Abstract

Background:

Cardiac remodeling is a specific response to exercise training and time exposure. We hypothesized that athletes engaging for long periods in high-intensity strength training show heart and/or vascular damage.

Objective:

To compare cardiac characteristics (structure and function) and vascular function (flow-mediated dilation [FMD] and peripheral vascular resistance [PVR]) in powerlifters and long-distance runners.

Methods:

We evaluated 40 high-performance athletes (powerlifters [PG], n = 16; runners [RG], n = 24) and assessed heart structure and function (echocardiography), systolic and diastolic blood pressure (SBP/DBP), FMD, PVR, maximum force (squat, bench press, and deadlift), and maximal oxygen uptake (spirometry). A Student’s t Test for independent samples and Pearson’s linear correlation were used (p < 0.05).

Results:

PG showed higher SBP/DBP (p < 0.001); greater interventricular septum thickness (p < 0.001), posterior wall thickness (p < 0.001) and LV mass (p < 0.001). After adjusting LV mass by body surface area (BSA), no difference was observed. As for diastolic function, LV diastolic volume, wave E, wave e’, and E/e’ ratio were similar for both groups. However, LA volume (p = 0.016) and BSA-adjusted LA volume were lower in PG (p < 0.001). Systolic function (end-systolic volume and ejection fraction), and FMD were similar in both groups. However, higher PVR in PG was observed (p = 0.014). We found a correlation between the main cardiovascular changes and total weight lifted in PG.

Conclusions:

Cardiovascular adaptations are dependent on training modality and the borderline structural cardiac changes are not accompanied by impaired function in powerlifters. However, a mild increase in blood pressure seems to be related to PVR rather than endothelial function.

Keywords:
Hypertrohy,Ventricular; Exercise; Exercise MovementTechniques; Blood Pressure; Resistance Training; Running/physiology

Resumo

Fundamento:

Remodelamento cardíaco é uma resposta específica ao tempo e modalidade de treinamento. Nós hipotetizamos que atletas de treinamento de força de alta intensidade, por longo tempo, mostram dano à estrutura cardíaca e/ou vascular.

Objetivo:

Comparar as características cardíacas (estrutura e funcionalidade) e função vascular (dilatação fluxo-mediada, FMD e resistência vascular periférica, PVR) em powerlifters e corredores.

Métodos:

Nós avaliamos 40 atletas de alto-desempenho (powerlifters [PG], n = 16; corredores [RG], n = 24). Mensuramos estrutura e funcionalidade cardíaca (ecocardiografia), pressão arterial (SBP/DBP), FMD, PVR, força máxima (agachamento, supino e levantamento terra) e consumo máximo de oxigênio (ergoespirometria). Foi utilizado teste T de Student e correlação linear de Pearson (p < 0,05).

Resultados:

PG mostrou maior SBP/DBP (p < 0,001), espessura de septo interventricular (p < 0,001), parede posterior (p < 0,001) e massa do VE (p < 0,001); após ajuste pela superfície corporal (BSA), não houve diferença na massa do VE. O volume do VE, onda E, onda e’, e a razão E/e’ foram similares entre os grupos. O volume do AE (p = 0,016), mesmo ajustado pela BSA (p < 0,001) foi menor no PG. A função sistólica (volume sistólico final e fração de ejeção) e FMD foram similares nos grupos. Contudo, foi observada maior PVR no PG (p = 0,014). Houve uma correlação direta entre as alterações cardíacas e a carga total levantada no PG.

Conclusões:

As adaptações cardiovasculares são dependentes da modalidade e os valores encontrados na estrutura do coração não são acompanhados por prejuízo na funcionalidade. Entretanto, um leve aumento na pressão arterial pode estar associado com maior PVR e não com a função endotelial.

Palavras-chave:
Hipertrofia Ventricular; Exercício; Técnicas de Exercício e Movimento Pressão Arterial; Treinamento de Resistência; Corrida/fisiologia

Introduction

Exercise training induces cardiovascular adaptations secondary to changes in blood pressure as well as other hemodynamic and metabolic changes in response to physical exertion. These adaptive changes can induce left ventricular (LV) hypertrophy in the long run.¹1 Maron BJ, Pelliccia A. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation. 2006;114(15):1633-44. Some authors claim that borderline physiological and anatomical changes occur as part of an adaptive process of high-performance training and they have sparked off debate on their implications.²2 McCann GP, Muir DF, Hillis WS. Athletic left ventricular hypertrophy: long-term studies are required. Eur Heart J.2000;21(5):351-3. They postulate that volume overload generally increases LV pumping ability producing eccentric hypertrophy while, in contrast, pressure overload decreases ventricular cavity size producing concentric hypertrophy. Moreover, peripheral vascular resistance (PVR) is an important factor of cardiac overload by specifically modulating LV afterload. Furthermore, the endothelium is central to vasodilation by producing nitric oxide (NO), which is a vasodilator and has a direct effect on PVR. Therefore, it is important to highlight that after exercise there is a stimulation of NO production and eNOS phosphorylation, which contributes directly to a reduction in PVR.³3 Goto C, Nishioka K, Umemura T, Jitsuiki D, Sakagutchi A, Kawamura M, et al. Acute moderate-intensity exercise induces vasodilation through an increase in nitric oxide bioavailiability in humans. Am J Hypertens.2007;20(8):825-30.^,44 Tanaka LY, Bechara LR, dos Santos AM, Jordao CP, de Sousa LG, Bartholomeu T, et al. Exercise improves endothelial function: a local analysis of production of nitric oxide and reactive oxygen species. Nitric Oxide.2015 Feb 15;45:7-14.

Aerobic exercise increases shear stress leading to increased release and synthesis of NO and higher active muscle vasodilation.⁵5 Heinonen I, Saltin B, Kemppainen J, Sipila HT, Oikonen V, Nuutila P. et al. Skeletal muscle blood flow and oxygen uptake at rest and during exercise in humans: a pet study with nitric oxide and cyclooxygenase inhibition. Am J Physiol Heart Circ Physiol. 2011;300(4):H1510-7. LV pressure overload is reduced over time.⁶6 Guindani G, Umpierre D, Grigoletti SS, Vaz M, Stein R, Ribeiro JP. Blunted local but preserved remote vascular responses after resistance exercise in chronic heart failure. Eur J Prev Cardiol.2012;19(5):972-82. However, high-intensity resistance training such as weightlifting and powerlifting involves a number of very slow-speed contractions that produce transient mechanical compression of resistance vessels, increasing PVR and LV pressure overload during exercise.⁷7 MacDougall JD, Tuxen D, Sale DG, Moroz JR, Sutton JR. Arterial blood pressure response to heavy resistance exercise. J Appl Physiol.1985;58(3):785-90. It has been postulated that chronic increase in afterload induces the parallel addition of new sarcomeres in the myocardium leading to concentric ventricular hypertrophy.⁸8 Lalande S, Baldi JC. Left ventricular mass in elite olympic weight lifters. Am J Cardiol.2007;100(7):1177-80. Yet, this form of ventricular hypertrophy has not been demonstrated in strength training athletes,⁹9 Haykowsky MJ, Dressendorfer R, Taylor D, Mandic S, Humen D. Resistance training and cardiac hypertrophy: unravelling the training effect. Sports Med. 2002;32(13):837-49. and it is thus an inconsistent finding.

Given the limited body of evidence in support of these cardiovascular adaptations as well as concerning endothelial function and PVR in strength athletes, this study aimed to compare structural and functional cardiac changes in powerlifters and long-distance runners. Secondarily, we compared endothelium-dependent vasodilation and PVR in these athletes. Our hypothesis is that athletes engaging in high-intensity strength training for long periods of time show changes in cardiac structure associated with reduced cardiac function when compared to long-distance runners. Furthermore, long-time exposure to high-intensity strength training could lead to a reduction of endothelial function caused by pressure overload.

Methods

Study participant selection and groups

The study convenience sample comprised 40 male individuals aged 18-40 years. We selected athletes of powerlifting (powerlifters group [PG], n = 16) and long-distance (over 10 km) running events (runners group [RG], n = 24). Eligible athletes were those competing for at least 3 years. Individuals with any medical condition in the preceding 6 months; those not competing in the preceding 6 months; those on use of illicit (doping) substances in the last 12 months; or those who refused to sign an informed consent were excluded.

The study sample was recruited using an open invitation at training sites (gyms, health clubs and sports centers) and selected after applying the inclusion criteria. Participants were assessed as follows: on the first visit they underwent blood pressure assessment, echocardiographic assessment, brachial artery flow-mediated dilation, peripheral vascular resistance assessments. In addition, they were administered a comprehensive questionnaire with questions about training including time of training experience; performance timeline; any awards/prizes; current training routine (volume, intensity, and duration of weekly training sessions, frequency of competitive participation, rest times, etc.) among others. On the next day, they underwent a maximum load test; and on the last visit (48 hours later), they underwent a maximum oxygen uptake test. All assessments were carried out within the same period of time (8 a.m. to 11 a.m.).

Blood pressure assessment

Blood pressure measurements were taken using a semi-automatic blood pressure monitor (OMROM 705CP), with the participant in a seated position with both feet on the floor, after a 10-minute rest; the cuff was placed and adjusted to the arm circumference. In a completely quiet room, blood pressure measurements were taken in duplicate on both arms, and the higher value of these readings was used in the study.

Echocardiographic examination

Transthoracic echocardiographic examinations were performed by an echocardiography specialist (G.B.G.). An ultrasound device (EnVisor CHD, Philips, Bothell, WA, USA) equipped with a sector transducer probe (2-4 MHz) was used to obtain longitudinal, cross-sectional, two-dimensional 2- and 4-chamber, and M module images. Continuous-wave, pulsed-wave, and color Doppler techniques were used to examine ventricular tissues and walls. All images were stored and sent to a second echocardiography specialist (D.P.K.) for blind evaluation of images. Body surface area (BSA) was calculated using Du Bois method.¹⁰10 DuBois D, DuBois EF. A formula to estimate the approximate surface area if height and weight be known. Arch Intern Med. 1916;17:862-71.

Brachial artery flow-mediated dilation and peripheral vascular resistance

We used a high-resolution two-dimensional Doppler ultrasound device (EnVisor CHD, Philips, Bothell, WA, USA) equipped with a high-frequency (7-12 MHz) linear vascular transducer probe and electrocardiographic imaging and monitoring software. Flow-mediated dilation (FMD) measurements were taken with the participants in the supine position, and a properly fitting pressure cuff was placed on the arm 5 cm above the cubital fossa.¹¹11 Corretti MC, Anderson TJ, Benjamin EJ, Celermajer D, Charbonneau F, Creager MA, et al. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J Am Coll Cardiol. 2002;39(2):257-65. Baseline brachial artery longitudinal diameters were assessed. Following that, the occlusion cuff was inflated to 50 mmHg above the systolic blood pressure (SBP) for 5 minutes and then deflated. Brachial artery diameters were measured for 60 seconds after deflation of the cuff. All analyses were performed offline and brachial artery measurements were made at the end of diastole (at R-wave peak on the electrocardiogram). FMD responses were expressed as percentage change from the baseline brachial artery diameter.

PVR was calculated from mean blood pressure (MBP) and baseline blood flow obtained in the FMD test (PVR = MBP/baseline blood flow in mmHg/cm.s^-).

Maximum load test

Maximum strength was assessed in the one-repetition maximum test (1-RM) for the squat, bench press and deadlift exercises, which are specifically performed at competitions, and through the total sum of these three exercises (total load). Distance runners attended a familiarization session within 48 hours of the test when the order of strength exercises and proper performance were introduced. For the 1-RM, the participants performed the maximum number of repetitions with the proposed load, up to a maximum of 10 repetitions. Exercise loads were increased according to Lombardi (1989)up to a point where participants were able to perform only one repetition with a maximum of 3 attempts to achieve the maximum load.

Maximum oxygen uptake

Maximum oxygen uptake (VO₂peak or VO₂max) was assessed through cardiopulmonary exercise test on a treadmill with respiratory gases collected (VO2000 model, Inbramed, Porto Alegre, Brazil). Powerlifters attended a familiarization session within 48 hours of the test where test procedures were introduced (Bruce protocol and mask placement for gas collection). The highest value, either VO₂ peak or VO₂ max was recorded at the end of the test as VO₂ max.

Statistical analyses

We performed the Shapiro-Wilk test to test normality of the data and homogeneity of variance was tested using Levene's test. All results are described as mean ± SD and confidence interval. We conducted Student's t Test for independent samples to assess differences between groups and calculated Pearson’s linear correlation coefficients (α = 0.05 for all tests). All statistical analyses were performed using SPSS Statistics (version 21 for Windows).

Results

The participants had similar age and height (Table 1). However, all anthropometric measurements for PG were greater compared to distance RG. In turn, Table 2 shows loads for the squat, bench press, and deadlift exercises and total load (total sum of these three exercises). For all types of exercises, weight loads were higher in PG than RG as expected. The total load was greater by ~133% in PG than RG. The differences remained unchanged when loads were adjusted for body mass.

Table 3 shows hemodynamic and cardiopulmonary parameters. Powerlifters had higher resting SBP (~10%) and resting DBP (~12%); the absolute differences between the two groups were 13.6 mmHg and 10.1 mmHg, respectively. Resting heart rate was higher in PG compared to RG (~19%, Δ15.7 bpm). VO₂max was much higher in RG than PG (~65%): the highest VO₂ max value among powerlifters was lower than the lowest VO₂ max value among runners.

Table 4 shows the echocardiographic results. As for cardiovascular adaptations, aorta diameter, left atrium (LA) diameter, right ventricle diameter, LV systolic diameter, and LV diastolic diameter were similar in both groups. However, PG showed greater interventricular septum thickness (Δ2.4 mm) and posterior wall thickness (Δ1.2 mm). They also showed greater LV mass (Δ46.5 g), but this difference disappeared after adjusting for BSA. As for diastolic function, LV diastolic volume, transmitral E wave, e' wave, and E/e' ratio were similar in both groups. However, LA volume (~22%), and LA volume adjusted for BSA (~40%) were found in PG, when compared to RG, but they were all within normal ranges. Although PG showed some degree of anatomical remodeling and different diastolic function parameters compared to RG, systolic function reflected in LV systolic volume, ejection fraction, and ejection fraction calculated by Simpson’s rule were similar in both groups. Of the 40 participants, 9 (22.5%) had physiological ventricular hypertrophy in response to exercise; 10 (all powerlifters) had interventricular septum thickness greater than 11 mm. Of the 27 participants with LV mass greater than 225 g and LV mass adjusted by BSA greater than 115g/m²2 McCann GP, Muir DF, Hillis WS. Athletic left ventricular hypertrophy: long-term studies are required. Eur Heart J.2000;21(5):351-3., 13 (82%) were PG and 14 (63%) RG.

Figure 1 shows FMD (%) and PVR measurements. Interestingly, FMD values were similar in both groups ([PG] 14.7 ± 2.3 vs. [RG] 15.9 ± 2.5%). However, PG had higher PVR values compared to RG ([PG] 12.6 ± 5.3 vs. [RG] 8.2 ± 3.8 mmHg/cm.s^(-1), Δ35%).

The correlations between training parameters and echocardiographic and cardiopulmonary variables in PG are displayed in Table 5. There was a direct correlation between interventricular septum thickness and weight load in the deadlift, squat, and total load. Interestingly, no correlation was found with time of exposure, i.e., duration in years of strength training among powerlifters. SBP levels were directly correlated with training intensity; and DBP showed a stronger correlation with duration of strength training. For runners, interventricular septum thickness and resting heart rate were inversely correlated with VO₂max and duration of strength training (Table 6).

Finally, FMD measurements were directly proportional to training intensity (% 1-RM) in PG and weight load for the squat (Table 7). For RG, no correlation of FMD values was found with cardiopulmonary variables and resting heart rate. Furthermore, FMD values were correlated with duration of powerlifting training (years) and daily duration of training session. However, this same correlation was not seen among runners.¹²12 Lombardi VP. Beggining weight training: the safe and effective way. Dubuqye: Dubuqye/Brown; 1989.

Discussion

Our study found that, compared with long-distance runners, powerlifters showed greater interventricular septum thickness, LV posterior wall thickness and LV mass. However, after adjusting for BSA, no difference was observed in LV mass.Cardiac function was similar in powerlifters and runners. Together, these parameters suggest that specific cardiac remodeling may occur as a result of training, but with no impairment of cardiac functions. A major finding of our study was similar FMD measurements in both powerlifters and runners despite PVR being higher in powerlifters.¹²12 Lombardi VP. Beggining weight training: the safe and effective way. Dubuqye: Dubuqye/Brown; 1989. Although our findings are comparative and derive from a cross-sectional design, they suggest that high-intensity strength training does not necessarily cause damaging cardiovascular changes as it has been generally believed.

Cardiac parameters

Regarding cardiac parameters (anatomical structure, and diastolic and systolic function), the echocardiographic assessments showed increased interventricular septum thickness with slight or no chamber diameter reduction and slight increase in posterior wall thickness in powerlifters compared to runners. These changes may be because powerlifting involves a great amount of slow-speed contractions using high loads close to the maximum¹³13 Hill AV. The heat of shortening and the dynamic constants of muscle. Proceedings of the Royal Society B- Biological Sciences. 1938;126:136-95. in daily training sessions leading to LV pressure overload.

As for the cutoff values, several studies with high-performance athletes have used to determine pathological hypertrophy cutoff values of 12-13 mm for maximum interventricular septum thickness and 55-60 mm for end-diastolic dimension, as described below.Whyte (2004) examined 306British elite male athletes (judo, n = 22; skiing, n = 10; pole vault, n = 10; kayak, n = 11; rowing, n = 17; cycling, n = 11; power lifters, n = 29; triathlon, n = 51; modern pentathlon, n = 22; middle distance, n = 45; rugby, n=30; tennis, n = 33; swimming, n = 19) and found interventricular septum thickness > 13 mm in ~3.0% of them. Riding (2012) examined 836 athletes (soccer, n = 586; basketball, n = 75; volleyball, n = 41 and handball, n = 35) and found interventricular septum thickness > 12 mm and typical features of concentric left ventricular hypertrophy in ~2.0%. Pelliccia (1999) examined 1,309 Italian elite athletes engaged in different sporting disciplines (soccer, n = 119; gymnastics, n = 87; rowing, n = 80; tennis, n = 64;basketball, n = 62; track and field, n = 59; alpine skiing, n = 59; shooting, n = 57; handball, n = 56; cycling, n = 49; water polo, n=43; ice hockey, n = 42; cross-country skiing, n = 41; canoeing, n = 39; rugby, n = 39; skating, n = 36; fencing, n= 35; yachting, n = 33; swimming, n = 29; equestrian sports, n = 24; karate, n = 24; volleyball, n = 21; bobsledding, n = 17; boxing, n = 15; wrestling, n = 14; judo, n = 13; luge, n = 13; field hockey, n = 13; table tennis, n=11; pentathlon, n = 7; weight-lifting, n = 7; golfing, n = 6; baseball, n=5; triathlon, n = 3; motor-racing, n = 3; body-building, n=3; other modalities n = 72) and found interventricular septum thickness > 13 mm in 1.1% of them. Moreover, they also found that 45% and 14% of the athletes studied exhibited end-diastolic dimension > 55 mm and > 60 mm, respectively. Thus, if we use these cutoffs, despite some anatomical cardiac changes, none of the study participants showed cardiac dimensions consistent with pathological hypertrophy. However, it is important to note a strong correlation between weight loads lifted in the squat and total load and cardiac dimensions including septum thickness, posterior wall thickness, and LV mass. Yet again, a possible explanation is that powerlifting involves a great amount of slow-speed contractions using high loads close to the maximum leading to a pressure overload.⁹9 Haykowsky MJ, Dressendorfer R, Taylor D, Mandic S, Humen D. Resistance training and cardiac hypertrophy: unravelling the training effect. Sports Med. 2002;32(13):837-49.

10 DuBois D, DuBois EF. A formula to estimate the approximate surface area if height and weight be known. Arch Intern Med. 1916;17:862-71.

11 Corretti MC, Anderson TJ, Benjamin EJ, Celermajer D, Charbonneau F, Creager MA, et al. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J Am Coll Cardiol. 2002;39(2):257-65.

12 Lombardi VP. Beggining weight training: the safe and effective way. Dubuqye: Dubuqye/Brown; 1989.

13 Hill AV. The heat of shortening and the dynamic constants of muscle. Proceedings of the Royal Society B- Biological Sciences. 1938;126:136-95.

14 Whyte GP, George K, Sharma S, Firoozi S, Stephens N, Senior R, et al. The upper limit of physiological cardiac hypertrophy in elite male and female athletes: the British experience. Eur J Appl Physiol. 2004;92(4-5):592-7.

15 Riding NR, Salah O, Sharma S, Carre F, O’Hanlon R, George KP, et al. Do big athletes have big hearts? Impact of extreme anthropometry upon cardiac hypertrophy in professional male athletes. Br J Sport Med. 2012;46( Suppl 1):i90-7.

16 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.^-1717 Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE. The athlete’s heart. A meta-analysis of cardiac structure and function. Circulation. 2000;101(3):336-44.

With regard to LV mass, Gardin et al.,¹⁸18 Gardin JM, Arnold A, Gottdiener JS, Wong ND, Fried LP, Klopfenstein HS, et al. Left ventricular mass in the elderly. The Cardiovascular Health Study. Hypertension. 1997;29(5):1095-103. reported values of 225 g and 115 g/m² adjusted by BSA in individuals chronically exposed to pressure overload. LV mass was also measured in our study and we found values of 282 g and 135 g/m^2, among powerlifters. Interestingly, runners also showed high LV mass (236 g and 128 g/m^{(2 )}adjusted by BSA). Regardless of the training modality, cardiac remodeling occurred in response to exercise training in both groups. Though still controversial, echocardiographic measurements indexed to BSA allow to comparing individuals of different body sizes. BSA is affected by fat mass, and fat mass is neither correlated with nor predicts LV mass.¹⁹19 Whalley GA, Gamble GD, Doughty RN, Culpan A, Plank L, MacMahon S, et al. Left ventricular mass correlates with fat-free mass but not fat mass in adults. J Hypertens. 1999;17(4):569-74. An alternative approach is to adjust echocardiographic parameters for lean mass. However, accurate measurements are not widely available and substitute methods such as skin-fold thickness measurements are relatively inaccurate.²⁰20 Di Paolo FM, Schmied C, Zerguini YA, Junge A, Quattrini F, Culasso F, et al. The athlete’s heart in adolescent Africans: an electrocardiographic and echocardiographic study. J Am Coll Cardiol. 2012;59(11):1029-36.^,2121 Kasikcioglu E, Akhan H. Echocardiographic limits of left ventricular remodeling in athletes. J Am Coll Cardiol. 2004;44(2):469-70.

Diastolic function assessment in the study revealed consistently normal values in long-distance runners.²²22 Pelliccia A, Di Paolo FM, Maron BJ. The athlete’s heart: remodeling, electrocardiogram and preparticipation screening. Cardiol Rev.2002;10(2):85-90. In contrast, lower LA volume and transmitral A-wave velocity measures were found in powerlifters although these values were within normal limits. The difference of LA volume measures between both groups was ~22%, and it was even more pronounced after adjustment for BSA (~40%). D’Andrea et al.,²³23 D’Andrea A, Riegler L, Cocchia R, Scarafile R, Salerno G, Gravino R, et al. Left atrial volume index in highly trained athletes. Am Heartt J. 2010;159(6):1155-61. and coworkers have assessed LA volume and BSA-indexed LA volume in 350 endurance athletes and 245 strength athletes.²³23 D’Andrea A, Riegler L, Cocchia R, Scarafile R, Salerno G, Gravino R, et al. Left atrial volume index in highly trained athletes. Am Heartt J. 2010;159(6):1155-61. For BSA-indexed measures, these authors defined values between 29 and 33 mL/m²2 McCann GP, Muir DF, Hillis WS. Athletic left ventricular hypertrophy: long-term studies are required. Eur Heart J.2000;21(5):351-3. as mild LA enlargement and values greater than 33 mL/m²2 McCann GP, Muir DF, Hillis WS. Athletic left ventricular hypertrophy: long-term studies are required. Eur Heart J.2000;21(5):351-3. as moderate LA enlargement. Thus, our results were all below the cutoff values set in D'Andrea et al.,²³23 D’Andrea A, Riegler L, Cocchia R, Scarafile R, Salerno G, Gravino R, et al. Left atrial volume index in highly trained athletes. Am Heartt J. 2010;159(6):1155-61. As for LV systolic function assessed through estimates of ejection fraction and ejection fraction calculated by Simpson's rule, the echocardiographic assessment showed values within the normal range in all cases.

Blood pressure

The association of aerobic training with lower resting blood pressure is well established.²⁴24 Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J. 2013;34(28):2159-219.^,2525 Pescatello LS, Franklin BA, Fagard R, Farquhar WB, Kelley GA, Ray CA et al. American College of Sports Medicine position stand. Exercise and hypertension. Med Sci Sports Exerc. 2004;36(3):533-53. But a growing body of evidence shows that strength training can have a similar effect on blood pressure,²⁶26 Cornelissen VA, Fagard RH. Effect of resistance training on resting blood pressure: a meta-analysis of randomized controlled trials. J Hypertens. 2005;23(2):251-9. though there is not yet a consensus in the literature.²⁷27 Cornelissen VA, Smart NA. Exercise training for blood pressure: a systematic review and meta-analysis. J Am Heart Assoc. 2013;2(1):e004473. However, high-intensity strength training has been reported to negatively affect blood pressure. A meta-analysis showed that training modalities that basically consist of strength training (powerlifting, bodybuilding, and Olympic weightlifting) are associated with a higher risk of high blood pressure with mean SBP of 131.3 ± 5.3 mmHg and mean DBP of 77.3 ± 1.4 mmHg.²⁸28 Berge HM, Isern CB, Berge E. Blood pressure and hypertension in athletes: a systematic review. Br J Sports Med. 2015;49(11):716-23. These values are consistent with those found in our study (SBP 130.0 ± 8.2 and DBP 82.1 ± 6.9 mmHg).

Vascular function

FMD measurements were similar in both powerlifters and runners. This is an interesting finding given that these two training modalities have different biomechanical and metabolic characteristics. Exercise training has been shown as an effective means for the improvement of endothelium-dependent vasodilation capacity.²⁹29 Higashi Y, Sasaki S, Kurisu S, Yoshimizu A, Sasaki N, Matsuura H, et al. Regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive as well as hypertensive subjects: role of endothelium-derived nitric oxide. Circulation. 1999;100(11):1194-202. Among high-performance athletes, long-distance runners with above average normal cardiac function show lower arterial stiffness, lower oxidative stress, and increased endothelium-dependent dilation³⁰30 Umpierre D, Stein R. Hemodynamic and vascular effects of resistance training: implications for cardiovascular disease. Arq Bras Cardiol. 2007;89(4):256-62. capacity when compared to sedentary individuals of the same age.³¹31 Florescu M, Stoicescu C, Magda S, Petcu I, Radu M, Palombo C, et al. “Supranormal” cardiac function in athletes related to better arterial and endothelial function. Echocardiography. 2010;27(6):659-67. These data suggest that outstanding cardiac performance in athletes may be associated with improved vascular function induced by aerobic exercise training.

It is well known that aerobic exercise improves endothelial function by producing increased shear stress on the vessel walls during exercise.³²32 Thijssen DH, Dawson EA, Black MA, Hopman MT, Cable NT, Green DJ. Brachial artery blood flow responses to different modalities of lower limb exercise. Med Sci Sports Exerc. 2009;41(5):1072-9. Yet, it has been suggested that strength training can increase hemodynamic stress due to the mechanical compression of blood vessels during active movements together with excessive vascular tension produced during strength exercises.⁷7 MacDougall JD, Tuxen D, Sale DG, Moroz JR, Sutton JR. Arterial blood pressure response to heavy resistance exercise. J Appl Physiol.1985;58(3):785-90. Thus, we can speculate that high-intensity strength training could acutely affect endothelium-dependent vasodilation and lead to permanent damage in the long run. In this regard, impaired vascular function has been demonstrated in strength athletes, though it appears to be related to the use of anabolic agents rather than an effect of training.³³33 Lane HA, Grace F, Smith JC, Morris K, Cockcroft J, Scanlon MF, et al. Impaired vasoreactivity in bodybuilders using androgenic anabolic steroids. Eur J Clin Invest. 2006;36(7):483-8.^,3434 Severo CB, Ribeiro JP, Umpierre D, Da Silveira AD, Padilha MC, De Aquino Neto FR, et al. Increased atherothrombotic markers and endothelial dysfunction in steroid users. Eur J Prev Cardiol.2013;20(2):195-201.

Heffernan et al. found increased forearm reactive hyperemia in healthy young individuals after 6-month strength training.³⁵35 Heffernan KS, Fahs CA, Iwamoto GA, Jae SY, Wilund KR, Woods JA, et al. Resistance exercise training reduces central blood pressure and improves microvascular function in African American and white men. Atherosclerosis. 2009;207(1):220-6. The most likely explanation for increased endothelium-dependent dilation in strength training is the assumption of the mechanical compression of resistance vessel walls during exercise, followed by blood flow release after cessation of exercise, producing a sharp increase in vessel wall shear stress.³⁶36 Tinken TM, Thijssen DH, Hopkins N, Dawson EA, Cable NT, Green DJ. Shear stress mediates endothelial adaptations to exercise training in humans. Hypertension.2010;55(2):312-8. Although training modalities involve different stimuli (running training: increased continuous blood flow; strength training: intermittent compression of the muscles and restoring blood flow) they ultimately produce the same effects on vessel wall shear stress.

It is important to note that, despite increased blood pressure levels and greater posterior wall thickness and LV mass found in our study among powerlifters, they showed no cardiac and endothelial function impairment when compared to runners and all the parameters were above average. Therefore, high blood pressure found in powerlifters seems to be related to increased PVR rather than endothelial function impairment.

Study strengths and limitations

The key strengths of our study are the use of a homogeneous sample (within each group) and that all echocardiographic images were assessed by two independent examiners, one of them blinded. However, our data should be interpreted with caution due to some limitations including the small sample size (due to recruitment challenges as anabolic steroid use is common among powerlifters and few met our inclusion criteria), and the challenge of recruiting a sample of untrained healthy subjects; however, all parameters evaluated were compared with those findings of other studies and/or current guidelines.

Conclusion

Our study showed that cardiac remodeling seems dependent on training modalities and not on structural difference, as in BSA-indexed LV mass in both powerlifters and long-distance runners. Systolic and diastolic functions were preserved in both modalities. Powerlifters showed higher resting blood pressure, which can be explained by increased PVR. However, FMD measurements were similar in both groups studied and were well above average. Although our findings are comparative in nature and derive from a cross-sectional design, it is possible to speculate that high-intensity strength training for a significant number of years (~5 years or more) may be associated to borderline structural cardiac changes, though they are not accompanied by reduced cardiac function.

References

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