Interrelation between Exercise Heart Rate, Post-Run Systolic Blood Pressure, and Myocardial Structure in Distance Runners

ng is an exercise practiced by athletes in many sports. Being benefi cial to health, it is also under- taken by a great number of non-athletic individuals. Rigorous endurance training frequently induces symmetric (i. e. both ventricular chamber dilation and wall thickening) myocardial hypertrophy, which is a physiological adapta- tion. Although distance running is a sport associated with haemodynamic volume rather than pressure overload, in addition to enlarged cardiac output, systolic arterial blood pressure also considerably increases during running. The extent of the cardiac hypertrophy was shown to be correlated with peak blood pressure measured during laboratory exercise. However, the predominant type of myocardial hypertrophy (the ratio between the myocardial wall thickness and chamber size) in endurance runners remains contradictory, and the majority of the responsible factors are still to be determined. The aim of this study was to determine possible correlations between post-run systolic blood pressure and myocardial hypertrophy in endurance runners. Standard transthoracic two-dimensional M-mode echocardiography was performed in white adult male distance runners (n = 49) of national level within four weeks of treadmill testing, which was a non-continuous incremental exercise test employed for the determination of the heart rate as well as post-exertional systolic blood pressure re- sponse. Runners’ training volume (evaluated as the average number of hours per week spent training averaged over the past four weeks) correlated (p < 0.05) positively with the left ventricular (LV) wall thickness but not with the cavity size or LV mass (p > 0.05). Training volume also positively correlated with systolic blood pressure response to exercise (p < 0.05), but negatively with submaximal exercise heart

the average number of hours per week spent training averaged over the past four weeks) correlated (p < 0.05) positively with the left ventricular (LV) wall thickness but not with the cavity size or LV mass (p > 0.05). Training volume also positively correlated with systolic blood pressure response to exercise (p < 0.05), but negatively with submaximal exercise heart rate (p < 0.01). Post-run systolic blood pressure correlated positively with LV wall thickness and LV concentricity (namely, the ratio between the myocardial wall thick- ness and chamber size) (p < 0.05), but no signifi cant correlation of any of the LV size parameters with resting heart rate, blood pressure, or systolic blood pressure in 2 to 4 min during the recovery period was revealed. Submaximal and maximal heart rate correlated signifi cantly and negatively with LV wall thickness, LV mass, and systolic blood pressure measured immediately after running (p < 0.05). Training volume and post-run systolic blood pressure have been found to correlate positively with LV wall thickness and concentricity in white adult male distance runners. Negative correlation of exercise heart rate has been found with the post-exercise systolic blood pressure, LV wall thickness, and LV mass. Keywords: myocardial hypertrophy, pressure overload, echocardiography, athlete’s heart. INTRODUCTION I n contrast to the majority of other mammals, humans are naturally equipped for endurance running (Bramble, Lieberman, 2004). Dis- tance running is a classical endurance exercise practiced by athletes of many sport disciplines. It is also undertaken by many non-athletic individu- als and has a positive impact on health. Regular endurance training suffi cient in volume and in- tensity triggers ‘symmetric’ (i. e. both ventricular chamber dilation and wall thickening) myocardial hypertrophy, which is considered a purely physio- logical adaptation (De Castro et al., 2006). Distance running is classifi ed as a sport as- sociated with haemodynamic volume rather than pressure overload (Mitchell et al., 2005). Howe- ver, in addition to both increased heart rate and

et al., 2006). Distance running is classifi ed as a sport as- sociated with haemodynamic volume rather than pressure overload (Mitchell et al., 2005). Howe- ver, in addition to both increased heart rate and

57INTERRELATION BETWEEN EXERCISE HEART RATE, POST-RUN SYSTOLIC BLOOD PRESSURE, AND MYOCARDIAL STRUCTURE IN DISTANCE RUNNERS systolic volume, systolic blood pressure (SBP) also considerably increases during running, and large fluctuations of pulse pressure are obser- ved, and the extent of the cardiac hypertrophy was shown to correlate with peak blood pressure measured during laboratory exercise (Palatini et al., 1989). The arterial pulse pressure response to exercise was shown to be one of the deter- minants of concentricity (i. e. more pronounced wall thickening rather than chamber dilation (Ha- ykowsky et al., 2002)) of runners’ myocardium (Kasikcioglu et al., 2005). While competitive distance runners in response to their training are believed to develop symmetrical (i. e. both cardiac dilation and wall thickening of similar degree) or even eccentric (Pluim et al., 2000) (i. e. more pronounced chamber dilation rather than wall thic- kening (Haykowsky et al., 2002)) physiological cardiac hypertrophy, the concentric myocardial hypertrophy has been reported in professional endurance athletes who practice running as a size- able component of their training and competition (Karjalainen et al., 1997; Palazzuoli et al., 2002; Venckunas et al., 2006). Anyway, the predominant type of myocardial hypertrophy in endurance runners remains clearly contradictory, as many authors have reported more pronounced chamber dilation as compared with wall thickening in these athletes (Morganroth et al., 1975; D’Andrea et al., 2002; Nagashima et al., 2003). There is even less understanding of the mechanisms involved in and the factors responsible for the development of the structural adaptation due to athletic conditioning (Kasikcioglu et al., 2005). As one of the most potent stimuli for cardiac hypertrophy is arterial blood pressure, we have hypothesized that running-triggered haemody- namic pressure overload, measured as post-run SBP, explains (is responsible for) a significant proportion of LV wall thickness. The aim of the study was to determine possible correlations be- tween post-run SBP and myocardial hypertrophy in endurance runners. METHODS Sample. The permission to conduct the study was given by the Regional Bioethics Committee. Forty-nine adult (18 to 42 years of age) male run- ners of national level who had been training for competitive distances from

LV wall thickness. The aim of the study was to determine possible correlations be- tween post-run SBP and myocardial hypertrophy in endurance runners. METHODS Sample. The permission to conduct the study was given by the Regional Bioethics Committee. Forty-nine adult (18 to 42 years of age) male run- ners of national level who had been training for competitive distances from 800 m to the marathon were included in the study after their informed consent had been obtained. All the athletes were Caucasian and in their active training season at the time of the examination. They completed questionnaires to report their age, training expe- rience in years, and weekly training volume in hours, averaged over the past four weeks. Athletes disclaimed usage of any chemical preparations. Clinical and training characteristics of the subjects are presented in Table 1. Treadmill testing. A progressive incremental non-continuous exercise test was performed on a motorized treadmill (H/p/Cosmos Mercury 4.0, Nussdorf-Traunstein, Germany). The runners did not train at least 16 h and did not have meals at least 2 h before the testing. All the subjects were familiar with treadmill running. The test consisted of 4-min running bouts of increasing intensity interspaced with 4-min passive rest spans in a seated position. The initial speed was 60% of the subject’s average running velocity achi- eved during his last 5000-m race. Then the speed was increased by 0.7 km / h each bout. Subjects ran on the treadmill a suffi cient number of times to increase the blood lactate concentration above the level of 4 mmol·L -1 . Blood samples from fi ngertips were analysed by an enzymatic membrane. After each running stage, the athletes dismounted from the treadmill and were seated immediately. Cuff SBP was measured within 20 s, and also at 2 and 4 min of the recovery period, always by the same investigator. Values of SBP measured immediately after cessation of running were carefully analysed. Maximal and minimal SBP values, as well as the SBP value after the last running stage were obtai- ned for each athlete. In addition, all the SBP values Age, years

20 s, and also at 2 and 4 min of the recovery period, always by the same investigator. Values of SBP measured immediately after cessation of running were carefully analysed. Maximal and minimal SBP values, as well as the SBP value after the last running stage were obtai- ned for each athlete. In addition, all the SBP values Age, years Height, m Body mass, kg BMI, kg·m -2 BSA, m 2 Systolic BP, mmHg Diastolic BP, mmHg Heart rate, beats·min -1 Training experience, years Training vo- lume, hours / week 24.6 (7.4) 1.80 (0.06) 69.9 (5.9) 21.5 (1.8) 1.89 (0.09) 133.0 (13.3) 73.0 (10.2) 56.6 (9.7) 9.8 (7.3) 8.1 (3.3) Note. BMI — body mass index; BSA — body surface area; BP — arterial blood pressure. Table 1. Subjects’ clinical and trai- ning characteris- tics

58 measured immediately after cessation of running were averaged for each subject. The difference between resting and exercise SBP was calculated by subtracting the averaged post-exercise SBP by resting SBP. As regards the later recovery period blood pressure, only the subject’s average SBP at 2 and 4 min (separately) was analysed. Heart rate (HR) was recorded continuously averaging each 5-s interval (HR monitor Polar Accurex-Plus, Kempe- le, Finland). Maximal HR was determined as the highest 10-s interval value during the fi nal stages of the treadmill test, and HR at the running speed of 15 km / h was extrapolated from the recorded exercise HR. Echocardiography. Standard two-dimensio- nal M-mode echocardiography, using ultrasound sonographer AU3 Partner (Esaote Biomedica, Genoa, Italy) with 2.5-MHz transducer, was per- formed within four weeks of treadmill testing, as described earlier (Venckunas et al., 2006). Internal LV diameter, interventricular septal (IVS) and LV posterior wall (PWT) thicknesses were measured at end-diastole as recommended by the American Society of Echocardiography. The same professio- nal cardiologist took three measurements of each of the parameters, and the average was calculated. Left ventricular mass (in g) was calculated using the following equation: LV mass=0.8 x {1.04 x ((IVS + LVED + PWT) 3 – (LVED) 3 )} + 0.6, where IVS is interventricular septum thickness, PWT is left ventricular posterior wall thickness and LVEDd is left ven- tricular internal diameter (all at end-diastole, in cm). Echocardiographic indices relative to body size were obtained by dividing absolute values by the body surface area (BSA) value of the same index order, i. e. LV wall thicknesses and diameter were divided by square rooted BSA, and LV mass was divided by square rooted and then cubed BSA. Body surface area was calculated according to the following formula (Du Bois, Du Bois, 1916): BSA (m 2 ) = [stature (cm)] 0.725 × [body mass (kg)] 0.425 × 0.007184. The relative wall thickness (RWT) was cal- culated by dividing the sum of end-diastolic in- terventricular septum and LV posterior wall thic- knesses by LV end-diastolic diameter. Resting cuff blood pressure (both systolic and diastolic) and

to the following formula (Du Bois, Du Bois, 1916): BSA (m 2 ) = [stature (cm)] 0.725 × [body mass (kg)] 0.425 × 0.007184. The relative wall thickness (RWT) was cal- culated by dividing the sum of end-diastolic in- terventricular septum and LV posterior wall thic- knesses by LV end-diastolic diameter. Resting cuff blood pressure (both systolic and diastolic) and heart rate were measured after the echocar- diographic examination. Statistics. The Pearson’s bivariate two-tai- led test was used in calculating the correlation coeffi cients. Echocardiographic LV size indices correlated with the following independent va- riables: SBP, HR, and training parameters. The signifi cance level was set at p value of 0.05. All the analyses were performed with the SPSS for Windows release 13.0. RESULTS Runners’ training volume correlated posi- tively with absolute and relative IVS, PWT, as well as RWT (r from 0.283 to 0.368, p < 0.05), but not LV cavity size, LV mass or LV mass index (p > 0.05). Training volume also positi- IVS IVSrel PWT PWTrel RWT LVM LVMi SBPaver 0.282 p = 0.049 0.306 p = 0.032 0.309 p = 0.031 0.319 p = 0.025 SBP@15km / h 0.292 p = 0.047 0.292 p = 0.047 0.294 p = 0.045 SBPmax 0.293 p = 0.043 0.348 p = 0.015 SBPlast 0.334 p = 0.043 0.338 p = 0.041 0.344 p = 0.037 SBPmin 0.301 p = 0.037 0.302 p = 0.037 HRmax –0.361 p = 0.014 –0.348 p = 0.018 –0.433 p = 0.003 –0.423 p = 0.003 –0.476 p = 0.001 –0.473 p = 0.001 HR@15km / h –0.327 p = 0.022 –0.292 p = 0.042 –0.322 p = 0.024 –0.290 p = 0.043 –0.429 p = 0.002 –0.375 p = 0.008 Note. IVS — interventricular septum thic- kness; IVSrel — relative interventricular septum thickness; PWT — left ventricular posterior wall thickness; PWTrel — relati- ve left ventricular posterior wall thickness; RWT — relative wall thickness; LVM — left ventricular mass; LVMi — left ven- tricular mass index; SBPaver — averaged systolic blood pressure immediately after running; SBP@15km/h — systolic blo- od pressure immediately

— interventricular septum thic- kness; IVSrel — relative interventricular septum thickness; PWT — left ventricular posterior wall thickness; PWTrel — relati- ve left ventricular posterior wall thickness; RWT — relative wall thickness; LVM — left ventricular mass; LVMi — left ven- tricular mass index; SBPaver — averaged systolic blood pressure immediately after running; SBP@15km/h — systolic blo- od pressure immediately after running at 15 km / h; SBPmax — maximal recorded systolic blood pressure immediately after running; SBPlast — systolic blood pres- sure immediately after the last running bout; SBPmin — the lowest recorded systolic blood pressure immediately after running; HRmax — maximal heart rate; HR@15km/h — heart rate immediately after running at 15 km / h. Table 2. Correlation of left ventri- cular structure to systolic blood pressure (SBP) and heart rate (HR) response to treadmill running. Signi- fi cant (p < 0.05) correlation coeffi ci- ents are presented Tomas Venckûnas, Birutë Maþutaitienë, Arvydas Stasiulis

59 vely correlated with SBP response to exercise (r from 0.41 to 0.48, p < 0.01), as well as SBPa- ver and HRmax product (r = 0.371, p = 0.011), but negatively with HR@15km / h (r = –0.422, p = 0.003). Signifi cant (p < 0.05) correlation coeffi cients of echocardiographic LV hypertrophy parameters to SBP and HR response to running are presented in Table 2. Absolute LV diastolic diameter, but not wall thickness or LV mass, showed positive correlation with BSA (r = 0.544, p = 0.001), pulse pressure at rest (r = 0.339, p = 0.018), and negative correlati- on with the difference between resting and exerci- se SBP (–0.340, p = 0.017). The latter parameter also correlated with RWT (0.329, p = 0.021). Pulse pressure at rest also correlated with relative LV diameter (r = 0.331, p = 0.022) and LV mass (r = 0.309, p = 0.033). However, no significant correlation of any of the LV size parameters with resting HR or blood pressure, or SBP in 2 to 4 min during the recovery period was observed. Both HRmax and HR@15km/h correla- ted negatively with the parameters of absolute and relative LV hypertrophy (Table 2), as well as SBP measured immediately after running (r ≈ –0.38, all p < 0.04). DISCUSSION The study has revealed a positive correlation of post-run systolic blood pressure with LV wall thickness and concentricity in distance runners. This could be explained by the ability of athlete’s heart with thicker myocardial wall to contract more powerfully during treadmill testing. An alternative interpretation is that more concentric myocardium hypertrophy is due to higher pressure response to daily training. These mechanisms may complement each other. The study has also shown that submaximal and maximal heart rate correlated negatively with LV wall thickness, LV mass, and systolic blood pressure measured immediately after running. Some echocardiographic characteristics were shown to be influenced by the sport undertaken (Barbier et al., 2006). Increased myocardial mass due to both cavity dilation and wall thickening is a usual finding in endurance runners (Pluim et al., 2000; Fagard, 2003). Professional

maximal heart rate correlated negatively with LV wall thickness, LV mass, and systolic blood pressure measured immediately after running. Some echocardiographic characteristics were shown to be influenced by the sport undertaken (Barbier et al., 2006). Increased myocardial mass due to both cavity dilation and wall thickening is a usual finding in endurance runners (Pluim et al., 2000; Fagard, 2003). Professional distance runners, though for a long time they were be- lieved to possess more pronounced LV chamber dilation than wall thickening (Morganroth et al., 1975), were also shown not to have considerably lower relative wall thickness as compared with athletes from many other sports (Fagard, 2003; Hoogsteen et al., 2004), and even to be similar in LV cavity diameter to sedentary controls at least in one study (Palazzuoli et al., 2002). Several physiological factors including en- docrine, pressure responses to exercise, as well as diastolic filling pattern influence structural cardiac adaptation to regular exercise. Dyna- mic exercises including running favour venous return (Crawford et al., 1985; Goldhammer et al., 1999; Sundstedt et al., 2004), diastolic fil- ling and accompanying distension of ventricular myocardium (mechanical stimulus to cardiac myocytes). Training volume and the duration of the haemodynamic overload as well as shifts in the hormonal milieu are also important factors which determine the extent of structural cardiac adaptation, namely myocardial mass. The results of the present study suggest that the amount of endurance running performed has an influence on distance runners’ LV wall thickness rather than chamber size. Longer mechanical stimulus of voluminous training, instead of triggering dila- tion of the chamber, seems to induce net cardiac protein synthesis (wall thickening) and in such a way ‘compensates’ for the lower pressure over- load during running as compared to the values triggered by strength / power athletes endeavour (MacDougall et al., 1985). This could plausibly explain the absence of lower (relative) myocar- dial wall thickness in long distance runners as compared with strength athletes (Fagard, 2003). Interestingly, runners’ training volume was not only negatively associated with submaximal heart rate, but also positively correlated with SBP incre- ase due to exercise. The latter

by strength / power athletes endeavour (MacDougall et al., 1985). This could plausibly explain the absence of lower (relative) myocar- dial wall thickness in long distance runners as compared with strength athletes (Fagard, 2003). Interestingly, runners’ training volume was not only negatively associated with submaximal heart rate, but also positively correlated with SBP incre- ase due to exercise. The latter correlation might be explained by the ability of a better trained my- ocardium to contract more powerfully, and by the lower concentration of vasodilative metabolites produced, which leads to higher peripheral resi- stance at the same absolute workload in a better trained endurance runner. Blood pressure during exercise is another pos- sible factor involved in the development of both the type and the extent of cardiac hypertrophy (Karjalainen et al., 1997; D’Andrea et al., 2002). It remains controversial whether the extent to which SBP increase to exercise is or is not rela- ted to cardiovascular risk (Tanaka et al., 1996; INTERRELATION BETWEEN EXERCISE HEART RATE, POST-RUN SYSTOLIC BLOOD PRESSURE, AND MYOCARDIAL STRUCTURE IN DISTANCE RUNNERS

This research investigates the relationship between exercise heart rate and myocardial structure in runners.