Background
Although cardiac adaptation to different sports has been extensively described, the potential relationship of training with aortic root (AR) elastic properties and diameters in top-level athletes remains not fully investigated. The aims of this study were to compare AR morphology and stiffness between highly trained athletes and sedentary subjects and to assess the independent determinants of AR stiffness and distensibility in athletes.
Methods
Four hundred ten elite athletes (220 endurance-trained athletes [ATE] and 190 strength-trained athletes [ATS]; 290 men; mean age, 28.3 ± 13.6 years; age range, 18–40 years) and 240 healthy controls underwent standardized comprehensive transthoracic echocardiography, including Doppler studies. End-diastolic AR diameters were measured at four locations: the aortic annulus, the sinuses of Valsalva, the sinotubular junction, and the maximal diameter of the proximal ascending aorta. The aortic distensibility index was calculated as 2 × (systolic proximal ascending aortic diameter − diastolic proximal ascending aortic diameter)/(diastolic proximal ascending aortic diameter) × (pulse pressure) (cm −2 · dyn −1 · 10 −6 ). AR stiffness index was defined as (systolic blood pressure/diastolic blood pressure)/(systolic proximal ascending aortic diameter − diastolic proximal ascending aortic diameter)/diastolic proximal ascending aortic diameter. Analysis of variance was performed to evaluate differences among groups.
Results
Left ventricular (LV) mass index did not significantly differ between the two groups of athletes but was lower in controls. ATS showed higher body surface area, sum of wall thickness (septum plus LV posterior wall), and circumferential end-systolic stress, while LV stroke volume and LV end-diastolic volume were greater in ATE. AR diameters at all levels and AR stiffness were significantly greater in ATS than in ATE and controls, while AR distensibility was significantly higher in ATE. However, AR dilatation was observed only in four male power athletes (1%). By multivariate analyses, in the overall population of athletes, age, LV stroke volume, endurance training, and duration of training were the only independent determinant of higher AR distensibility. On the other hand, age, circumferential end-systolic stress, strength training, and duration of training were independently associated with AR stiffness in ATS.
Conclusions
AR diameters and stiffness were significantly greater in strength-trained athletes, while aortic distensibility was higher in endurance athletes compared with age- and sex-matched healthy controls.
The athlete’s heart reflects cardiac adaptation to long-term intensive training, which includes changes in cavity diameters, wall thickness, and left ventricular (LV) mass, produced to degrees consistent with sport activity and exercise programs.
Recently, the potential impact of intensive physical training on aortic root (AR) morphology has been investigated, providing reference values for AR dimensions and identifying the relative influence of anthropometric parameters and different long-term training protocols among large series of endurance and strength elite athletes.
Arterial stiffness is emerging as the most important determinant of increased systolic and pulse pressure and therefore as the cause of several cardiovascular complications and events, including LV hypertrophy and failure, aneurysm formation and rupture, and a major contributor to atherosclerotic and small-vessel disease.
Aerobic exercise has well-documented efficacy for cardiovascular risk reduction, and it appears that at least part of its benefit derives from modification of arterial properties. Previous studies have indicated that blood pressure (BP) can be increased by a static weight-training program. However, the potential relationship of sport activity with aortic elastic properties and diameters in top-level athletes remains not fully investigated.
The aims of this study were therefore (1) to compare AR morphology and stiffness between highly trained athletes and sedentary subjects and (2) to assess the independent determinants of AR stiffness and distensibility in athletes.
Methods
From June 2008 to April 2010, 420 Caucasian elite athletes (mean age, 28.3 ± 13.6 years; age range, 18–40 years) and 240 healthy controls were referred to the Sports Medicine Ambulatory Service of Monaldi Hospital (Naples, Italy) for cardiovascular preparticipation screening and afterward to our echocardiographic laboratory for the purposes of the present study. Among these 420 athletes, 360 had been previously involved in our previous study of the effects of competitive sport training on myocardial function.
We also studied 240 sex-matched and age-matched (by age in years) normal-weight Caucasian sedentary subjects without detectable cardiovascular disease and/or risk factors. Volunteer controls were all recruited in Naples, were selected from our departments of cardiology among an initial cohort of 370 subjects investigated for work eligibility, and were examined at a single center (Monaldi Hospital). None of the control subjects had cardiovascular structural or functional abnormalities or received any medication.
All subjects underwent detailed histories, physical examinations, electrocardiography, chest radiography, and comprehensive transthoracic echocardiography, including Doppler studies.
Physical examinations at the study visits included measurements of height, weight, and BP and were conducted according to standardized protocols by trained and certified staff members. Three BP measurements were obtained in the right arm using a mercury manometer after the patient had been sitting for ≥5 min, with a break of ≥30 sec between readings. Five cuff sizes were available. Phase 1 and phase 5 Korotkoff sounds were used for systolic BP (SBP) and diastolic BP (DBP), respectively. The mean of the three measurements was calculated for this analysis on the same day as the echocardiographic studies.
Exclusion criteria were Marfan syndrome, coronary artery disease, arterial hypertension, valvular abnormalities of more than mild degree, congenital heart disease, bicuspid aortic valve, congestive heart failure, cardiomyopathies, diabetes mellitus, use of anabolic steroids and of other illicit drugs, and echocardiograms of inadequate quality. The diagnosis of Marfan syndrome was made according to the clinical criteria defined by Pyeritz and McKusick. Any subject believed to have Marfan syndrome was referred for slit-lamp examination with dilated pupils by an ophthalmologist and a complete evaluation of the skeletal system by an orthopedist. According to these criteria, we excluded three athletes for bicuspid aortic valve, one for hypertrophic cardiomyopathy, three for use of anabolic steroids, one for Marfan syndrome, and two for echocardiograms of inadequate quality.
On the basis of their training protocols and types of sports activity (mainly dynamic or static), and for the purposes of the present study, athletes were categorized into two groups: endurance-trained athletes (ATE; n = 220) and strength-trained athletes (ATS; n = 190). The study was approved by the local ethics committee.
All athletes had been trained intensively for 15 to 20 hours/week for >4 years. The ATE group (long-distance and middle-distance swimming or running, soccer, basketball) had submitted to intensive aerobic isotonic dynamic exercise at incremental workloads of 70% to 90% of maximal heart rate. In particular, they performed 3 hours/day of incremental long-distance swimming (7,000 m/day divided into series of 400–800 m) or 3 hours/day of long-distance running and only 2 hours/week of weightlifting at low workloads. On the other hand, the ATS group (weightlifting, martial arts, windsurfing) had undergone anaerobic isometric static exercise at incremental workloads of at 40% to 60% of maximal heart rate. Their training protocol included 3 hours/day of short-distance running and 3 hours/day of weightlifting at high workloads.
Standardized transthoracic echocardiography and Doppler examinations were performed using commercially available equipment in all subjects (Vivid 7, GE Healthcare, Milwaukee, WI). All studies were reviewed and analyzed offline by two independent observers blinded to the clinical characteristics of the study population. Specific measurements were made by the average of three to five cardiac cycles.
M-mode measurements (LV diastolic and systolic diameters, interventricular septal and posterior wall thicknesses) were performed in the parasternal long-axis view with the patient in the left lateral position. LV mass was calculated using the Penn convention and indexed to height (Cornell adjustment). Relative diastolic wall thickness was determined as the ratio between the sum of septal and posterior wall thicknesses and LV end-diastolic diameter. Circumferential end-systolic stress (ESSc) was calculated as a measurement of LV afterload using a cylindrical model according to the following formula:
ESSc ( g / cm ) = SBP × 1 2 D s 2 { 1 + [ ( 1 2 D s + P s ) 2 / ( 1 2 D s + 1 2 P s ) 2 ] } / ( 1 2 D s + P s ) 2 − 1 2 D s 2 ,
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