). These findings indicate that regardless of training volume or intensity, 10 to 30 percent of the variability in VO2max is genetically determined. The genetic influence on VO2max has been attributed to both central and peripheral factors, with the genetic effect on cardiac output reported as high as 50 percent (McArdle, Katch & Katch 1996). Similarly, training improvements in economy and lactate threshold are also genetically regulated.
Genetic differences in the proportion of muscle fiber types (slow twitch and fast twitch) are also common. Slow-twitch muscle fibers, characterized by more mitochondrial mass and higher enzyme levels than fast-twitch muscle fibers, have an increased capacity for mitochondrial respiration. Elite endurance athletes generally possess high percentages of slow-twitch muscle fibers in muscles contributing to their respective exercise. In fact, some elite marathoners have been reported to have more than 90 percent slow-twitch muscle fibers in their leg muscles (Costill, Fink & Pollock 1976). The advantages of more slow-twitch muscle fibers include greater mitochondrial capacity and increased oxygen consumption, leading to improved performance. High correlations between slow-twitch muscle fibers and endurance performance have been reported in both running and cycling (Costill, Fink & Pollock 1976; Ivy et al. 1980). Individual fiber-type proportions also genetically regulate the training adaptability to the physiological parameters of VO2max, exercise economy and lactate threshold (Robergs & Roberts 1997).
Although the physiological mechanisms regulating endurance performance are quite complex, the main factors limiting prolonged exercise have a straightforward interpretation. To continue exercise for extended durations, sustained muscle contraction must be maintained and is dependent on the continuous provision of both oxygen and fuel. Although each of the physiological factors limiting performance is modifiable through endurance training, it is important to recognize that genetic factors play a tremendous role in determining capacity and trainability. Therefore, when designing training programs to improve your clients’ endurance exercise capacity, it is critical to recognize all the physiological components that contribute to—and limit—performance.