The Physiological Limitations to Endurance Exercise Capacity

Len Kravitz, Ph.D. and Lance C. Dall

Endurance exercise can be defined as the ability to perform cardiovascular

exercise, whether it be cross-country skiing, spinning, running, aerobic exercise
or swimming, for an extended period of time (Robergs & Roberts 1997).

One is limited in this pursuit by a complex integration of multiple physiological

functions. Despite the multifaceted nature, endurance exercise is characterized
by one simple requirement – the necessity to sustain repeated muscle
contraction. This criterion is fulfilled through two basic functions – the ability to
consume enough oxygen and an adequate fuel provision. The capacity for
oxygen consumption is reliant upon the physiological parameters of maximal
oxygen uptake, lactate threshold, and economy of movement in the given
activity. Fuel, or food substrate, is supplied mostly through carbohydrates and
fats. Hydration levels and genetic factors also play influential roles in the
capacity for endurance exercise. This article will review the main physiological
mechanisms limiting endurance exercise and performance.

Maximal Oxygen Uptake

Maximum oxygen uptake (VO2max) refers to the highest rate at which oxygen
can be taken up and consumed by the body 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 performance. A
classic study, conducted in the 1970’s at Ball State University, confirmed the
importance of VO2max to endurance performance with findings indicating a
strong correlation between VO2max and 10-mile run times (Costill 1970).

Prolonged exercise requires sustained energy provision to maintain muscle

contraction and is accomplished through the continual production of ATP
(adenosine triphosphate), the universal energy molecule. The production of ATP
is accomplished through three metabolic pathways (breakdown of a fuel to
release energy), which include the phosphagen system (the production of ATP
from creatine phosphate), glycolysis (glucose breakdown), and mitochondrial
respiration (aerobic metabolism within the mitochondrion of the cell). The first
two pathways are only capable of energy production for short durations;
consequently, ATP regeneration for extended exercise is accomplished
predominantly through mitochondrial respiration.
The biochemical reactions involved in mitochondrial respiration depend on
continuous oxygen availability for proper functioning. Enhanced oxygen delivery
and utilization during exercise will improve mitochondrial respiration and
subsequently the capacity for endurance exercise. Both central (heart, lungs,
blood vessels) and peripheral (tissue extraction of oxygen) physiological
functions can limit VO2max. The relative importance of each function in limiting
endurance performance has been discussed, researched and debated by
exercise physiologists for decades.

Central Limitations to VO2max

The ability of the cardiorespiratory system to transport oxygen to the exercising

muscles refers the central component of VO2max (Roberts & Robergs 1997). The
role of the central component is for oxygen to be transported from the
atmosphere and delivered to the muscles where it is utilized during
mitochondrial respiration to produce ATP. The main central limitations to oxygen
delivery are pulmonary diffusion, cardiac output, and blood volume and flow
(Bassett & Howley 2000).

Pulmonary diffusion

The lungs serve a primary function of transferring oxygen from the atmosphere
to the blood, and for the removal of 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 limiting
factor to VO2max. However, in well-trained endurance athletes, with much
higher cardiac outputs (which is the product of heart rate and stroke volume),
pulmonary diffusion may become a limiting factor to VO2max. The very high
cardiac outputs that highly trained athletes attain shortens the time period for
blood to pick up oxygen in the lungs, possibly leading to lower blood oxygen
saturation levels (Robergs & Roberts 1997). Despite this possibility, pulmonary
diffusion is thought to play a minor role in the overall limitation of oxygen
delivery for endurance performance.

Cardiac Output

Cardiac output (defined above as the product of heart rate and stroke volume
which is reported in liters per minute) is commonly identified as one of the main
limiting factors to oxygen delivery and VO2max (Bassett & Howley 2000). In fact,
some researchers have concluded that 70-85% of the limitation in VO2max can
be attributed to maximal cardiac output (Cerretelli & DiPrampero 1987). A
person’s maximal heart rate is quite stable and remains unchanged with
endurance training. Maximal heart rate is much more dependent on a person’s
age, decreasing as one ages. Contrariwise, stroke volume (the amount of blood
pumped per heart beat) increases substantially from endurance training. Much of
this rise is due primarily to the increased chamber size and wall thickness of the
left ventricle (the heart’s hardest working chamber because it pumps blood
throughout the body). However, from endurance training, both the left and right
ventricles have expanded capacity to fill with blood. The heart, being a muscle
with the ability to extend, also attains a greater stretch from the increased blood
volume, which results in a stronger elastic recoil for ejecting the blood to the
body tissues. The variation in individual maximal stroke volume explains most of
the range observed in VO2max in trained and untrained individuals. During
incremental exercise to maximal, untrained individuals experience a plateau in
stroke volume at an intensity approximately 50% VO2max, whereas with highly
trained endurance athletes, stroke volume continues to increase up to VO2max
(Robergs & Roberts 2000). This allows for further increases in cardiac output and
improved endurance performance.

Blood Volume and Flow

Working muscles demand considerably more oxygen and nutrients. To meet

these needs, more blood must be allocated to the muscles during endurance
exercise. The final link in the oxygen delivery chain (from the lungs and heart) is
the oxygen carrying capacity of the blood. Oxygen is transported in the blood
bound to a molecule called hemoglobin located within red blood cells. Regular,
intense endurance training will increase blood volume via two mechanisms: 1) an
increase in hormones (antidiuretic hormone and aldosterone) causes the kidneys
to retain water, increasing blood plasma (fluid portion of blood), and 2) a boost in
plasma proteins production also leads to more blood plasma (Wilmore & Costill
1999). This increase in fluid reduces the blood’s viscosity. A reduced viscosity
may improve blood flow through the blood vessels, especially the smallest
vessels which will enhance oxygen delivery to working muscle mass (Wilmore &
Costill 1999). An increase in red blood cell volume is also possible with
endurance training (not consistent with every person), which could lead to an
additional increase in the blood’s oxygen carrying capacity. Research has shown
increasing the number of red blood cells in the body through blood infusions
concurrently increases VO2max values by 5 to 10% (Gledhill 1982; Spriet,
Gledhill, Froese, & Wilkes 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.

To briefly recap all of the above, oxygen delivery to muscles during endurance
exercise may be limited by central factors including pulmonary diffusion,
maximal cardiac output, and blood oxygen carrying capacity (volume and flow).
Despite the apparent central limiting factors to VO2max and endurance exercise,
research has also suggested the influence of peripheral limiting factors, which is
where we now shift our focus.

Peripheral Limitations to VO2max

The ability of exercising muscles to extract and utilize oxygen, which has been
transported by the cardiorespiratory system, refers to the peripheral component
of VO2max (Robergs & Roberts 1997). The potential sites for VO2max limitation
in the peripheral component include muscle diffusion capacity, mitochondrial
enzyme (molecules that facilitate ATP production in mitochondria) levels, and
capillary density (Bassett & Howley 2000).

A pressure gradient (difference) existing 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. Endurance training results in a two-fold
increase in mitochondrial enzymes levels (which allows the working muscles to
use more oxygen), resulting in a higher VO2max, and also indicates this potent
peripheral limitation to VO2max (Honig, Connett, & Gayeski 1992). In addition, a
20% increase in capillary density (the anatomical location of oxygen exchange
between the blood and muscle) has also been reported with endurance training,
signifying an improved distribution and extraction of blood within the muscle
(Robergs & Roberts 1999).

Which is More Crucial to VO2max: The Central or Peripheral Component?

It is intriguing to note that although the average increase in VO2max is 15% to

20% (person sedentary prior to training), increases up to 93% have been
reported in the literature (Wilmore and Costill 1999). Although most current
research supports the central component to be the main limitation to VO2max
(Wilmore and Costill 1999), the importance of peripheral components to VO2max
should not be minimized. However, due to the logistical constraints of studying
the consumption of oxygen at the cellular level, at highly intense levels, the
entire picture of oxygen utilization is still developing (Robergs 2001).

Exercise Economy

The term economy is used to express the oxygen consumption required to

perform a given exercise workload, whether it be spinning, running, or any other
endurance activity (Daniels 1985). Differences in oxygen consumption between
individuals at similar exercise workloads illustrate the individual variation found
in exercise economy. Consequently, individuals with similar VO2max values can
have much different endurance performances depending on their economy of
movement. In fact, high correlations between 10-km running performance and
economy have been reported between runners with comparable VO2max values
(Conley & Krahenbuhl 1980). Individual exercise economy is enhanced with
endurance training and has been explained by improvements in biomechanical
techniques in performing the specific physical activity (Roberts & Robergs 1997).

The Lactate Threshold

The lactate threshold refers to the intensity of exercise at which there is an

abrupt increase in blood lactate levels (Roberts & Robergs, 1997). Many
scientists consider the lactate threshold to be a primary indicator of endurance
performance (Wilmore & Costill 1999). Additionally, the lactate threshold
(compared to VO2max and economy) appears to be the most responsive
physiological parameter to endurance training (McKardle et 1996).

In untrained endurance individuals, the lactate threshold occurs at

approximately 50-60% of VO2max. Following endurance training, individuals
generally improve the lactate threshold to 75% of VO2max; with values at 80-
90% of VO2max having been reported in elite, world-class endurance athletes
(McKardle, Katch, & Katch 1996). The performance benefit of this training
adaptation is that an individual is capable of maintaining a higher steady state
exercise intensity (below the lactate threshold) during the endurance exercise.
This allows the endurance exerciser to maintain faster steady state tempos
during training or racing, leading to improved endurance performance. In fact,
research has consistently reported high correlations between the lactate
threshold and performance in a variety of endurance events including running,
cycling, and race-walking (McKardle, Katch, & Katch 1996). It has been proposed
that the best predictor of endurance performance is the maximal steady state
workload achieved near VO2max (Weltman 1995).

To better understand and appreciate the lactate threshold, a physiological

explanation describing its mechanism is warranted. The primary pathway for ATP
regeneration during endurance exercise is mitochondrial respiration, which
initially shares the same metabolic pathway as glycolysis, where muscle
glycogen (glycogen is the store form of glucose in muscle or the liver) or blood
glucose is converted into another chemical molecule called pyruvate. Depending
on exercise intensity, pyruvate will either enter the mitochondria or be converted
to lactate. At exercise intensity levels below the lactate threshold, pyruvate
enters the mitochondria and muscle contraction continues through oxidative ATP
production. However, at exercise intensity levels above the lactate threshold, the
capacity to produce ATP through mitochondrial respiration is compromised, and
pyruvate is converted to lactate. The metabolic pathways supporting exercise
intensity above the lactate threshold are only capable of sustaining muscle
contraction for short durations, thus limiting endurance activity (Bassett &
Howley 2000).

The physiological explanations for lactate threshold improvements following

endurance training are related to increased mitochondria size, numbers, and
enzyme levels. Following endurance training, mitochondria size and numbers
have been reported to increase by 50-100%, thus increasing the mitochondrial
respiration capacity (Holloszy & Coyle 1984). Additionally, the previously
mentioned 2-fold increase in mitochondrial enzymes will also enhance
mitochondrial respiration capacity. The combined result of these adaptations is a
delayed timeline to lactate threshold and greater capacity to perform endurance
exercise.

Maximizing Endurance Performance

The potential for endurance performance according to the physiological

parameters we have examined thus far is limited by the complex interaction of
VO2max, economy, and lactate threshold. An individual would achieve their
endurance potential by maximizing their physiological capacities in each of these
components. In an effort to investigate the endurance potential of humans,
researchers have input VO2max, 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
ml/kg/min, a lactate threshold of 85% VO2max, and an ideal running economy
would be able to maintain a marathon pace of 21.46 km/hr. These optimal
performances in each physiological component would result in an amazing time
of 1:57:58 (hr:min:sec), which is nearly 8 minutes faster than the current world
record.

Substrate Availability and Utilization

Thus far, we have focused on the metabolic machinery (VO2max, economy, and
lactate threshold) necessary for endurance exercise and performance. However,
the ability to exercise for extended periods requires not only adequate metabolic
machinery but also fuel (food substrates) for continual muscle contraction. The
human body is dependent on fats (lipids), and carbohydrates (blood glucose and
muscle glycogen) to support ATP regeneration for sustained muscle contraction
(Roberts & Robergs 1997). Availability and utilization of these substrates plays a
significant role in the limitations to endurance exercise.

The intensity of endurance exercise regulates the substrate utilized for the
provision of energy. During low-intensity endurance exercise (<60% VO2max),
fats and carbohydrates are used to support metabolism. With increasing exercise
intensity (at or above 70% VO2max), there is a shift towards more carbohydrate
metabolism to support continuous exercise (Roberts & Robergs 1997). While
carbohydrate substrate supply is limited, lipid supply in most individuals is
unlimited. After approximately 2 hours of intense steady state exercise, muscle
glycogen stores become significantly depleted resulting in fatigue, regardless of
the presence of an adequate oxygen supply. Research has demonstrated that
the ingestion of carbohydrates during exercise can prolong the duration of
exercise beyond the time supplied by muscle glycogen stores (Coggan & Coyle
1989). 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”.

One of the most noted physiological adaptations to endurance training is an

increased reliance on fats at the same relative intensity workload. This
carbohydrate sparing modification increases an individual’s potential for
endurance activity and performance at lower intensity (<60% VO2max)
endurance exercise. However, regardless of training status, at exercise
intensities nearing lactate threshold, there is a greater predominance of
carbohydrate utilization for substrate supply because the metabolism of
carbohydrates (resulting in the formation of ATP) is more efficient with regards to
the oxygen consumption (Robergs & Roberts 1997).

Most endurance competitions are performed at intensities near the lactate

threshold in which substrate utilization relies almost entirely on blood glucose
and muscle glycogen. Long-term training in multiple 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 the endurance exercise prior to muscle glycogen depletion, and
subsequent fatigue becomes prolonged.

Since the 1960’s, research has indicated a modified diet strategy, known as
glycogen supercompensation (commonly referred to as carbohydrate loading),
used in the week preceding endurance events could enhance muscle glycogen
stores. The 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 – resulting in enhanced 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 higher-than-normal carbohydrate diet the week prior to competition
(>70% carbohydrate) sufficiently increases muscle glycogen stores (Robergs &
Roberts 1997).
In ultra-endurance events in which the exercise intensity (<60% VO2max) is far
below the lactate threshold, the primary substrate utilized becomes fats, which
are circulating in the blood (known as Free Fatty Acids or FFA’s) or stored within
the muscles (intramuscular lipids). During these activities, 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.

Hydration and Endurance Exercise

Sweating is a normal physiological response to prolonged exercise, required for

the dissipation of heat produced during energy metabolism. Unfortunately, this
natural 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 events
including increased heart rates and temperatures. Research has suggested that
rising body core temperatures may cause fatigue in the muscles (by impairing
mitochondrial respiration) and central nervous system (Fitts 1994). Dehydration
also results in higher heart rate values for the same submaximal intensity due to
decreased stroke volumes, resulting from the lower blood plasma volumes. It is
possible for heart rate values to approach maximal levels despite the
submaximal nature of endurance exercise during severe dehydration (Roberts &
Robergs 1997).

Although dehydration is a naturally occurring physiological limitation to

endurance exercise, it can be countered to a certain degree by adequate
hydration practices both prior to and during endurance exercise. Currently, there
are many different approaches and products used by endurance enthusiasts for
pre-exercise and exercise hydration, including the ingestion of solutions
comprised of water, salt, simple carbohydrates, electrolytes and glycerol.

Genetic Limitations to Endurance Exercise

The physiological limitations to endurance exercise examined thus far including

VO2max, economy, lactate threshold, substrate availability/utilization, and
hydration may all 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, 10-30% 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 having been reported to be as
high as 50% (McCardle, Katch, & Katch 1996). Similarly, training improvements
in economy and lactate threshold are parameters that are also genetically
regulated.

Genetic differences in muscle fiber type proportion (slow-twitch and fast-twitch)

are also commonly found in individuals. Slow-twitch muscle fibers, characterized
by more mitochondrial mass and 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 endurance exercise. In fact, elite
marathoners have been reported to have greater than 90% slow-twitch muscle
fibers in muscles of the leg (Costill, Fink, & Pollock 1976). The advantage of more
slow-twitch muscle fibers includes greater mitochondrial capacity, increased
oxygen consumption, and increased performance in endurance exercise. 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, economy, and lactate
threshold (Robergs & Roberts, 1997).

Conclusion

The purpose of our article was to review the major physiological limitations to
endurance exercise. Though 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 limitations is modifiable through endurance training, it is important
to recognize that genetic factors play a tremendous role in the trainability of
these limitations and their capacity. It is therefore critical for coaches, fitness
instructors, and personal trainers to recognize the all of the physiological
components limiting endurance performance as they design exercise programs
to improve endurance capacity.