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Endurance exercise performance: The physiology of champions


Abstract and Figures

Efforts to understand human physiology through the study of champion athletes and record performances have been ongoing for about a century. For endurance sports three main factors--maximal oxygen consumption (.VO(2,max)), the so-called 'lactate threshold' and efficiency (i.e. the oxygen cost to generate a given running speed or cycling power output)--appear to play key roles in endurance performance. and lactate threshold interact to determine the 'performance .VO(2)' which is the oxygen consumption that can be sustained for a given period of time. Efficiency interacts with the performance .VO(2) to establish the speed or power that can be generated at this oxygen consumption. This review focuses on what is currently known about how these factors interact, their utility as predictors of elite performance, and areas where there is relatively less information to guide current thinking. In this context, definitive ideas about the physiological determinants of running and cycling efficiency is relatively lacking in comparison with .VO(2,max) and the lactate threshold, and there is surprisingly limited and clear information about the genetic factors that might pre-dispose for elite performance. It should also be cautioned that complex motivational and sociological factors also play important roles in who does or does not become a champion and these factors go far beyond simple physiological explanations. Therefore, the performance of elite athletes is likely to defy the types of easy explanations sought by scientific reductionism and remain an important puzzle for those interested in physiological integration well into the future.
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J Physiol 586.1 (2008) pp 35–44 35
Endurance exercise performance: the physiology
of champions
Michael J. Joyner1and Edward F. Coyle2
1Departments of Anaesthesiology and Physiology, Mayo Clinic College of Medicine Rochester, MN 55905, USA
2Department of Kinesiology and Health Education, University of Texas Austin, Austin, TX 78712, USA
Efforts to understand human physiology through the study of champion athletes and record
performances have been ongoing for about a century. For endurance sports three main factors –
maximal oxygen consumption ( ˙
VO2,max), the so-called ‘lactate threshold’ and efficiency (i.e. the
oxygen cost to generate a give running speed or cycling power output) – appear to play key roles
in endurance performance. ˙
VO2,max and lactate threshold interact to determine the ‘performance
VO2‘ which is the oxygen consumption that can be sustained for a given period of time. Efficiency
interacts with the performance ˙
VO2to establish the speed or power that can be generated at this
oxygen consumption. This review focuses on what is currently known about how these factors
interact, their utility as predictors of elite performance, and areas where there is relatively less
information to guide current thinking. In this context, definitive ideas about the physiological
determinants of running and cycling efficiency is relatively lacking in comparison with ˙
and the lactate threshold, and there is surprisingly limited and clear information about the
genetic factors that might pre-dispose for elite performance. It should also be cautioned that
complex motivational and sociological factors also play important roles in who does or does
not become a champion and these factors go far beyond simple physiological explanations.
Therefore, the performance of elite athletes is likely to defy the types of easy explanations sought
by scientific reductionism and remain an important puzzle for those interested in physiological
integration well into the future.
(Received 24 August 2007; accepted after revision 26 September 2007; first published online 27 September 2007)
Corresponding author M. J. Joyner: Departments of Anaesthesiology and Physiology, Mayo Clinic College of Medicine,
200 First Street SW, Rochester, MN 55905, USA. Email:
Faster, Higher, Stronger: these simple descriptions have
been of interest to humans since the beginning of recorded
history. In this context, integrative physiology has long
been served by so-called ‘experiments in nature.’ These
include asking fundamental questions about the ability of
various animal species to function in harsh environments
and studies on unique human patients with clinical
conditions that offer the opportunity to ask important
questions about physiological regulation (for examples see
Hagberg et al. 1982; Faraci et al. 1984; Schrage et al. 2005).
Along similar lines, studies on both human and animal
performance in athletic events can provide important
insights and raise critical questions about oxygen
transport, muscle performance and metabolism, cardio-
vascular control, and the operation of various components
of the nervous system (Joyner, 1991).
Historical note
One of the first analyses of world records from A. V. Hill
in 1925 (Hill, 1925) related the decline in running speed
as race distance increased to the topic of muscle fatigue
(Fig. 1). Even before then, the Italian physiologist Mosso,
who was interested in fatigue associated with manual
labour, noted ‘It is not will, not the nerves, but it is the
muscle that finds itself worn out after the intense work of
the brain.’ But Mosso hedged his bets and also commented
that ‘fatigue of brain reduces the strength of the muscles’
(DiGiulio et al. 2006).
In Hill’s analysis he speculated that the factors limiting
performance in events of less than a minute and more
than an hour are probably not dependent solely on the
energy supply to the contracting muscles and discussed the
physiological determinants of performance in the context
of ideas about energy stores, oxygen demand and oxygen
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36 M. J. Joyner and E. F. Coyle J Physiol 586.1
debt. He also speculated that there were ‘three types of
fatigue’ (a concept he found to be inexact) including:
(1) one associated with short violent efforts; (2) the
exhaustion ‘which overcomes the body when an effort
of moderate intensity is continued for a long time’; and
(3) fatigue associated with a more general ‘wear-and-tear’.
The first two types of fatigue were thought to be primarily
Additionally, for the second and third types of fatigue,
which occur during endurance exercise, Hill speculated
thatas distancesincrease beyondabout 10miles (16 km),
‘The continued fallin the curve,as theeffort isprolonged, is
probably due to the second and third types of fatigue which
we discussed above, either to the exhaustion of the material
of the muscle, or to the incidental disturbances which may
make a man stop before his muscular system has reached
its limit. A man of average size running in a race must
expend about 300 g of glycogen per hour; perhaps a half
of this may be replaced by its equivalent of fat. After a very
few hours therefore the whole glycogen supply of his body
will be exhausted. The body, however, does not readily use
fat alone as a source of energy; disturbances may arise in
the metabolism; it will be necessary to feed a man with
carbohydrate as the effort continues. Such feeding will be
followed by digestion; disturbances of digestion may occur
– other reactions may ensue. For very long distances the
case is far more complex than for the shorter ones, and
although, no doubt, the physiological principles can be
Figure 1. A. V. Hill’s (Hill, 1925) original plot of world record performance time on the X-axis versus
performance speed on the Y-axis
The top tracing is for speed-skating, the middle tracing is for running by males, and the bottom tracing is for
running by women. The shape of the curve led to Hill’s original ideas about differing causes of muscle fatigue for
exercise bouts of different durations.
ascertained, we do not know enough about them yet to be
able further to analyse the curves.’ These comments and
the work of Scandinavian physiologists in the 1930s set the
stagefor theconceptof carbohydrateloading anda number
of dietary and feeding strategies that have been shown to
delay fatigue (Christensen, 1939; Sherman & Costill, 1984;
Murray, 1998).
Focus of this review
In this review for The Journal of Physiology’s 2008
Olympic Issue, we will focus on current models of human
performance, review the physiological ‘ideas’ that led to
these models, and ask what these models explain and more
importantly do not explain. Figure 2 presents our concepts
using a model like Hill’s that is focused on ‘performance
velocity’ and how it is determined by maximum rates
of aerobic energy production, anaerobic capacity and
how efficiently the energy being used is converted to
In general, we focus on endurance exercise performance
because it is our area of expertise, and there are relatively
more data on the physiological adaptations that contribute
to endurance performance, and (especially for running)
there are accurate records extending for more than
100 years. There is also at least some physiological data
on champion athletes over almost the same period of
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Overview of current ideas about human performance
As noted above, most models of athletic performance focus
on distance running and endurance cycling. First, there
are excellent records and standard events. Second, there
is comprehensive physiological data on a large number
of elite athletes. Third, it is possible, using treadmills and
cycle ergometers, to reasonably simulate in a laboratory
what is happening during actual competition. We should
also note that for the purposes of this review we assume
that environmental conditions are ideal and do not add
anyadditional challengesto physiological regulation(most
notably the challenges associated with high altitude and/or
high environmental temperatures).
VO2,max.Several well-accepted concepts (Joyner, 1991,
1993; Coyle, 1995; Bassett & Howley, 2000) have emerged
related to endurance exercise performance velocity and the
first component issue is the level of aerobic metabolism
that can be maintained during a race (i.e. performance
VO2; Fig. 2). The upper limit for this is ‘maximal’ oxygen
uptake. This is usually achieved during relatively large
muscle mass exercise and represents the integrative ability
of the heart to generate a high cardiac output, total body
haemoglobin, high muscle blood flow and muscle oxygen
extraction, and in some cases the ability of the lungs to
oxygenate the blood (Mitchell et al. 1958; Kanstrup &
Ekblom, 1984; Rowell, 1986; Dempsey, 1986; Saltin &
Strange, 1992; Bassett & Howley, 2000). By the 1930s
very high values for ˙
VO2,max in athletes were observed and
identified as a marker of elite performance (Robinson
et al. 1937). Champion endurance athletes have ˙
values of between 70 and 85 ml kg1min1, with values in
women typically averaging about 10% lower due to lower
haemoglobin concentrations and higher levels of body fat
Figure 2. Overall schematic of the multiple
physiological factors that interact as
determinants of performance velocity or
power output
This figure serves as the conceptual framework
for the ideas discussed in this review.
(Saltin & Astrand, 1967; Pollock, 1977; Durstine etal. 1987;
Pate et al. 1987).
In summary, ˙
VO2,max values 50–100% greater than those
seen in normally active healthy young subjects are seen
in champion endurance athletes and the most striking
adaptations to training that contribute to these high
VO2,max values include increased cardiac stroke volume,
increased blood volume, increased capillary density and
mitochondrial density in the trained muscles (Costill et al.
1976). Of these, the most dominant factor is a high stroke
volume (Ekblom & Hermansen, 1968; Coyle et al. 1984;
Martin et al. 1986).
Once it became reasonably clear that elite runners
had high values for ˙
VO2,max it also became clear that for
events lasting beyond 10 or 15 min, most or all of the
competition was performed at an average pace that did not
evoke ˙
VO2,max, with much of the 42 km marathon run at
approximately 75–85% ˙
VO2,max while 10 km is performed
at 90–100% ˙
VO2,max and 5 km at close to ˙
VO2,max (Costill
et al. 1973; Bassett & Howley, 2000). Along these lines, it
has recently been shown that maximal aerobic metabolism
can decline acutely during the course of a 5–8 min
laboratory performance bout. This decline is caused by
a fall in stroke volume and accelerated muscle fatigue
due to reduced blood and oxygen delivery and increased
anaerobic metabolism (Gonzalez-Alonso & Calbet, 2003;
Mortensenet al.2005). This doesnot invalidatethe concept
of ˙
VO2,max, but rather indicates that the maximal rate of
aerobic ATP resynthesis during a race is dynamic and that
truly accurate models of energy turnover during actual
competition would require instantaneous measurements
and calculation of fluxes through multiple metabolic
pathways (e.g. total ATP turnover with contributions from
both aerobic and anaerobic components as well as energy
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Figure 3. Plot or blood lactic acid concentration
versus race distance (Costill, 1970)
This figure is an example of the diminishing contribution
of so-called ‘anaerobic’ energy sources as race distance
increases. This paper also set the stage for a number of
later investigations related to the fraction of ˙
(e.g. performance ˙
VO2) that could be sustained in
Lactate threshold. Based on the concepts above the
question then became what fraction of ˙
VO2,max might be
sustained for periods of time extending to several hours
(i.e. the marathon) and what is the rate of glycolysis in
the active muscles at this rate of mitochondrial oxidation.
This question led to observations showing a curvilinear
relationship between blood lactate values during exercise
and the distance of the effort (Fig. 3; Costill, 1970) and
Figure 4. Individual record of treadmill velocity and ˙
blood lactate concentration in subject capable of breaking
2:30 h for the marathon (Farrell et al. 1979)
In untrained subjects the upturn in lactic acid concentrations is seen at
about 60% of ˙
VO2,max. Trained subjects can usually exercise at
75–85% of ˙
VO2,max before there is a marked increase in blood lactate
concentration. This figure also illustrates the concept of performance
VO2and performance velocity.
led to the concept that the rate of aerobic metabolism
maintained during a performance bout (i.e. performance
VO2; Fig. 2) can be better described by the degree of muscle
glycolytic stress reflected in lactate production in addition
to ˙
VO2,max (Farrell et al. 1979; La Fontaine et al. 1981).
In this context, as running speed or power output on
a cycle ergometer increases in untrained subjects there is
typically no sustained rise in blood lactate concentration
until about 60% of ˙
VO2,max is reached. In trained
subjects this value can be 75–90% of ˙
VO2,max (Fig. 4). There
is a long history of investigation about what causes this
rise in blood lactate levels and also how lactate (and/or
hydrogen ion) does or does not contribute to fatigue. For
this review the important summary points include: (1) the
initial appearance of blood lactate is not synonymous with
hypoxia in the skeletal muscle, and (2) the lactate molecule
per se does not ‘cause’ muscle fatigue (Holloszy et al. 1977;
Holloszy & Coyle, 1984; Robergs et al. 2004).
What appears to be occurring is that the maximum
rate of fat oxidation is inadequate to meet the ATP
demands of muscles contracting at moderate and high
intensities. This causes intracellular signalling events to
occur which stimulate glycogenolysis and glycolysis and
ultimatelythe rateofpyruvate deliverytothe mitochondria
progressively exceeds the ability of the mitochondria to
oxidize pyruvate and this leads to accelerated generation
of lactic acid (Holloszy et al. 1977; Holloszy & Coyle, 1984;
Robergs et al. 2004). The associated hydrogen ion is then a
likely culprit in muscle fatigue and also activates group III
and IV skeletal muscle afferents that evoke important
cardiovascular and autonomic reflexes (Pryor et al. 1990).
While the physiological determinants of the lactate
threshold are extremely complex, they are determined
mainly by the oxidative capacity of the skeletal muscle
(Holloszy et al. 1977; Davies et al. 1982; Holloszy & Coyle,
1984; Gregg et al. 1989a,b). This capacity is highly plastic
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J Physiol 586.1 Factors that make champions 39
and can essentially increase more than twofold in the
trained skeletal muscle of humans or animals who engage
in 20–120 min of training at a requisite intensity (Holloszy
et al. 1977; Dudley et al. 1982; Holloszy & Coyle, 1984).
This more than doubling of oxidative capacity is one of
the factors that is linked to the high ‘lactate threshold’
values seen in elite endurance athletes (Fig. 2). As noted
above, these elite athletes have ˙
VO2,max values that are
50–100% above those seen in normally active sedentary
young people and their lactate threshold occurs at a higher
percentage of their ˙
VO2,max. This means that in elite athletes
the absolute oxygen consumptions (power output and/or
speed) that can be generated for long periods of time
before reaching the lactate threshold is essentially doubled
allowing sustained running speeds of 20 km h1or cycling
power outputs of 400 W.
Other key factors that reduce muscle fatigability and
lactate production during exercise at 85–90% ˙
when only a fraction of the total limb muscle mass
is simultaneously recruited, is the quantity of muscle
mass that the athlete can recruit to share in sustaining
power production (Fig. 2). Elite cyclists appear capable
of rotating power production through 20–25% more
muscle mass throughout a 1 h bout of cycling, thus
reducing the relative power production and stress on a
givenfibre(Coyleet al. 1988; Coyle, 1995). Additionally,
this ‘power sharing’ among fibres would also reduce the
glycolytic stress and lactate production per fibre due to
more total mitochondrial sharing for a given rate of
aerobic metabolism. These factors should operate in
a complementary way that reduces the stress per
mitochondria and muscle fibre.
As exercise extends beyond about 2 h the problem
becomes one of fuel availability as (Hill predicted) the
glycogen content in skeletal muscle becomes depleted and
the modest ability of active muscle to take up glucose
from blood (via either the liver or from feeding) can
limit the rate of oxidative ATP generation and thus
the pace that can be sustained. In some (but not all)
subjects the associated reductions in blood glucose evoke
frank symptoms of hypoglycaemia that limit the ability
of the individual to continue exercising (Christensen,
1939; Coyle et al. 1983, 1986). Other highly trained
subjects show remarkable resistance to hypoglycaemia and
for these athletes muscle glycogen depletion is probably
more important. In response to these events, a number
of pre-competition dietary strategies and during-exercise
energy replacement regimens and products have been
developed (Murray, 1998). When these are used in an
optimal manner muscle glycogen stores can be augmented
by 40% before exercise, and hypoglycaemia can be avoided
with the net effect being that the duration of exercise
at about the lactate threshold can be extended by about
one-third (from 2 to 3 h to 4 h) (Coyle et al. 1983, 1986;
Sherman & Costill, 1984).
Performance ˙
VO2and anaerobic metabolism. Without
practical direct calorimetric methods to measure
instantaneous rates of heat and work production during
endurance exercise (Webb et al. 1988; Scott, 2000),
the best practical estimation of the rates of actual
metabolic energy production and ATP turnover is
obtained from measures of oxygen consumption (i.e.
indirect calorimetry) during an endurance performance
bout. During marathon running the relative amount
of anaerobic metabolism is small yet in events lasting
13–30 min (i.e. 5 and 10 km running), it will be significant,
contributing perhaps 10–20% of total ATP turnover. This
anaerobic contribution to ATP turnover during endurance
performance bouts is noted in Fig. 2 and has classically
been estimated from measures of post-exercise oxygen
consumption and may equal the energy provided by
50–80 ml kg1of oxygen uptake (Fig. 2) (Bangsbo et al.
1993). However, the rate at which this energy might
be generated and consumed is difficult to estimate in a
definitive way.
Figure 2 also makes the point that the rate of total
ATP turnover during endurance performance reflects
the interplay of aerobic and anaerobic metabolism with
lactate generation serving to maintain the NAD+needed
for continued glycolysis and generation of pyruvate. An
example of this interplay appears to be the influence of
high skeletal muscle capillary density, serving to remove or
recycle within muscle fatiguing metabolites (e.g. hydrogen
ions). As shown in Fig. 5, exercise time to fatigue at 88%
VO2,max in a population of cyclists (n=14, individually
numbered) possessing the same ˙
VO2,max (i.e. 4.9 l min1),
as expected, was related to the percentage of ˙
VO2,max at
the blood lactate threshold. However, some subjects (see
upper line in Fig. 5) were able to exercise longer than
normal (see lower line in Fig. 5) even when accounting
for their lactate threshold (i.e. subjects 1, 2, 7 and 8 in
Fig. 4). For the most part, these individuals (i.e. 1, 2, 7 and
8) possessed an unusually high muscle capillary density
which may have allowed their exercising muscles to better
tolerate anaerobic metabolism and lactic acid production.
For this reason, Fig. 2 indicates that ‘Performance ˙
might be directly influenced by muscle capillary density,
independent of its important role in delivering oxygen
and reducing diffusion gradients, but also by removing
waste products and limiting acidosis in the contracting
An additional point from Fig. 5 is that much remains
to be learned about subtle factors that delay or accelerate
fatigue during events performed at intensities above
80–90% of ˙
VO2,max. Small increases in total energy
expenditure or reductions in oxygen delivery will have
disproportionate effects and accelerate fatigue (Mortensen
et al. 2005) during very intense exercise. At this time it
remains unclear if laboratory tests can detect the subtle
adaptationsin thevery bestperformers who seemto beable
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40 M. J. Joyner and E. F. Coyle J Physiol 586.1
manage their metabolism in a way that permits maximum
efficient energy use.
Efficiency. The next factor that makes an important
contribution in endurance exercise performance velocity
has been termed ‘economy’ or ‘efficiency.’ In the above
sections we outlined how ˙
VO2,max and the lactate threshold
operate to determine ‘Performance ˙
VO2, (Fig. 2). The
next question then is how much speed or power can
be generated for that level of oxygen consumption? The
oxygen cost of endurance running (ml kg min1)atagiven
speed can vary about 30–40% among individuals (Farrell
et al. 1979; Conley & Krahenbuhl, 1980; Joyner, 1991), as
shown in Fig. 6. When cycling at a given power output,
the oxygen cost and thus gross mechanical efficiency also
varies from oneperson toanother,but by asomewhat lesser
amount compared with running (i.e. 20–30%) (Coyle,
Gross mechanical efficiency when endurance-trained
cyclists generate 300 W can vary from 18.5 to 23.5% and
it appears that more than one-half of this variability is
related to the percentage of type I (slow twitch) muscle
fibres of the vastus lateralis muscle (Coyle et al. 1992).
The efficiency with which the chemical energy of ATP
hydrolysis is converted to physical work depends greatly
on the velocity of sarcomere and muscle fibre shortening.
Type I (slow twitch) fibres display greater mechanical
efficiency when cycling at cadences of 60–120 r.p.m.
Therefore, it is not surprising that elite endurance cyclists
Time to
Fatigue at
88% VO2max
(min) 9
%VO2max at LT
%VO2max at LT
Time to
Fatigue at
88% VO2max
Subjects with High Capillary Density
Subjects with High Capillary Density
60 70
70 80
80 90
Figure 5. Time to fatigue during exercise at 88% of ˙
plotted against lactate threshold (LT) in 14 highly trained cyclists
and triathletes (data plotted from Coyle et al. 1988; Coyle, 1995)
These athletes all had similar ˙
VO2,max values and uniformly high muscle
oxidative enzymes. A subgroup of 4 athletes (subjects 1, 2, 7 and 8)
with exceptionally high capillary density seemed to ‘overachieve’ in
comparison with their lactate threshold values compared with other
members of the group.
typically possessa higherpercentage of type Imuscle fibres,
given that they are more efficient. Although type I muscle
fibres in untrained humans possess higher mitochondrial
density compared with type II fibres (fast twitch), it is
important to note that with intense interval training,
mitochondrial activity can be increased to equally high
levels in both fibre types (Chi et al. 1983). Thus, with
intense endurance training over years, the main functional
advantage of type I fibres appears to be efficiency when
cycling rather than total oxidative ability, although type I
fibre seem to retain a greater ability to oxidize fat.
It is also of note that many champion cyclists chose
pedal cadences of around 90 r.p.m. This is a cadence that
may actually increase whole body oxygen consumption
slightly for a given total body power output from the
VO2minimum which usually occurs at 50–60 r.p.m.
In a comprehensive engineering/physiology analysis of
this problem Hansen et al. (2002) noted that subjects
with higher levels of myosin heavy chain I (MHC I, the
predominant myosin in type I fibres) self-selected higher
pedal rates and these rates closely matched the rate of peak
mechanical efficiency. In this context, they speculated that
motor control patterns in these subjects might favour a
faster cadence so that relatively low total muscle forces
(probably from fatigue-resistant motor units) per pedal
stroke could generate the needed power so that the higher
force (and more fatigable) motor units could be conserved.
On a speculative note, with lower force per contraction
there might be less compression of the microcirculation
Figure 6. Regression lines for high, average and low running
economy (efficiency) in elite endurance athletes based on
values gleaned from a number of sources (Joyner, 1991)
Since there has been little systematic data collected above
18 km h1the filled triangles in the figure are individual data from a
limited number of champions with exceptional running economy. This
figure emphasizes the importance of efficiency among groups of elite
performers with relatively uniform ˙
VO2,max and lactate threshold
values. It is also of note that the physiological determinants of
efficiency (especially for running) are poorly understood.
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in the active muscle and better distribution of blood flow
in a way that is consistent with the concepts presented in
Fig. 5.
Running is a more complicated movement than cycling
in that it elicits more stretch on the muscle prior
to contraction and there is more potential to capture
mechanical energy in the elastic elements of tissue.
However, although there has been long-standing interest
in identifying the biomechanical and anatomical factors
that allow one person compared with another to expend
30–40% less energy per kilogram of body to move at
a given velocity, the aetiology of differences in running
economy generally remain a mystery, and biomechanical
descriptions of running are not good predictors of running
economy (Kyr¨
ainen et al. 2001; Williams, 2007).
Elite endurance runners typically possess a
predominance of type I muscle fibres and it would
seem logical that they are more mechanically efficient
at the velocities of distance running (Costill et al. 1976;
Fink et al. 1977; Bosco et al. 1987). However, running and
walking economy has not often been highly correlated
with a person’s percentage of type I muscle fibres (Morgan
& Craib, 1992; Hunter et al. 2005). This agrees with the
idea that running economy reflects the interaction of
numerous factors including muscle morphology, elastic
elements and joint mechanics in the efficient transfer of
ATP to running speed.
The extent to which cycling efficiency or running
economy can be improved with training has also been
of long-standing interest. Until recently, it was generally
believed that cycling efficiency and running economy did
not improve much with training (Moseley et al. 2004).
At best, running economy might sometimes increase
slightly over the course of 2 months when explosive-type
weight training is added to an endurance training program
(Paavolainen et al. 1999; Millet et al. 2002). However, the
conclusion that efficiency does not change with training
was based on cross-sectional comparisons of relatively
small numbers of endurance athletes (Moseley et al. 2004).
In this context, there are no comprehensive longitudinal
data on groups of endurance athletes followed over several
years to determine the trainability of cycling efficiency or
running economy. However, there are at least two cases
reporting that running economy can be improved over
years of training in elite athletes (Conley et al. 1984;
Jones, 2006). In fact, the current world record holder
for the women’s marathon displayed a remarkable 14%
improvement in running economy over the course of
5 years of training (Jones, 2006). Furthermore, cycling
efficiency was observed to increase 8% over the course
of 7 years in an elite endurance cyclist (Coyle, 2005). In
general, these case reports suggest that muscular efficiency
and running economy might indeed improve with
continued endurance training at a rate of approximately
1–3% per year. One possible contributing factor is that
at least some of the fast myosin in endurance-trained
muscle shifts to a different and perhaps more efficient iso-
form (Green et al. 1984). Additionally, in some models of
extreme muscle use there can be a complete conversion of
fast twitch to slow twitch muscle fibres, whether this occurs
in elite athletes who train for two or more hours per day
for many years is not known and it is further not known if
such a shift would explain any improvements in efficiency
that might occur with years of training (Pette, 2001).
Integrating current ideas about physiological
limiting factors
The concepts above and in Fig. 2 suggest that ˙
VO2,max and
lactate threshold interact to determine how long a given
rate of aerobic and anaerobic metabolism can be sustained
(i.e. performance ˙
VO2) and efficiency then determines how
much speed or power (i.e. performance velocity) can be
achieved at a give amount of energy consumption. These
relationships were hinted at by Hill in his 1925 paper (Hill,
1925) and were clearly defined in the period between 1970
and the early 1990s (Costill, 1970; Costill etal. 1973; Joyner,
1991; Joyner, 1993; Coyle, 1995; Bassett & Howley, 2000).
The Marathon. In 1991, these concepts were used (Joyner,
1991) to predict that a much faster world record for the
marathon was ‘physiologically’ possible based on the idea
that marathon running speed was essentially predicted by
the equation:
VO2,max ×lactate threshold percentage×running economy
When reasonable estimates of the ‘best’ values ever
recorded for these three parameters were used in this
equation a predicted optimal marathon time of around
1:45 h emerged. Even when assumptions about wind
resistance were added, times well under 2 h seemed
possible. In retrospect, one overlooked possibility was
that the ˙
VO2,max values used in the estimates came
from laboratory studies typically conducted while the
subjects ran up a grade of 5–10% and these values may
be 10% higher than those seen during level running
(Morgan et al. 1989). However, even if the highest ˙
values seen during graded running protocols are not
attainable during level running in many people, there
are high enough ˙
VO2,max and lactate threshold values that
might result in sustainable oxygen uptakes, which in
combination with outstanding running economy, would
generate a marked improvement in current world record
time. These comments reinforce the conclusions of this
earlier modelling effort that either there are unknown
factors that operate at high speeds that make such time
‘not’achievable orthat forsome reason‘best inclass’ values
for every factor are unlikely to occur in the same person
(Lucia et al. 2002).
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42 M. J. Joyner and E. F. Coyle J Physiol 586.1
Some unanswered questions
In the context of the ideas above there are a number
of fundamental unanswered questions. We have already
highlighted questions about the determinants of efficiency
especially for running, and for both running and cycling a
key question is how ‘trainable’ this factor is. Additionally,
we have discussed several factors beyond mitochondrial
content and oxidative enzymes that may permit some
athletes to operate for prolonged periods at especially
high fractions of their ˙
VO2,max. These factors may also
be important in events like long distance cycling and
cross country skiing that occur over varied terrain and
are not conducted at an even physiological pace. In these
competitions there are frequent bursts of more intense
near-maximal activity lasting from a few seconds to a few
minutes that are followed by periods of relative recovery.
A fundamental question is the role genetics plays in the
attainment of world class status and truly elite athletic
performance. There are a number of studies showing that
key elements of the response to training in sedentary
persons is widely variable and has a genetic component
(Rankinen et al. 2006). There have also been reports
suggestingthat commonsingle nucleotidepolymorphisms
might be over represented in either groups of elite
endurance athletes or in sedentary subjects that respond
most to training. The most notable example is the idea
that I (for insertion) variant of the angiotensin converting
enzyme (ACE) gene is over represented among elite end-
urance athletes. However, in the largest cohort of elite
athletes who have been both rigorously phenotyped and
genotyped this association has not been confirmed and
to date there are no genetic markers identified in humans
that have been clearly shown to be more frequent in elite
endurance athletes (Rankinen et al. 2000).
Another interesting example relates to the gene
encoding for the skeletal muscle isoform of AMP
deaminase. There is a common mutation of this gene
that may be associated with lower exercise capacity and
‘trainability’ in untrained subjects (Rico-Sanz et al. 2003).
While the frequency of the gene may be lower in elite
endurance athletes there are still a number of elite
performers who carry it so it does not appear to pre-
clude the attainment of elite status and there is at least
one example of an elite performer with essentially no AMP
deaminase activity (Lucia et al. 2007; Rubio et al. 2005).
In this context, finding genetic markers that are
strongly predictive of either success in endurance athletic
performance or somehow preclude it is likely to be
a daunting task because of the many cultural and
environmental factors that contribute to success in
sport, the many physiological factors that interact as
determinants of performance, and the heroic nature of the
training required. Ideas about culture are highlighted by
the observation that while East African runners currently
dominate international competition previously athletes
from Australia and New Zealand, preceded by Eastern
Europeans and even earlier the Finns showed remarkable
levels of success. This geographical diversity argues against
a simple genetically based set of answers to the problem of
elite performance in endurance competition. In a parallel
way, there is a low signal to noise ratio for many proposed
genetic factors that might contribute to multifactorial
medical conditions like heart disease, diabetes and
hypertension and clear causal associations between
genotype and phenotype are slow to emerge (Morgan et al.
Concluding remarks
Our concepts about factors that regulate and potentially
limit endurance performance are not a radical departure
from the intuitive logic introduced by Mosso and Hill. Elite
athletic performance involves integration of muscular,
cardiovascular and neurological factors that function
cooperatively to efficiently transfer the energy from
aerobic and anaerobic ATP turnover into velocity and
power. The past four decades of research have described
in great detail the cardiovascular and muscular factors
that govern oxygen delivery to active muscles, oxidative
ATP rephosphorylation and markers of metabolic stress.
However, little advancement seems to have been made in
identifying neurological factors that might alter motor
unit recruitment during prolonged exercise in ways
that limit fatigue. Although it has become increasingly
apparent that muscular efficiency and economy are hugely
important, the physiological determinants of running
economy remain a mystery while myosin type appears
important to cycling efficiency at cadences chosen in
The outcome of all Olympic endurance events is
decided at intensities above 85% ˙
VO2,max and most require
athletes to be relatively fatigue resistant at intensities that
stimulate significant anaerobic metabolism. At this time,
the literature contains insufficient data that specifically
describe the actual total energy demands of competition,
the amount of muscle that is active during competition,
and the complex neural patterns by which power and
velocity are maintained as fatigue and failure develop in the
nervous, cardiovascular and muscular systems. Such data
are needed both in absolute and temporal terms. In this
context, more work is needed on highly trained athletes
performing very intense exercise in real or simulated
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... Endurance performance is mainly determined by aerobic power (VO 2max ), fractional utilization, and working economy (Joyner and Coyle, 2008). World-leading athletes have maximized these determinants through years with high volumes of systematic training. ...
Full-text available
Purpose: To compare training characteristics and aerobic power (VO 2max ) between the most successful junior and senior seasons of world-class cross-country (XC) skiers and to identify differences between sexes and among sprint and distance skiers. Methods: Retrospective analysis was conducted on self-reported training and VO 2max tests of ten male and seven female world-class XC-skiers, collectively holding 38 Olympic medals. Training was categorized by form (endurance, strength, speed, other) and mode (specific, unspecific) and was divided into low- (LIT), moderate- (MIT), and high-intensity training (HIT). Results: Total training increased by 203 ± 130 h (35% ± 31%, p < .001, large effect) and 78 ± 69 sessions (21% ± 24%, p < .001, very large effect). Junior training volume (658 ± 107 h) did not correlate with senior volume (861 ± 74 h) but correlated negatively with changes in volume ( r = −.822, p < .001). No sex differences were observed related to total volume, but distance skiers increased their total volume more than sprint skiers ( p = .037, large effect). Endurance training increased by 197 ± 117 h ( p < .001; large effect) tied to increased low-intensity training (186 ± 115 h, p < .001; large effect) and moderate-intensity training (13 ± 7 h, p < .001; large effect). Training intensity distribution (% LIT/MIT/HIT) was 91/3/6 in junior and 92/4/4 in senior season. Women demonstrated greater increase of unspecific modes (100 ± 58 vs. 37 ± 44 h, p = .022; large effect) and strength training (25 ± 23 vs. −3 ± 17 h, p = .010, large effect). Men improved absolute (8% ± 5%; p = .009; large effect) and relative VO 2max (6% ± 4%; p = .016; large effect) from junior to senior, while women only increased relative VO 2max (7% ± 5%, p = .012; large effect). Conclusion: This study provides novel information regarding changes in training characteristics and aerobic power from junior to senior age in world-class XC-skiers. Overall, the enhanced training volume during this transition was primarily driven by increased LIT and MIT and the exceptionally high relative VO 2max at junior age further increased in both sexes.
... Aerobic fitness, encompassing critical aspects such as maximal oxygen uptake (VO2max) and endurance performance [1], plays a pivotal role in promoting health and overall well-being through a variety of mechanisms [2]. Among these mechanisms, one of the most prominent is its favorable impact on the cardiovascular system. ...
Aerobic fitness is a critical aspect of overall health and well-being, essential for maintaining a high quality of life. Unfortunately, sedentary behavior has been on the rise among young adults, and this has had a negative impact on their aerobic fitness levels. Therefore, it is crucial to identify enjoyable physical exercise training programs that can play a pivotal role in improving aerobic fitness. The objective of this study was to systematically review the experimental studies concerning the impact of small-sided games (SSGs) training programs, implemented across various team sports, on the enhancement of aerobic fitness in a youth sedentary population. A literature search was conducted in PubMed, Scopus, and the Web of Science on August 01, 2023. Our eligibility criteria focused on studies involving sedentary youth populations (aged <18 years) as the target population. These studies needed to incorporate interventions based on SSGs as the intervention of interest, comparing them to passive or control groups as the comparator. The primary outcomes of interest were related to maximal oxygen uptake (VO2max), assessed either directly or indirectly, or the results of field-based cardiorespiratory tests. We specifically considered two- or multi-arm randomized controlled studies as the study design of interest. Out of the initial pool of 1980 studies, we reviewed 38 full-text articles, ultimately selecting and analyzing 13 studies for inclusion in our review. Among the studies included, a total of 1281 participants were enrolled in SSG-based interventions, while 744 participants acted as part of the control groups. Regarding the impact on VO2max, the six studies that investigated this outcome showed varying improvements, ranging from 2.2 % to 31.3 % when participants were exposed to SSGs. In terms of the outcome related to endurance performance in field-based tests, the eight studies that examined this aspect found that participants exposed to SSGs showed improvements ranging from 0.1 % to 79.8 %. In conclusion, this systematic review suggests that SSG-based interventions conducted among sedentary youth populations can play a positive role in improving their aerobic fitness. This improvement in aerobic fitness can have potential positive impacts on their overall health and quality of life.
... This consists of power production on one side of the equation and power losses on the other side, with velocity as outcome. Factors that influence power production are the aerobic and anaerobic energy production systems and the gross mechanical efficiency [5,6]. Factors that influence the power losses are air friction, rolling resistance, and internal friction, such as bearing friction and frictional losses in the chain drive system [7]. ...
Full-text available
Tandem cycling is a paralympic discipline, in which two cyclists ride on one tandem bicycle. Their performance can be improved by minimizing power losses. This study aimed to quantify power loss due to the chain drive of a tandem bicycle and influence of power input, location of power input, and rear chain wheel size. Power loss was determined by the difference between power input applied on the cranks (front or back rider) and power output measured at the rear wheel. Power output values were set from 100 to 400 W, with 50 W increments, and using two gear ratios, 53-11 and 53-13. Power input was generated at the back crank (with only the primary chain—solo bicycle—and with primary and secondary chain attached) and at the front crank (with primary and secondary chain attached). The power loss for the solo bicycle was 2.1% (± 1.5%). A significantly larger power loss was found for the tandem in the back (3.7 ± 2.4%, p < 0.001) and front positions (3.0 ± 1.8%, p < 0.001), with marginal differences between positions at higher power output. Power loss for the tandem was lower with gear 53-13 (2.9% ± 1.7%) compared to 53-11 (4.0 ± 2.8%, p < 0.001, effect size is medium). Therefore, findings suggest that back and front riders experience similar power losses due to the chain drive, but more than on a solo bicycle. Tandem cyclists can reduce their power loss in the chain drive by selecting larger gear ratios. Coaches may consider these findings for selecting and coaching their tandem cyclists.
... Host energy production, ROS modulation, and inflammations are caused by gut microbiota and its metabolites in the gut by attenuating TNFα-mediated immune responses and inflammasomes such as NLRP3. The intestinal microbiota composition and activity have recently been shown to be affected by genetic variants within the mitochondrial genome, while we know that gut microbiota is regulated by mitochondrial ROS production [64,67]. ...
Full-text available
Multiple diseases can decrease levels and changes in gut microbial populations, while increasing microbiota diversity causes an increase in the immune response. Evidence shows that exercise can affect the gut microbiota and, subsequently, the health of individuals. Also, regular exercise provides many benefits for health, protection against the spread of chronic diseases, and improved quality of life. Exercise can increase the number of helpful microbiota species, enrich microflora diversity, and improve the growth of commensal microbiota. This article reviews recent findings on the interaction of gut microbiota and exercise. Also, another purpose of this research is to suggest different mechanisms that using them can provide the way that the exercise factor can change the gut microbiota.
... The time ≥90% of maximal heart rate (HR max ) is of interest as it is seen as an approximation for the time ≥90% of maximal oxygen uptake. The latter is considered as a large stimulus to elicit cardiovascular and peripheral adaptations leading to a higher maximal oxygen uptake (VO 2max ) capacity, a main factor of (endurance) exercise performance (Joyner and Coyle, 2008;Laursen, 2010;Buchheit and Laursen, 2013). The percentage thresholds applied for the relative speed thresholds (i.e., 55 and 70) are explained by the fact that they correspond to the recommended fixed thresholds (Miguel et al., 2021) for a maximum speed of 36 km/h. ...
Full-text available
Extensive research has led to evidence-based methodological recommendations for appropriate prescription and implementation of different training drills to improve the physical performance of professional soccer players, while also pointing out limitations of drills. Less is known about the current methods used in an ecological context and the extent to which evidence-based considerations are applied. Knowledge of current practices might also enable to identify pitfalls in successful implementation and/or deficiencies in the communication of scientific knowledge. Thus, the aim of this study was to quantify and compare the load that players experience in an ecological context during drills that are frequently used, and in which there is an intention to improve the players’ physical capacities. Therefore, a retrospective observational cohort study was conducted over a 14-month period, analyzing 9 load measures during training drills of 39 players of a team competing in the highest Swiss league. The load experienced by players was statistically significant different between the assessed drill categories for each load measure (all p < .001). This indicates different drills provide different stimuli. HIIT drills proved to be a more powerful tool of getting players to cover distances at high-speed and to spend time at an intensity ≥90% HR max compared to sided games. The sprint distance of players was very low in all sided games and in most cases also in HIIT drills, in the latter the players also hardly performed any deceleration. In small goal-oriented sided games, players covered a greater distance per minute when outside floaters were present. Particularly regarding an improvement of the players’ aerobic capacity, the present data emphasize the relevance for coaches to ensure an appropriate exposure. In general, the importance of individual load management in professional soccer is highlighted.
Background/Aims Creatine supplementation is an effective ergogenic nutrient for athletes, as well as for people starting a health or fitness program. Resistance training has previously been identified as an important method of increasing muscle mass and strength, especially in people with cancer to avoid sarcopenia. The potential of creatine supplementation for adaptations produced by resistance training in patients with cancer is still unknown. The primary aim of this study is to evaluate the effectiveness of a supervised resistance training program intervention with and without creatine supplementation in patients with breast cancer. Methods Is a multicentre, randomized, blind, placebo-controlled study. Patients will be randomly assigned to a control group and 2 experimental groups. The first training resistance group (RG) will perform resistance training, while the second experimental resistance-creatine group will perform the same resistance training as the RG and will also receive a 5 g/d creatine supplementation during the intervention. RG participants will follow the same daily dosing protocol, but in their case, with dextrose/maltodextrin. Resistance training will be a 16-week supervised workout that will consist of a series of resistance exercises (leg press, knee extension, knee bends, chest press, sit-ups, back extensions, pull-ups, and shoulder press) that involve the largest muscle groups, performed 3 times a week on nonconsecutive days. Both the RG and the resistance-creatine group will receive a supplement of soluble protein powder (20 to 30 g) daily. Conclusions This intervention will help to better understand the potential of nonpharmacological treatment for improving strength and well-being values in patients with breast cancer with and without creatine supplementation.
Full-text available
Endurance athletes offer unique physiology and metabolism compared to sedentary individuals. Athletes training at high intensities for prolonged periods are at risk for gastrointestinal disturbances. An important factor in endurance performance is the integrity and function of the gut barrier, which primarily depends on heavily O -glycosylated mucins. Emerging evidence shows a complex bidirectional dialogue between glycans on mucins and gut microorganisms. This review emphasizes the importance of the crosstalk between the gut microbiome and host mucus mucins and some of the mechanisms underlying this symbiosis. The contribution of mucin glycans to the composition and functionality of the gut microbiome is discussed, as well as the persuasive impact of the gut microbiome on mucin composition, thickness, and immune and metabolic functions. Lastly, we propose natural and synthetic glycans supplements to improve intestinal mucus production and barrier function, offering new opportunities to enhance endurance athletes’ performance and gut health.
Cardiovascular disease, especially heart failure (HF) is the leading cause of death in patients with diabetes. Individuals with diabetes are prone to a special type of cardiomyopathy called diabetic cardiomyopathy (DCM), which cannot be explained by heart diseases such as hypertension or coronary artery disease, and can contribute to HF. Unfortunately, the current treatment strategy for diabetes-related cardiovascular complications is mainly to control blood glucose levels; nonetheless, the improvement of cardiac structure and function is not ideal. The transient receptor potential cation channel subfamily V member 1 (TRPV1), a nonselective cation channel, has been shown to be universally expressed in the cardiovascular system. Increasing evidence has shown that the activation of TRPV1 channel has a potential protective influence on the cardiovascular system. Numerous studies show that activating TRPV1 channels can improve the occurrence and progression of diabetes-related complications, including cardiomyopathy; however, the specific mechanisms and effects are unclear. In this review, we summarize that TRPV1 channel activation plays a protective role in the heart of diabetic models from oxidation/nitrification stress, mitochondrial function, endothelial function, inflammation, and cardiac energy metabolism to inhibit the occurrence and progression of DCM. Therefore, TRPV1 may become a latent target for the prevention and treatment of diabetes-induced cardiovascular complications.
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In brief: American mile record holder Steve Scott was tested for maximal aerobic capacity and running economy on three occasions over nine months, a period that included off-season, preseason, the indoor season, and the early part of the outdoor season. The laboratory results demonstrated that Scott's training raised his maximal aerobic capacity approximately 8% and improved his running economy 5%. In comparing Scott's data with that of former American record holder Jim Ryun, it appears that Scott's better economy, which allowed him to perform at a lower percentage of his maximal aerobic capacity, was the essential difference between the two runners.
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The accumulated O2 deficit (the difference between the estimated energy demand and the actual O2 uptake) was determined during intense exhaustive exercise (2-7 min) in elite athletes, and its relationship with muscle buffer capacity, muscle enzymes and muscle morphology was examined. Five oarsmen, fifteen soccer players, and fourteen distance runners ran, and three sprint cyclists cycled intensely to exhaustion (2-7 min). The oarsmen also performed exhaustive rowing. Blood lactate was measured immediately after several submaximal exercise bouts. A muscle biopsy was taken at rest from m. gastrocnemius of the soccer players and runners, and from m. vastus lateralis of the cyclists. The accumulated O2 deficit for the oarsmen, soccer players and runners during treadmill running was 47.3 (range: 29.6-62.4), 49.5 (34.3-73.7) and 51.9 (26.5-85.5) ml O2 equivalents ("O2-Eq").kg-1 b.w., respectively, and it was 56.5 (47.5-73.2) ml "O2-Eq".kg-1 for the cyclists during cycling. The O2 deficit was not related to blood lactate during submaximal exercise, muscle enzyme activity (citrate synthase, 3-hydroxyacyl-CoA-dehydrogenase, lactate dehydrogenase), number of muscle capillaries, %ST fibres or muscle buffer capacity. The accumulated O2 deficit was 36% higher (p < 0.05) during rowing compared to running. The present data suggest that the anaerobic energy production during intense exercise is related to the muscle mass involved. However, it appears that the anaerobic energy turnover is not determined by muscle fibre type distribution, muscle buffer capacity or muscle endurance capacity.
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Relationships between muscle oxidative capacity, anemia, endurance, whole-body maximal O2 consumption (V̇O2 (max)), and V̇O2(max) work load (maximal treadmill speed at 15% grade, rat weight constant) were investigated in iron deficiency and during dietary iron repletion. Young rats were made severely iron deficiency by a diet containing 2 mg iron/kg. Control animals received the same diet but with 50 mg iron/kg. Blood hemoglobin was decreased to 3.6 ± 0.5 g/dl compared to 13.7 ± 0.6 in control animals. The combination of decreased mitochondrial enzyme specific activities and a 30% reduction in the mitochondrial content of muscle resulted in 60-85% decreases in muscle oxidative capacities. V̇O2 (max) and V̇O2(max) work load were both 50% lower in deficient rats, whereas endurance capacity was 90% lower in deficient animals than controls. The iron-sufficient control diet was then given to deficient rats and the course of dietary repletion followed. Hemoglobin increased substantially within 3 days in parallel with V̇O2(max) and V̇O2(max) work load. No significant improvements in mitochondrial bioenergetic functions, mitochondrial content of muscle, muscle oxidative capacity, or endurance capacity occurred until the 5th day. We conclude that V̇O2(max) and V̇O2(max) work load capacity were not limited by muscle oxidative capacity. Conversely, endurance capacity was not restricted by oxygen supply, but was primarily determined by the oxidative capacity of muscle.
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LUCÍA, A., J. HOYOS, M. PÉREZ, A. SANTALLA, and J. L. CHICHARRO. Inverse relationship between V̇O2max and economy/efficiency in world-class cyclists. Med. Sci. Sports Exerc., Vol. 34, No. 12, pp. 2079–2084, 2002. Purpose: To determine the relationship that exists between V̇O2max and cycling economy/efficiency during intense, submaximal exercise in world-class road professional cyclists. Methods: Each of 11 male cyclists (26 ± 1 yr (mean ± SEM); V̇O2max: 72.0 ± 1.8 mL·kg−1·min−1) performed: 1) a ramp test for V̇O2max determination and 2) a constant-load test of 20-min duration at the power output eliciting 80% of subjects’ V̇O2max during the previous ramp test (mean power output of 385 ± 7 W). Cycling economy (CE) and gross mechanical efficiency (GE) were calculated during the constant-load tests. Results: CE and GE averaged 85.2 ± 2.3 W·L−1·min−1 and 24.5 ± 0.7%, respectively. An inverse, significant correlation was found between 1) V̇O2max (mL·kg−0.32·min−1) and both CE (r = −0.71;P = 0.01) and GE (−0.72;P = 0.01), and 2) V̇O2max (mL·kg−1·min−1) and both CE (r = −0.65;P = 0.03) and GE (−0.64;P = 0.03). Conclusions: A high CE/GE seems to compensate for a relatively low V̇O2max in professional cyclists.
To investigate the effects of simultaneous explosive-strength and endurance training on physical performance characteristics, 10 experimental (E) and 8 control (C) endurance athletes trained for 9 wk. The total training volume was kept the same in both groups, but 32% of training in E and 3% in C was replaced by explosive-type strength training. A 5-km time trial (5K), running economy (RE), maximal 20-m speed ( V 20 m ), and 5-jump (5J) tests were measured on a track. Maximal anaerobic (MART) and aerobic treadmill running tests were used to determine maximal velocity in the MART ( V MART ) and maximal oxygen uptake (V˙o 2 max ). The 5K time, RE, and V MART improved ( P < 0.05) in E, but no changes were observed in C. V 20 m and 5J increased in E ( P < 0.01) and decreased in C ( P < 0.05).V˙o 2 max increased in C ( P < 0.05), but no changes were observed in E. In the pooled data, the changes in the 5K velocity during 9 wk of training correlated ( P< 0.05) with the changes in RE [O 2 uptake ( r = −0.54)] and V MART ( r = 0.55). In conclusion, the present simultaneous explosive-strength and endurance training improved the 5K time in well-trained endurance athletes without changes in theirV˙o 2 max . This improvement was due to improved neuromuscular characteristics that were transferred into improved V MART and running economy.
Seven endurance exercise-trained subjects were studied 12, 21, 56, and 84 days after cessation of training. Maximal O2 uptake (VO2 max) declined 7% (P less than 0.05) during the first 21 days of inactivity and stabilized after 56 days at a level 16% (P less than 0.05) below the initial trained value. After 84 days of detraining the experimental subjects still had a higher VO2 max than did eight sedentary control subjects who had never trained (50.8 vs. 43.3 ml X kg-1 X min-1), due primarily to a larger arterial-mixed venous O2 (a-vO2) difference. Stroke volume (SV) during exercise was high initially and declined during the early detraining period to a level not different from control. Skeletal muscle capillarization did not decline with inactivity and remained 50% above (P less than 0.05) sedentary control. Citrate synthase and succinate dehydrogenase activities in muscle declined with a half-time of 12 days and stabilized at levels 50% above sedentary control (P less than 0.05). The initial decline in VO2 max was related to a reduced SV and the later decline to a reduced a-vO2 difference. Muscle capillarization and oxidative enzyme activity remained above sedentary levels and this may help explain why a-vO2 difference and VO2 max after 84 days of detraining were still higher than in untrained subjects.
Muscle biopsies were obtained from the gastrocnemius of 14 elite distance runners, 18 middle distance runners, and 19 untrained men. The middle distance runners were all highly trained, but had significantly slower performance times than the elite runners at distances greater than 3 miles. Fiber composition and mean cross sectional areas were determined from muscle sections incubated for histochemical activity. A portion of the specimen was used to determine succinate dehydrogenase (SDH), lactate dehydrogenase (LDH) and phosphorylase activities. All subjects were tested for maximal oxygen uptake on a treadmill. As previously demonstrated by others, the elite runners' muscles were characterized by a high percentage (79%) of slow twitch (ST) fibers. On the average, the cross sectional area of their ST fibers was found to be 22% larger than the FT fibers (P<0.05). SDH activity of whole muscle homogenates from elite and middle distance runners was 3.4 and 2.8 fold greater, respectively, than that measured in the untrained men. Since the LDH and phosphorylase activities were similar for the runners and untrained men, it appears that training for distance running has little influence on the enzymes of glycogenolysis.