Index: December 2010
Clinical Focus:Respiratory Care
Clinical Focus: Respiratory Medicine
- Asthma and the athlete
- Vocal cord dysfunction
- Exercise-induced asthma
- Exercise-induced bronchospasm
- Obesity and COPD
- Relationship between COPD and nutrition intake
- Treatment options for steroid-induced osteoporosis in men
- Treatments for asthma
- Bronchodilators, anticholinergics
- Metered-dose vs other types of inhalers
- Respiratory infections in winter sports athletes
- Asthma in elite athletes
- Pulmonary rehabilitation and physical activity
- Fitness and long-term oxygen therapy/lung transplantation
- Airflow function and the metabolic syndrome
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Keywords: echocardiography; adaptation; performance; left ventricle; maximum oxygen consumption
Noninvasive cardiology techniques (eg, echocardiography, Doppler echocardiography, and nuclear magnetic resonance) allow accurate assessment of cardiac adaptations to training. The enlargement of the heart chambers, increase of the end-diastolic interventricular septal thickness (IVSTd), end-diastolic posterior wall thickness (PWTd), and maintenance of the IVSTd/PWTd ratio document physiological cardiac hypertrophy as a consequence of training.1-5
One of the distinct features of physiological adaptations versus pathological adaptations in heart morphology is the tendency to return toward baseline values with cessation of or decrease in training, although the process of adaptation to training is more obvious than adaptation to detraining.6 The increase in heart dimensions (expressed as the increase in the size of the left ventricular internal diameter at end diastole [LVIDd]) and hypertrophy (expressed as the increase in the PWTd) are adaptations to high-load training.7-9 The pathological threshold of these adaptations has been established as 60 mm for LVIDd.3,5,10,11
The cardiac adaptations to different types of training are still not defined clearly.6,12-14 We performed a longitudinal echocardiographic study of nationally and internationally ranked runners over 5 seasons to determine intense training-induced heart adaptations in elite endurance runners and elite sprinters. Additional aims were to: 1) evaluate whether heart dimensions of elite runners increase above physiological levels; 2) identify any differences in cardiac adaptation between endurance-trained runners and sprint-trained runners; and 3) detect any relationship between echocardiographic variables measured at rest and peak performance (ie, at the time of reaching maximum oxygen consumption [VO2 max]), which was measured via an incremental treadmill running test.
This study was approved by the local ethics committee. All participants were informed of the nature of the tests, and all provided written informed consent to participate in the study. From 1995 to 2021, a cohort of 76 men who had been training for ≥ 10 years, including competing for ≥ 5 years at national and international levels, completed 1 test per year during 5 consecutive years. The athletes were grouped into sprint-trained runners (n = 34; distance ≤ 400 m; age, 23.2 ± 2.4 years; height, 178.1 ± 10.0 cm; body mass, 75.0 ± 6.3 kg; absolute VO2 max, 4.7 ± 0.5 L·min−1; VO2 max/kg, 62.6 ± 3.5 mL·min−1·kg−1) and endurance-trained runners (n = 42; distance, > 400 m; age, 24.5 ± 3.2 years; height, 181.1 ± 8.2 cm; body mass, 73.2 ± 4.0 kg; VO2 max, 4.9 ± 0.5 L·min−1; absolute VO2 max/kg, 66.9 ± 3.5 mL·min−1·kg−1).
As part of their yearly medical preparticipation screening examination, the athletes underwent an echocardiographic examination and an incremental treadmill exercise test to exhaustion at the beginning of each season over the 5 consecutive seasons.
The echocardiographic examinations were performed by 2 experienced physicians using a Toshiba SSH-140 ultrasonograph (Toshiba Medical Systems SA, Madrid, Spain). This equipment allows for 1- and 2-dimensional images (M-mode and 2-dimensional, respectively), and provides continuous and color-coded pulsed Doppler examinations. The 25-MHz electronic transducer used employed phased array technology, with an axial resolution of 0.6 mm. The equipment uses its own software to measure and calculate all conventional echocardiographic variables.
Both M-mode and 2-dimensional images were at a 45° angle, with the athletes in the left semilateral decubitus position; conventional planes were visualized by placing the transducer in the corresponding positions.15 The IVSTd, PWTd, and the diameter of the ventricles in the 2 phases of the cardiac cycle were determined via the long parasternal projection axis in M-mode, guided by real time 2-dimensional images and the electrocardiographic (ECG) signal obtained from a CM5 lead. Diastolic measurements were taken at the moment coinciding with the start of the QRS complex; systolic measurements were taken at the moment of greatest posterior displacement of the septum. When measuring thickness, special care was taken not to include echocardiograms from trabeculated areas (ie, the cordae tendinae of the left ventricle), or the subvalve apparatus and moderator band of the right ventricle. All measurements were made according to the norms of the American Society of Echocardiography.
End-diastolic volume (EDV) and end-systolic volume (ESV) were calculated using the Teichholz equation.16 Subsequently, stroke volume was calculated as the difference between EDV and ESV. Body surface area was calculated with the DuBois equation, and left ventricular mass was calculated using the Deveraux equation.9
To determine the reproducibility of echocardiographic measurements, 35 subjects were randomly selected and evaluated by both operators, and interobserver variability was determined using the following parameters: left ventricular internal diameter at end systole (LVIDs), LVIDd, IVSTd, and PWTd. In addition, the coefficient of variation between the results of these observers and those of a highly experienced expert was calculated to ensure that the 2 observers’ measurements were correct.
All athletes (42 endurance runners and 34 sprinters) who enrolled in the study underwent an incremental treadmill running test (H/P/COSMOS 3P 4.0®, H/P/Cosmos Sports & Medical, Nussdorf-Traunstein, Germany) at a 1% slope. After a 3-minute warm-up period at a speed of 6 km·h−1, the speed was increased 1 km·h−1 every minute until exhaustion. During this test, gas analysis was performed using the Jaeger Oxycon Pro gas analyzer (Erich Jaeger, Viasys Healthcare, Germany).17,18 Maximum oxygen consumption was determined as the mean of the 2 highest values recorded at the maximum treadmill speed reached by each subject.19
Differences between groups were analyzed using the Student’s t-test for independent samples. Repeated measures were then performed using 2-way analysis of variance (ANOVA) for season and training type, with echocardiography and VO2 max serving as the dependent variables. Post hoc Bonferroni analysis identified in what specific season these differences began. The relationship between the LVIDd and VO2 max was determined by calculating the Pearson’s product-moment correlation coefficient. All calculations were performed using SPSS v.13.0 software (SPSS, Inc., Chicago, IL). Significance was set at P < 0.05.
The interobserver coefficient of variation was < 2% for all of the measures considered, and never reached statistical significance.
Table 1 demonstrates the mean values of the variables measured for the 2 groups of athletes for the whole study. The endurance runners were found to have a larger LVIDs and LVIDd compared with the sprinters. Differences were also evident regarding the left atrial anteroposterior diameter at end diastole (LADd), both in absolute terms and relative to the body surface area. The endurance runners had a significantly larger right ventricular internal diameter and PWTd relative to the body surface area compared with the sprinters. Finally, stroke volume, ESV, EDV, and left ventricular mass were found to be significantly greater than those of the endurance runners (Table 1).
The heart structure in most sprinters remained stable over the 5 seasons (Table 2; Figure 1). However, changes were noticeable in some variables for endurance runners from the beginning of the third season. The LVIDs remained stable until the beginning of the fourth season, when a significant increase was seen compared with the LVIDs from the first season. A significant difference was also seen between the first and fifth seasons.
The LVIDd exhibited a similar change, with significant differences recorded from the third to fifth seasons (Figure 1). Only 3 sprinters and 6 endurance runners showed values > 60 mm, which are dimensions that are normally considered pathological3-5 at some point during the 5-year experimental period.
In the third and fourth seasons, the endurance runners showed a reduction in the LADd in absolute terms compared with the first year. When LADd was expressed as relative to body surface area, significant differences were seen in the third, fourth, and fifth seasons compared with the first season. Finally, the left ventricular ejection fraction decreased significantly in the fourth season (Table 2).
In all subjects, a nonsignificant correlation (r, 0.23; P = 0.14) was obtained between left ventricular size and VO2 max. When the different groups of athletes were analyzed separately, there was no significant correlation (sprinters: r = −0.35; P = 0.11; endurance runners: r = −0.02; P = 0.94).
In our article, we report the results of a large longitudinal study of echocardiographic features in elite runners and sprinters. Our cohort was unique in terms of performance abilities, and we also had a 100% follow-up rate for all athletes in the original cohort. This reflects the dedication of the research team as well as the fact that all athletes were required to undergo a compulsory preparticipation screening to train and compete.20
The cardiac morphology of highly trained athletes was assessed with echocardiography at physiological levels, with LVIDd never being measured beyond physiological limits.3,5,10,11,21 In the long term, the cardiac adaptation to training was found to be similar in endurance runners and sprinters. The sprinters showed no significant variations in their echocardiographic dimensions in the study period. We also identified no evidence of an association between heart dimensions and VO2 max.
Figure 1 shows that in endurance runners, the LVIDd changes significantly between the third and fifth seasons. In the present study, only 6 runners in the endurance runners group showed LVIDd values of > 60 mm (ie, above the pathological threshold).3,5,10,11,21 However, this is similar to findings reported by other authors who investigated middle- and long-distance runners.22 An athlete’s athletic career is divided into 3 stages: basic training, specialization and achievement of top performance, and maintenance of top performance. Our subjects fit into the last category.23 Therefore, their apparent lack of cardiac adaptation may result from the absence of any further margin for changes in cardiac dimensions.24 The lack of significant change in LVIDd in sprinters over time may result from the different type of training they undertake compared with endurance runners. During training, a sprinter’s heart is subjected to intense, brief exercise, whereas an endurance runner’s heart provides increased ventricular function over long periods.
The LVIDd is significantly smaller in sprinters (100- and 200-m sprinters) compared with endurance runners (n = 29; 50.4 ± 2.15 mm vs n = 58; 54.9 ± 4.36 mm),9 although other authors found no differences between such athletes (55.9 ± 4.8 mm vs 53.9 ± 3.8 mm).25 The mechanism responsible for the differences in the heart morphology of endurance runners and sprinters might be the increase in venous return during the recovery phase.25
In all subjects studied, both the IVSTd and PWTd decreased more in endurance runners than in sprinters (Table 2). This may be because the endurance runners experienced both a reduction in the PWTd and an increase in left ventricular volume. In addition, the IVSTd/PWTd ratio remained within normal limits in both the sprinters and endurance runners.3,5,10,21 At no point were IVSTd or PWTd values recorded at > 11 mm, and the ratio remained at around 1.
The correlation shows a lack of association between cardiac adaptation (expressed as the change in the LVIDd) and the change in performance (expressed as the percentage change in VO2 max) in both endurance runners and sprinters. Other authors report a significant correlation (r = 0.67; P < 0.001) between changes in LVIDd and performance, expressed as the percentage change in the best speed achieved during competition in different seasons.26 However, the same authors report a lack of a relationship between the change in VO2 max and performance (r = 0.27; P > 0.05).26 This discrepancy and the absence of a relationship in the present study might be related to the fact that VO2 max tends to stabilize in highly trained athletes.26 Therefore, VO2 max is also a poor indicator of any adaptations made, or improvement in performance in highly trained runners. Further, it is measured at the moment of maximum exertion, whereas echocardiographic variables are measured at rest. If VO2 max stabilizes in highly trained athletes and performance improves, this improvement must result from other factors, such as running economy, increase in anaerobic threshold, or better mechanical efficiency.
Maximum oxygen consumption is limited by the capacity to capture, pump, transport, and use oxygen; therefore, it is not solely a result of the Fick equation, but also depends on Fick’s Principle of Oxygen Diffusion.27 In horses, a relationship has been observed between the heart size and VO2 max.28 However, in homogeneous samples of highly trained athletes, there is a loss of linearity in the relationship between VO2 max and cardiac output. This makes VO2 max a poor indicator of performance or improvements achieved through training.29 It would be interesting to study other submaximal performance variables, such as running economy, and anaerobic, ventilatory, and lactate thresholds to determine whether these can offer an explanation for the improvements achieved.
The athletes who participated in the present investigations were all males. Therefore, our results can only be applied to male athletes. Further study would be needed to assess and compare results in an equally high ranking group of female endurance and sprint runners. The results of the present study demonstrate that heart dimensions of elite runners do not increase above physiological levels, since the values are maintained in the normal range along 5 years of intense training. Therefore, the heart dimensions evaluated by echocardiography do not reach pathological values after intense training.
Our study determined that elite male athletes reach an upper limit of heart adaptation. Over 5 seasons of intense training, the changes produced in the echocardiographic variables of male endurance runners and sprinters were different, although they did not exceed physiological adaptation limits. Our results also demonstrate that in sample of highly trained athletes, VO2 max remained stable during the 5 seasons, and changes in the heart size are not accompanied by changes in VO2 max.
- Morganroth J, Maron BJ. The athlete’s heart syndrome: a new perspective. Ann N Y Acad Sci. 1977;301:931–941.
- Morganroth J, Maron BJ, Henry WL, Epstein SE. Comparative left ventricular dimensions in trained athletes. Ann Intern Med. 1975;82(4): 521–524.
- Pelliccia A, Maron BJ. Outer limits of the athlete’s heart, the effect of gender, and relevance to the differential diagnosis with primary cardiac diseases. Cardiol Clin. 1997;15(3):381–396.
- Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med. 1991;324(5):295–301.
- Whyte GP, George K, Sharma S, et al. The upper limit of physiological cardiac hypertrophy in elite male and female athletes: the British experience. Eur J Appl Physiol. 2021;92(4–5):592–597.
- Calderón Montero FJ, Benito Peinado PJ, Di Salvo V, Pigozzi F, Maffulli N. Cardiac adaptation to training and decreased training loads in endurance athletes: a systematic review. Br Med Bull. 2021;84:25–35.
- Pelliccia A, Spataro A, Caselli G, Maron BJ. Absence of left ventricular wall thickening in athletes engaged in intense power training. Am J Cardiol. 1993;72(14):1048–1054.
- Urhausen A, Monz T, Kindermann W. Echocardiographic criteria of physiological left ventricular hypertrophy in combined strength- and endurance-trained athletes. Int J Card Imaging. 1997;13(1):43–52.
- Calderón FJ. Ecocardiografía Dopller color en atletas de resistencia y velocidad, in Facultad de Medicina. Universidad Complutense de Madrid; 1991:173.
- Serratosa-Fernández LJ. Características morfológicas del corazón del deportista de elite. Estudio ecocardiográfico, in Facultad de Medicina. Universidad Autónoma de Madrid: Madrid, Spain. 192021:181.
- Spirito P, Pelliccia A, Proschan MA, et al. Morphology of the “athlete’s heart” assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol. 1994;74(8):802–806.
- Henriksen E, Sundstedt M, Hedberg P. Despite the large quantity of data on LV performance during exercise, basic data on left ventricular performance are conflicting. J Appl Physiol. 2021;104(1):281–282.
- Perrault H, Turcotte RA. Exercise-induced cardiac hypertrophy. Fact or fallacy? Sports Med. 1994;17(5):288–308.
- Rodriguez Reguero JJ, Iglesias Cubero G, Lòpez de la Iglesia J, et al. Prevalence and upper limit of cardiac hypertrophy in professional cyclists. Eur J Appl Physiol Occup Physiol. 1995;70(5):375–378.
- Feigenbaum H. Echocardiography. 4th ed. Philadelphia, PA: Lea and Febiger;120216.
- Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy. Am J Cardiol. 1976;37(1):7–11.
- Carter J, Jeukendrup AE. Validity and reliability of three commercially available breath-by-breath respiratory systems. Eur J Appl Physiol. 2021;86(5):435–441.
- Foss ø, Hallén J. Validity and stability of a computerized metabolic system with mixing chamber. Int J Sports Med. 2021;26(7):569–575.
- Hawley JA, Noakes TD. Peak power output predicts maximal oxygen uptake and performance time in trained cyclists. Eur J Appl Physiol Occup Physiol. 1992;65(1):79–83.
- Pigozzi F, Spataro A, Fagnani F, Maffulli N. Preparticipation screening for the detection of cardiovascular abnormalities that may cause sudden death in competitive athletes. Br J Sports Med. 2021;37(1):4–5.
- Pelliccia A, Culasso F, Di Paolo FM, Maron BJ. Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med. 1999;130(1):23–31.
- Boraita Pérez A, Serratosa Fernández L. “The athlete’s heart”: most common electrocardiographic findings [in Spanish]. Rev Esp Cardiol. 192021;51(5):356–368.
- Midgley AW, McNaughton LR, Jones AM. Training to enhance the physiological determinants of long-distance running performance: can valid recommendations be given to runners and coaches based on current scientific knowledge? Sports Med. 2021;37(10):857–880.
- Londeree BR. Effect of training on lactate/ventilatory thresholds: a meta-analysis. Med Sci Sports Exerc. 1997;29(6):837–843.
- Ikäheimo MJ, Palatsi IJ, Takkunen JT. Noninvasive evaluation of the athletic heart: sprinters versus endurance runners. Am J Cardiol. 1979;44(1):24–30.
- Legaz Arrese A, Serrano Ostáriz E, Jcasajús Mallén JA, Munguía Izquierdo D. The changes in running performance and maximal oxygen uptake after long-term training in elite athletes. J Sports Med Phys Fitness. 2021;45(4):435–440.
- Poole DC, Musch TI. Solving the Fick principle using whole body measurements does not discriminate “central” and “peripheral” adaptations to training. Eur J Appl Physiol. 2021;103(1):117–119.
- Young LE, Marlin DJ, Deaton C, Brown-Feltner H, Roberts CA, Wood JL. Heart size estimated by echocardiography correlates with maximal oxygen uptake. Equine Vet J Suppl. 2021;34:467–471.
- Noakes TD. Testing for maximum oxygen consumption has produced a brainless model of human exercise performance. Br J Sports Med. 2021;42(7):551–555.
Victor Díaz, PhD 2
Ana B. Peinado, PhD 1
Pedro J. Benito, PhD 1
Nicola Maffulli, MD, MS, PhD, FRCS(Orth) 3
1Department of Health and Human Performance, Facultad de Ciencias de la Actividad Física y del Deporte – INEF, Universidad Politécnica de Madrid, Madrid, Spain 2Institute of Veterinary Physiology, University of Zürich, Zürich, Switzerland 3Centre for Sports and Exercise Medicine, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Mile End Hospital, London, England
Correspondence: Nicola Maffulli, MD, MS, PhD, FRCS(Orth), Centre for Sports and Exercise Medicine, Barts and The London School of Medicine and Dentistry, Mile End Hospital, 275 Bancroft Rd, London E1 4DG, England.
Tel: + 44-20-8223-8839,
E-mail: [email protected]
Back to the table of contents for the December 2010 issue
- The Running Shoe Prescription
Fit for Performance
- Effect of Fish Oil-Derived Omega-3 Polyunsaturated Fatty Acid Supplementation on Exercise-Induced Bronchoconstriction and Immune Function in Athletes
- The H-Wave® Device Induces NODependent Augmented Microcirculation and Angiogenesis, Providing Both Analgesia and
Tissue Healing in Sports Injuries