Professional Documents
Culture Documents
Physiology of Professional
Road Cycling
Alejandro Luca,1,2 Jess Hoyos2,3 and Jos L. Chicharro2,4
1
2
3
4
Contents
Abstract
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Main Characteristics of the Sport . . . . . . . . . . . . . . . . . . . . . . .
1.1 Racing Calendar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2 Tour Races . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2.1 Flat Stages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2.2 Time Trials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2.3 High Mountain Ascents . . . . . . . . . . . . . . . . . . . . . . .
2. Anthropometric Variables . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3. Physiological Variables . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1 Maximal Power Output and Maximal Oxygen Uptake . . . . . . . .
3.2 Submaximal Variables . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.1 Anaerobic Threshold . . . . . . . . . . . . . . . . . . . . . . . .
3.2.2 Isocapnic Buffering and Hypocapnic Hyperventilation Phases
3.2.3 Oxygen Uptake Kinetics during Submaximal Exercise . . . . .
4. Cardiovascular Responses and Adaptations . . . . . . . . . . . . . . . . .
4.1 Heart Rate (HR) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.1 The HR Response to Incremental Exercise: the Conconi Test .
4.1.2 HR as an Indicator of Exercise Intensity . . . . . . . . . . . . . .
4.2 Cardiovascular Adaptations . . . . . . . . . . . . . . . . . . . . . . .
4.2.1 Cardiac Adaptations . . . . . . . . . . . . . . . . . . . . . . . .
4.2.2 Vascular Adaptations . . . . . . . . . . . . . . . . . . . . . . . .
5. Pulmonary Responses and Adaptations . . . . . . . . . . . . . . . . . . .
6. Physiological Adaptations during a Sports Season . . . . . . . . . . . . .
6.1 Maximal Variables . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.2 Submaximal Variables: Metabolic and Neuromuscular Adaptations
7. Endocrine System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8. Haematological Variables and Blood Doping . . . . . . . . . . . . . . . .
9. Nutritional Habits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.1 Tour Races . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.2 Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
10.Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Abstract
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
325
326
326
326
326
327
327
328
328
328
328
328
329
329
330
330
330
330
331
331
332
332
332
333
333
333
334
334
334
335
335
326
Luca et al.
such as the Tour de France last 21 days (~100 hours of competition) during which
professional cyclists (PC) must cover >3500km. In some phases of such a demanding sport, on the other hand, exercise intensity is surprisingly high, since
PC must complete prolonged periods of exercise (i.e. time trials, high mountain
.
ascents) at high percentages (~90%) of maximal oxygen uptake (V O2max) [above
the anaerobic threshold (AT)]. Although numerous studies have analysed the
physiological responses of elite, amateur level road cyclists during the last 2
decades, their findings might not be directly extrapolated to professional cycling.
Several studies have recently shown that PC exhibit some remarkable physiological responses and adaptations such as: an efficient respiratory system (i.e. lack
of tachypnoeic shift at high exercise intensities); a considerable reliance on fat
metabolism even at high power outputs; or several neuromuscular adaptations
(i.e. a great resistance to fatigue of slow motor units). This article extensively
reviews the different responses and adaptations (cardiopulmonary system, metabolism, neuromuscular factors or endocrine system) to this sport. A special emphasis is placed on the evaluation of performance both in the laboratory (i.e. the
controversial Conconi test, distinction between climbing and time trial ability,
etc.) and during actual competitions such as the Tour de France.
327
Table I. Main characteristics of flat and high mountain stages, and time trials for professional cyclists in tour races[1-7]
FS
HMS
TT
~200
~200
4-5
5-6
~1
Low-to-moderate
High
Prevailing metabolism
Aerobic (fat)
Distance (km)
~45
Cadence (rpm)
~90
~70
~90
Cycling position
Traditional (sitting)
Main requirements
Technical
Physiological
Specific concerns
Moderate hypoxia
Aerodynamics
<250W
CHO = carbohydrate; FS = flat stages; HMS = high mountain stages; TT = time trials.
328
Luca et al.
329
.
It is well documented that oxygen uptake (VO2)
tends to slowly rise during any constant-load cycle
ergometer test involving sustained lactic acidosis
[i.e. above the lactate threshold (LT) or above VT]:
this phenomenon is called the slow component of
.
VO2 and is typically defined as the continued rise
.
in VO2 beyond the third minute of exercise.[27] Although several aetiological factors have been proposed (i.e. lactic acidosis, temperature, potassium
or cardiorespiratory work), what appears to be the
most important factor is a progressive recruitment
of less efficient motor units (i.e. type II fibres),
with exercise duration.[27] In this regard, we recent.
ly studied VO2 kinetics in a group of PC during
20-minute cycle ergometer tests performed at 400W
.
or ~80% of VO2max.[22] Gas exchange and blood
variables and electromyographic (EMG) data from
the vastus lateralis muscle were recorded during
the tests. The average magnitude of the slow component (7.6 ml/min) was considerably lower than
that reported by previous research (22 ml/min) using the same cycle ergometer protocol.[28]
Such a finding is suggestive of a great cycling
efficiency of PC which is thought to contribute to
their renowned ability to sustain high workloads
over long periods (i.e. >60 minutes), as shown by
previous field studies.[1-3] On the other hand, EMG
.
data suggested that the primary origin of the VO2
slow component in PC is not attributable to neuromuscular fatigue, at least at intensities up to 80%
.
of VO2max. These athletes, indeed, exhibit a considerable resistance to fatigue of recruited motor units,
at least at submaximal intensities. Such adaptation
is probably attained after years of highly demanding training (i.e. ~35 000km per year) as suggested
Sports Med 2001; 31 (5)
330
in a previous study which compared the physiological response of PC with that of their elite, amateur
counterparts.[17]
Although further research is needed, the origin
.
of the VO2 slow component in PC appears to be
multifactorial, with a non-negligible contribution
of central factors.[22] On the other hand, there seems
to exist an inverse correlation between pre-exercise
levels of thyroid hormones and the magnitude of
the slow component in these athletes.[29] This in
turn suggests, at least partly, an involvement of thyroid function on their neuromuscular efficiency during constant load cycling.[29]
Luca et al.
4. Cardiovascular Responses
and Adaptations
4.1 Heart Rate (HR)
4.1.1 The HR Response to Incremental Exercise:
the Conconi Test
Although a great controversy exists in the literature concerning the so-called Conconi test, previous research by Conconis team and by other authors has confirmed both the existence of a deflection
point (HRd) in the heart rate (HR) response to an
incremental exercise protocol and its coincidence
with the AT in elite athletes (including PC).[30] Indeed, the Conconi test, applicable in field conditions, has become one of the most frequently used
exercise tests in sports medicine. Because of the
ease of repeated measurements, it is commonly used
by elite athletes such as European PC to establish
optimum training intensity.
We have recently evaluated the applicability of
this test for AT determination in 21 PC using a ramplike protocol (workload increases of 25 W/min).[20]
The later type of test was chosen following the most
recent recommendations made by Conconi et al.[30]
for HRd determination. According to Conconis team,
the fact that some authors have previously failed to
detect HRd may be explained by the protocol used,
such as step-like workload increases rather than the
more gradual ramp method, which allows increases
in HR of <8 beats/min per min of exercise. The HR
response showed a deflection point in most PC (~2/3)
and was linear in the rest (~1/3). When occurring
Adis International Limited. All rights reserved.
331
190
180
170
y = 0.163x + 97.952
(r = 0.984)
HR (beats/min)
160
150
140
130
120
110
y = 0.274x + 53.147
(r = 0.972)
100
90
200
300
400
500
Workload (W)
Fig. 1. Determination of the point of heart rate deflection (HRd) in 1 professional cyclist (former world champion) from the heart rate
(HR)/workload (W) relationship. At times (such as in this example), the initial data points (i.e. below 100 to 110 beats/min) do not fall
on the straight line and should be ignored according to the methodology of Conconi and co-workers.[30] (From Lucia et al.,[20] with
permission).
332
derived cardiac dimensions in 21 top-level PC, including world champions and winners of major 3week tour races (mean age of 25 years and mean
competition experience in the category of 4 2
years).[20] We found a lower degree of ventricular
hypertrophy (i.e. mean ventricular mass index of
~116 g/m2) compared with the study by Rodrguez
Reguero et al.[38] Our data were similar to those
reported in previous studies for highly trained endurance athletes in general,[41-44] that is, PC show
a cardiac profile expected of endurance athletes with
predominantly eccentric left ventricular hypertrophy (enlarged left ventricular end-diastolic internal
diameter and proportional increase in wall thickness).
The incidence of electrocardiographic abnormalities (i.e. ST-T segment alterations) is very low among
PC.[34,38] Even extreme endurance events such as
3-week races do not appear to have a deleterious
effect on the hearts of PC. In a study conducted
during the Giro dItalia, Bonetti and co-workers
showed no evidence of myocardial damage throughout the 3-week period in any of the participants
using a marker of myocardial ischaemia such as
cardiac troponin T.[45]
4.2.2 Vascular Adaptations
Luca et al.
aerodynamic cycling positions.[51] Surgical mobilisations or reconstructions of the iliac arteries are
possible types of treatment.[51] Although long term
follow-up reports are lacking, some Spanish PC
have performed successfully after surgery (unpublished data).
5. Pulmonary Responses
and Adaptations
Pulmonary volumes of PC do not differ from
those of amateur, elite counterparts (i.e. vital capacity of ~6.0L for a height of 175 to 180cm).[24]
.
Similarly, maximal values of VE do not differ between PC and amateurs (180 to 190 L/min in both
groups).[17,24,52] In contrast, the breathing pattern
of the former during incremental exercise shows 2
unique characteristics, compared with other well
trained endurance athletes (including amateur cyclists):[53-55] (i) a prolongation of expiratory duration, especially at high workloads; and (ii) a lack
of tachypnoeic shift at high exercise intensities,
that is, tidal volume (VT) does not show a plateau at
near-maximal intensities.[24] Both characteristics
might be interpreted as an adaptation to the demands of professional cycling.[24] The fact that PC
do not adopt the tachypnoeic shift can be viewed
as a particularly efficient respiratory adaptation to
training from both metabolic and mechanical
points of views.[24]
6. Physiological Adaptations during a
Sports Season
The prevailing specific adaptations to training
incurred by already well-trained endurance athletes
is, in general, a controversial issue. Four prospective reports have evaluated the physiological adaptations which occur in PC as a response to training
and competition during the main part (~7 months)
of a typical sports season.[14,19,56,57] The sports season of PC generally includes 3 different periods in
terms of training volume and/or intensity, i.e. precompetition or training (winter), competition (spring
and summer, usually with an active rest period in
between) and postcompetition or active rest periods (fall) [table II].[14,19,56,57] During 2 to 3 weeks
Sports Med 2001; 31 (5)
.
Some authors have shown that the VO2max of
elite cyclists increases during the season.[14,58,59]
The data from our laboratory,[56] however, are in line
with those of most previous studies which showed
no significant effects of training intervention on
.
VO2max in well-trained athletes such as runners,[60]
swimmers,[61] and elite amateur cyclists.[62] Further, we have detected no difference in maximal
power output throughout the season.[19,56] Based
on these findings, it seems that once a certain training status is reached (i.e. professional cycling category), further increases in training intensity and
volume are no longer associated with improvements
.
in VO2max. It would appear that other physiological
characteristics, such as the ability to maintain high
.
percentages (i.e. 90%) of VO2max during prolonged
periods (>30 minutes), play a more relevant role in
successful endurance cycling. It is consequently
felt that training programmes should be designed
to improve this ability.
6.2 Submaximal Variables: Metabolic and
Neuromuscular Adaptations
In a recent study,[57] we found no overall training effect throughout the season in the ventilatory
.
response of 13 PC during a ramp-protocol (i.e. VE,
VT, ventilatory equivalents for O2 and CO2, timing of respiration, etc.), despite a significant improvement in performance (i.e. increases in both the
.
power output and the percentage of VO2max eliciting
RCP). In contrast, several metabolic and neuromuscular variables showed major changes during the
season in the same participants, such as: (i) lower
circulating lactate levels and possibly increased reliance on oxidative metabolism at a given submaximal intensity (up to 400W); and (ii) an enhanced
recruitment of motor units in active muscles, as
suggested by EMG data.[56] No significant improvements, however, were found in the cyclists buffering capacity during the season (i.e. no significant changes in blood pH and HCO3- levels for a
Adis International Limited. All rights reserved.
333
Average weekly
training (km)
Rest
(fall)
Precompetition Competition
(winter)
(spring-summer)
~270
~700
~800
Exercise intensitya
low (%)
~88
~78
~77
moderate (%)
~11
~17
~15
high (%)
~1
~5
~8
.
Exercise intensity: low (<65% VO2max), moderate (65-90%
.
.
VO2max), high (>90% VO2max).
.
VO2max = maximal oxygen uptake.
334
literature concerning the adaptations of other hormonal systems to professional cycling. It has nevertheless been reported that the resting activity of
the renin-angiotensin-aldosterone system is normal
in these athletes.[39]
8. Haematological Variables and
Blood Doping
Sports haematology and blood doping have become a contentious topic in elite sports in the last
3 decades. Since recombinant human erythropoietin (r-HuEPO) is demonstrably effective in increas.
ing haemoglobin levels, VO2max and physical work
capacity,[66-68] the lack of a reliable test (until most
recently) to confirm its use may have presumably
induced many PC to experiment with this drug over
the last 15 years. In fact, the possible health risks
of hyperviscosity and thrombogenicity associated
with the misuse of this drug could have caused the
mysterious deaths of some European riders between
1987 and 1990.[69] The suspected association between elite cycling and blood doping with r-HuEPO
was confirmed by both the discovery of vials of this
drug in a car belonging to a professional cycling
team during the 1998 Tour de France and the recent
finding of abnormally high erythropoietin levels in
several frozen urine samples collected during the
aforementioned race.[70]
To dissuade the use of r-HuEPO and to minimise
the health risks associated with the abuse of this
drug, the International Cycling Union has imposed
an upper limit of 50% on haematocrit levels since
1997. Disadvantages of using this threshold however, include: postural effects,[71] ease of manipulations through interventions such as saline infusion,[68]
and large natural variations among individuals.[68,72]
Concerning the latter, it has been recently documented that a subset of endurance athletes including elite cyclists (i.e. 2 to 8% of total) might naturally surpass the 50% threshold.[73-75] In fact, some
authors have suggested that those athletes with high
haematocrit levels (i.e. close to 50%) might be more
genetically predisposed to perform successfully in
endurance sports.[73] Other authors, in contrast, have
reported haematocrit levels consistently below 50%
Adis International Limited. All rights reserved.
Luca et al.
Few studies have evaluated the feeding pattern of PC during 3-week tour races, in both actual[23,79] and simulated conditions.[80,81] During
these races, average daily energy intake is as high
as 23 to 25MJ.[23,79] One of the main concerns in
these types of events is to replenish bodily glycogen stores within 18 hours (from the end of each
daily stage, at ~5pm, to the beginning of the next one,
at ~12pm) over a 3-week period. Although reports
with muscle biopsies are not available during acSports Med 2001; 31 (5)
tual cycling races, cyclists carbohydrate intake during these extreme events appears to be sufficient
(~60% of total caloric intake or >800g/24h period
or 12 to 13 g/kg bodyweight per day),[23,79] based
on the recommendations of previous research.[82,83]
In particular, the high carbohydrate intake during
the first 6 hours after the race (1.1 g/kg bodyweight)
is crucial.[79]
Additionally, an interesting factor for muscle glycogen resynthesis is the addition of protein (0.35
g/kg bodyweight) to carbohydrate in the first hour
after exercise.[79] The latter is achieved by consuming prepared semi-solid foods consisting basically
of a mixture of cereals, dairy products and fruits.
Carbohydrate intake during exercise, however, is
rather low (average 25 g/h),[79] and below the recommendations (30 to 60 g/h) for maintenance of a
high rate of carbohydrate oxidation during prolonged
strenuous exercise.[83]
Another remarkable characteristic is the high
protein intake (approximately 3 g/kg bodyweight
per 24 hour period),[23,79] clearly above that recommended for endurance athletes in general (1.2 to
1.4 g/kg bodyweight per day).[84] This protein intake is mainly because of the high overall energy
intake, since the relative contribution of protein to
energy is not higher than 14 to 18%.[23,79] On the
other hand, the diet of PC during tour races provides 23 to 25% of energy from fat, with biscuits
and confectionery providing as much as 27 to 43%
of this energy substrate.[23,79]
There exists considerable variation regarding
the fluid intake reported during tour races, i.e. 3.3L
per 24 hours in the study by Garca-Rovs et al.[79]
versus 6.7L per 24 hours in that by Saris et al.[23]
Such variability comes mainly from the carbohydrate feeding pattern adopted during exercise, since
the participants in the study by Saris et al. consumed a large amount of carbohydrates in the form
of sports drinks (4L per stage).
9.2 Training
335
tein intake during the latter.[78] Vitamin intake during both training and competition periods seems to
be well above the recommended daily amount for
healthy adult males, especially when considering
that most riders consume vitamin supplements.[23,78]
10. Conclusion
To date, some descriptive studies have analysed
the physiological responses and adaptations to such
an extreme endurance sport as professional road
cycling.[1-6,9,10,14-22,24,29,34,36-39,45,56,57] Furthermore,
a great amount of data have been collected during
actual races. As a result, the body of knowledge concerning cycling physiology has considerably increased in the last decade. For instance, we know that
the results from previous research with elite, amateur
cyclists, might not be directly extrapolated to professional riders. Further nondescriptive research is however needed in the field. Given the great performance
level of the participants, this sport could serve as a
model to better understand the mechanisms involved
in the human responses/adaptations to endurance exercise.
Acknowledgements
We are indebted to Asociacin Deportiva Banesto for
supporting our research.
References
1. Luca A, Hoyos J, Carvajal A, et al. Heart rate response to
professional road cycling: the Tour de France. Int J Sports
Med 1999; 20: 167-72
2. Fernndez-Garca B, Prez-Landaluce J, Rodrguez-Alonso M,
et al. Intensity of exercise during road race pro-cycling competition. Med Sci Sports Exerc 2000; 32: 1002-6
3. Padilla A, Mujika I, Cuesta G, et al. Level ground and uphill
cycling ability in professional road cycling. Med Sci Sports
Exerc 1999; 31: 878-85
4. Luca A, Hoyos J, Chicharro JL. Preferred pedalling cadence in
professional cycling. Med Sci Sports Exerc. In press
5. Luca A, Hoyos J, Chicharro JL. Physiological response to professional road cycling: climbers vs. time trialists. Int J Sports
Med 2000; 21: 505-12
6. Padilla S, Mujika I, Orbaanos J, et al. Exercise intensity during
competition time trials in professional road cycling. Med Sci
Sports Exerc 2000; 32: 850-6
7. Bassett DR, Chester JR, Passfield L, et al. Comparing cycling
world hour records, 1967-1996: modeling with empirical data.
Med Sci Sports Exerc 1999; 31: 1665-76
8. McCole SD, Claney K, Conte J-C, et al. Energy expenditure
during bicycling. J Appl Physiol 1990; 68: 748-53
336
Luca et al.
30. Conconi F, Grazzi G, Casoni C, et al. The Conconi test: methodology after 12 years of application. Int J Sports Med 1996;
17: 509-19
31. Skinner JS, McLellan TH. The transition from aerobic to anaerobic metabolism. Res Q Exerc Sport 1980; 51: 234-8
32. Jeukendrup A, Van diemen A. Heart rate monitoring during
training and competition in cyclists. J Sports Sci 1998; 16
Suppl.: S91-S99
33. Wilmore JH, Stanforth PR, Gagnon J, et al. Endurance exercise
training has a minimal effect on resting heart rate: The HERITAGE Study. Med Sci Sports Exerc 1996; 28: 829-35
34. Nishimura T, Yamada Y, Kawai CH. Echocardiographic evaluations of long-term effects of exercise on left ventricular hypertrophy and functions in professional bicyclists. Circulation
1980; 61: 832-40
35. Cohen A, Diebold B, Raffoul H, et al. Evaluation par echocardiographie Doppler des functions systolique et diastolique
du ventricule gauche du coeur datlte. Arch Mal Coeur 1989;
82: 55-62
36. Missault L, Duprez D, Jordaens L, et al. Cardiac anatomy and
diastolic filling in professional road cyclists. Eur J Appl Physiol 1993; 66: 405-8
37. Urhausen A, Kinderman W. Cardiac anatomy and diastolic filling in professional road cyclists [letter]. Eur J Appl Physiol
1993; 67: 567-8
38. Rodrguez Reguero JJ, Iglesias Cubero G, Lpez de la Iglesia
J, et al. Prevalence and upper limit of cardiac hypertrophy in
professional cyclists. Eur J Appl Physiol 1995; 70: 375-8
39. Iglesias Cubero G, Rodriguez Reguero JJ, Terrados N, et al.
Aldosterone levels and cardiac hypertrophy in professional
cyclists. Eur J Appl Physiol 1995; 16: 475-7
40. Abergel E, Linhart A, Chatellier G, et al. Vascular and cardiac
remodeling in world class professional cyclists. Am Heart J
1998; 136: 818-23
41. Fagard RH. Athletes heart: a meta-analysis of the echocardiographic experience. Int J Sports Med 1996; 17 Suppl.:
S140-S144
42. Huonker M, Knig D, Keul J. Assessment of left ventricular
dimensions and functions in athletes and sedentary subjects
at rest and during exercise using echocardiography, doppler
sonography and radionuclide ventriculography. Int J Sports
Med 1996; 17 Suppl.: S173-S179
43. Pelliccia A, Maron BJ, Spataro A, et al. The upper limit of
physiologic hypertrophy in highly trained elite athletes. N
Engl J Med 1991; 324: 295-301
44. Kaimal KP, Franklin BA, Moir TW, et al. Cardiac profiles of
national-class race walkers. Chest 1993; 104: 935-8
45. Bonetti A, Tirelli F, Albertini R, et al. Serum cardiac troponin T
after repeated endurance exercise events. Int J Sports Med
1996; 17: 259-62
46. Chevalier JM, Enon B, Walder J, et al. Endofibrosis of the external iliac artery in bicycle racers: an unrecognized pathological state. Ann Vasc Surg 1986; 1: 297-303
47. Rousselet MC, Saint-Andr JP, LHoste PH, et al. Stenotic intimal thickening of the external iliac artery in competition cyclists. Hum Pathol 1990; 21: 524-9
48. Abraham P, Chevalier JM, Leftheriotis G, et al. Lower extremity
disease in sports. Am J Sports Med 1997; 25: 581-4
49. Abraham P, Saumet JL, Chevalier JM. External iliac artery endofibrosis in athletes. Sports Med 1997; 24: 221-6
50. Chevalier JM. Pathologie vasculaire du cycliste. Encyclopedie
Medico-Chirurgicale. 1997; A10: 11-675
337
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.