Exercise training elicits morphological adaptations in the left ventricle (LV) and large-conduit arteries that are specific to the type of training performed (i.e., endurance vs. resistance exercise). We investigated whether the mode of chronic exercise training, and the associated cardiovascular adaptations, influence the blood pressure responses to orthostatic stimulation in 30 young healthy men (10 sedentary, 10 endurance trained, and 10 resistance trained). The endurance-trained group had a significantly larger LV end-diastolic volume normalized by body surface area (vs. sedentary and resistance-trained groups), whereas the resistance-trained group had a significantly higher LV wall thickness and aortic pulse wave velocity (PWV) compared with the endurance-trained group. In response to 60° head-up tilt (HUT), mean arterial pressure (MAP) rose in the resistance-trained group (+6.5 ± 1.6 mmHg, P < 0.05) but did not change significantly in sedentary and the endurance-trained groups. Systolic blood pressure (SBP) decreased in endurance-trained group (−8.3 ± 2.4 mmHg, P < 0.05) but did not significantly change in sedentary and resistance-trained groups. A forward stepwise multiple regression analysis revealed that LV wall thickness and aortic PWV were significantly and independently associated with the MAP response to HUT, explaining ∼41% of its variability (R2 =0.414, P < 0.001). Likewise, aortic PWV and the corresponding HUT-mediated change in stroke volume were significantly and independently associated with the SBP response to HUT, explaining ∼52% of its variability (R2 = 0.519, P < 0.0001). Furthermore, the change in stroke volume significantly correlated with LV wall thickness (r = 0.39, P < 0.01). These results indicate that chronic resistance and endurance exercise training differentially affect the BP response to HUT, and that this appears to be associated with training-induced morphological adaptations of the LV and large-conduit arteries.
- cardiovascular adaptation
- endurance training
- resistance training
- head-up tilt
arterial blood pressure (BP) is typically well regulated during short-term central hypovolemia (e.g., orthostatic stress, hemorrhage) as the unloading of the arterial and cardiopulmonary baroreceptors compensates for the decrease in stroke volume (SV) by evoking neurally and hormonally mediated increases in heart rate (HR) and peripheral vascular resistance (12, 20). However, exercise training-induced adaptations in cardiovascular structure may modify the functional regulation of BP. It is well known that there is a high prevalence of orthostatic hypotension in elite endurance athletes (2, 5, 6, 15). High-intensity endurance training, which is characterized by volume overload associated with the high cardiac output during exercise, induces an increase in left ventricle (LV) volume with a proportional increase in wall thickness (i.e., eccentric hypertrophy) (14), increases LV compliance (6), and reduces the stiffness of large-conduit arteries (13). These cardiovascular adaptations are favorable for achieving the high rates of oxygen consumption required for elite endurance exercise performance. However, the structural adaptations of the LV that occur with endurance training also result in a steeper Frank-Staring cardiac function curve (6). This is associated with a substantial drop in SV during orthostatic stress and likely contributes to the increased incidence of orthostatic hypotension and syncope in well-trained endurance athletes (6).
In contrast, there is a lack of information regarding the impact of regular resistance training on the hemodynamic response to the orthostatic stress. Although a few studies have suggested that resistance training is associated with superior orthostatic tolerance (8, 17), the precise etiology is unknown. The marked and repetitive increase in BP with high-intensity resistance training may elicit a thickening of the LV wall with unchanged LV chamber size (i.e., concentric hypertrophy) (14) and stiffening of the large-conduit arteries (10, 13). Such LV concentric hypertrophy may limit the distension of the LV chamber and attenuate the reduction in SV during orthostatic stimulation. On the other hand, baroreceptor sensitivity may be blunted by a stiffening of the central conduit arteries in which these mechanoreceptors are embedded (e.g., ascending aorta and carotid artery), thus leading to impaired BP regulation during orthostatic stress. Such a mechanism is suggested to contribute to age-related alterations in BP control (9). However, the influence of large-artery stiffening caused by vigorous resistance training on the BP response to orthostatic stimulation remains unknown.
We aimed to investigate the influence of habitual training modality on the BP responses to the orthostatic stimulation and to examine the underlying mechanism(s). We hypothesized that endurance-trained and resistance-trained individuals exhibit distinct BP responses to the orthostatic stimulation and that such divergent BP responses would be associated with exercise training-induced morphological adaptations of LV and large-conduit vessels.
A total of 30 apparently healthy Japanese men (10 sedentary, 10 endurance trained, and 10 resistance trained) were studied. Habitual physical activity status of each subject was determined upon initial screening prior to the experiment (via e-mail), then subsequently verified and explored in detail at the experimental visit (by interview and questionnaire). All subjects had no apparent cardiovascular disease as assessed by medical history. Subjects who were current smokers or smoked within the past two years were excluded. None of the sedentary subjects had engaged in regular physical activity (>2 days/wk). The endurance-trained group was comprised of long distance runners and triathletes who trained for competition more than 5 days/wk and did not engage in resistance training. Resistance-trained subjects were athletes who played American football. Their training program consisted mainly of regular heavy resistance training (2–3 days/wk) and anaerobic exercise (5–6 days/wk). On average, endurance-trained and resistance-trained men had been exercising for 7.1 ± 1.8 and 2.6 ± 0.1 yr, respectively. This study was reviewed and approved by the Institutional Review Board of the National Institute of Advanced Industrial Science and Technology and was conducted in Japan. All potential risks and procedures of the study were explained to the subjects, and they gave their written informed consent to participate in the study.
Subjects were instructed to avoid regular exercise training at least 24 h before the experimental visit to minimize the acute impact of exercise on the studied variables. All measurements were performed in a quiet, temperature-controlled room (24–26 C°) after at least 4 h of fasting and abstinence from caffeinated beverage. However, subjects were instructed to consume a little water prior to the measurements to maintain adequate hydration. After the physical characteristics measurements, cardiovascular measurements were conducted in a quiet room, and following >10 min of supine rest, subjects underwent a Doppler-echocardiography examination. Following this hemodynamic variables were continuously monitored during supine rest and 60° head-up tilt (HUT) (5 min each). Aortic pulse wave velocity was evaluated during supine rest only. During HUT, subjects stood on the foot rest of a tilt bed and were instructed not to move or voluntarily contract muscles in lower limbs.
Height, body mass (via a digital scale, BWB-200, TANITA, Tokyo, Japan), body mass index, thigh circumference (via a nonelastic tape measure), and leg volume (via water replacement method with a bathtub) were measured.
LV dimension, wall thickness, and LV function were determined using echocardiography according to established guidelines (1). LV mass (LVM), LV wall thickness (LVWT), and fractional shortening (FS) were calculated according to following equation: where LVEDD is LV end-diastolic internal diameter, PWT is posterior wall thickness, IVST is interventricular septal thickness, and LVESD is LV end-systolic internal diameter.
SV was calculated as the product of the cross-sectional area of the aortic annulus and the time-velocity integral. The cross-sectional area of the aortic annulus was calculated from its diameter during early systole (M-mode image from parasternal long-axis view). The velocity of LV outflow was measured with the sample volume positioned at the aortic annulus immediately proximal to the aortic valve leaflets from the apical five-chamber view [e.g., LV outflow method (7); average of five cardiac cycles]. Echocardiographically determined measures of SV were used to calibrate Modelflow measures of SV as described below.
Aortic pulse wave velocity.
To quantify aortic arterial stiffness, aortic (i.e., carotid-femoral) pulse wave velocity (PWV) was measured as previously described (18). Carotid and femoral arterial pulse waveforms were simultaneously measured throughout the BP measurement in supine position with a vascular testing device (Form PWV/ABI, Colin Medical Technology, Komaki, Japan). PWV was calculated from the distance between two arterial recording sites divided by the transit time. Carotid and femoral artery pulse waves were measured with arterial applanation tonometry incorporating an array of 15 micropiezoresistive transducers attached on the left common carotid and left common femoral arteries. The transit time between carotid and femoral arterial pressure waveforms was acquired using the foot-to-foot method. Arterial path length was assumed as the straight distance between carotid and femoral recording sites.
Heart rate was recorded with ECG (ML 132 Bio Amp, ADInstruments, Colorado Springs, CO). Finger arterial pressure wave forms were continuously recorded at right index finger fixed at the heart level by a noninvasive beat-to-beat blood pressure monitoring system (Finometer, TNO TPD Biomedical Instruments, Amsterdam, The Netherlands). Brachial systolic (SBP), diastolic (DBP), and mean arterial BP (MAP) were estimated by a filtering of the finger arterial pressure waveform (BeatScope 1.1, TNO TPD Biomedical Instruments, Amsterdam, The Netherlands). SV and cardiac output (Q) were computed from the blood pressure waveform using the validated Modelflow method, incorporating age, sex, height, and weight (19, 21), and then calibrated by a constant, the ratio of mean Modelflow SV to baseline (before HUT) SV by echocardiography. Total peripheral resistance (TPR) was calculated as MAP/Q. SV, Q, and TPR were normalized by body surface area and defined as SV index, cardiac index, and TPR index, respectively. Continuous data for the last 1 min during each posture (Supine, HUT) were averaged and reported.
One-way ANOVA was used to determine the effects of habitual training modality on physiological characteristics. Mixed-design AVOVA with both between-subject (i.e., sedentary, resistance, endurance) and within-subject factors (i.e., supine vs. tilt) were performed to determine the effects of habitual training on hemodynamic responses to HUT. In the case of a significant F-value, a Tukey HSD post hoc test was used to identify significant differences among mean values. Product-moment correlation analyses were performed to determine relations among physiological characteristics and hemodynamic responses to HUT. Using a forward stepwise multiple regression analysis, we examined which physiological characteristics were significantly and independently associated with the MAP and SBP responses to orthostatic stress. Physiological characteristics and changes in hemodynamic variables (except for blood pressure) were included in the model if first identified as being significantly associated in product-moment correlation analyses. All data are reported as means ± SE. Statistical significance was set a priori at P < 0.05.
Selected physiological characteristics are summarized in Table 1. Resistance-trained men had a significantly greater body mass, body mass index, thigh circumference, and leg volume compared with the sedentary and endurance-trained group. LVEDV and body surface area-normalized LVEDV (i.e., LVEDV index) were significantly larger in the endurance-trained group than in the other groups. Significantly greater LVWT was seen in the resistance-trained group compared with the other groups. There was no significant difference in FS among the three groups. Aortic PWV was significantly higher in the resistance-trained group than in the endurance-trained group.
Figure 1 depicts the BP responses to the HUT. There were no significant differences in baseline BP between groups. With HUT, SBP significantly decreased by 8 ± 2 mmHg in the endurance-trained group but remained unchanged in the resistance-trained and sedentary groups. DBP rose significantly with HUT in the resistance-trained and sedentary groups, but not in the endurance-trained group. MAP increased with HUT in the resistance-trained group but not in the sedentary and endurance-trained groups. PP was reduced with HUT in the endurance-trained and sedentary groups, but not in the resistance-trained group. Consequently, HUT-mediated BP responses of the endurance- and resistance-trained groups were divergent, as seen in Fig. 2.
Other hemodynamic responses to orthostatic stimulation are summarized in Table 2. There were no significant intergroup differences in these variables. HR significantly increased during HUT in all groups presumably due to a significant reduction in SV (ΔSV correlated significantly with ΔHR, r = −0.49, P < 0.01). SV index significantly decreased with HUT in all groups (P < 0.05 for all). Main effects for group and treatment (i.e., HUT) were not significant in Q, cardiac index, TPR, and TPR index. The group-treatment interactions were also nonsignificant
Table 3 summarizes the results of product-moment correlation analyses among baseline physiological characteristics and hemodynamic responses to HUT. Changes in MAP (ΔMAP) during HUT were significantly correlated with LVWT, LVM, and corresponding changes in SV (ΔSV) (r = 0.38–0.52). A forward stepwise multiple regression analysis revealed that LVWT and aortic PWV were significantly and independently associated with ΔMAP, explaining ∼41% of its variability (R2 = 0.414, P < 0.001, Table 4). Changes in SBP (ΔSBP) during HUT significantly correlated with body mass, BMI, LVWT, LVM, aortic PWV, and ΔSV (r = 0.47–0.69). Aortic PWV and ΔSV were significantly and independently associated with ΔSBP, explaining ∼52% of its variability (R2 = 0.519, P < 0.0001, Table 4). ΔSV was significantly correlated with LVWT (r = 0.39).
Our most salient findings are twofold. First, MAP rose with orthostatic stimulation in resistance-trained men but not in sedentary and endurance-trained men. LV wall thickening and aortic stiffening were independently associated with HUT-related MAP responses. Second, SBP decreased with orthostatic stimulation in endurance-trained men but not in sedentary and resistance-trained men. HUT-related SBP responses were independently related to aortic PWV and the corresponding change in SV, which itself was associated with LV wall thickness. Our findings suggest that the BP response to HUT varies as a function of habitual training modality, and that this is associated with exercise training-induced morphological adaptations in LV and large-conduit vessels.
Resistance training seems to be associated with superior orthostatic tolerance (8, 17). For example, Lightfoot et al. (8) indicated that men who were chronically resistance trained exhibited an elevation in MAP with maximal lower-body negative pressure administered until the onset of presyncopal signs. However, the exact mechanisms underlying the observations are unclear. Levine et al. (6) suggested that in endurance-trained athletes greater LV chamber compliance (i.e., a steeper Frank-Staring cardiac function curve) could lead to a substantial fall of SV during orthostatic stress, and hence orthostatic hypotension. Therefore, we reasoned that an increase in LV wall thickness in resistance-trained individuals would result in a reduction in LV chamber compliance, and thus may improve orthostatic tolerance. As expected, endurance-trained and resistance-trained individuals exhibited distinct BP responses to the orthostatic stimulation. During short-term orthostatic stimulation (e.g., 5 min HUT) resistance-trained men exhibited a significant increase in MAP and an unchanged SBP, whereas endurance-trained men showed an unchanged MAP and a significant reduction in SBP. Furthermore, forward stepwise multiple regression analyses in pooled subjects indicated that the MAP response to HUT was independently associated with LV wall thickness, whereas the SBP response to HUT was independently associated with the corresponding change in SV, which itself was modestly associated with LV wall thickness. LV wall thickening may be accompanied with lower LV chamber compliance and limit a drop of SV with HUT. Taken together, these results suggest that the divergent BP responses to HUT are associated with exercise training-specific morphological adaptations of the heart.
Regular endurance training reduces central arterial stiffness, whereas regular vigorous resistance exercise training elicits a stiffening of the central arteries (10, 13). In line with these previous findings, we observed that resistance-trained individuals have significantly higher aortic PWV compared with endurance-trained individuals. It should be emphasized that a forward stepwise multiple regression analysis showed that aortic PWV was positively associated with both MAP and SBP responses to HUT, such that greater conduit artery stiffness was related to a greater BP increase to HUT. These results are inconsistent with a previous observation made in an elderly cohort, in which an increase in central arterial stiffness was suggested to precipitate falls in BP during orthostatic stress. Although the precise contribution of exercise training-related adaptations of the central arteries on BP regulation during orthostatic stress remains unclear, our findings might imply that age-related and resistance training-induced alterations of central arterial stiffness are functionally different.
Overall, the results of the present study suggest that the morphological adaptations in the LV and large-conduit arteries resulting from chronic exercise training are accompanied by alterations in BP regulation during orthostatic stimulation. Our findings support and extend the notion advanced by Levine et al. (6) that LV morphological adaptations are associated with orthostatic intolerance in endurance-trained individuals. However, in the present study training-related cardiovascular morphological adaptation explained only ∼41–52% of the variance in the MAP and SBP responses to HUT. The physiological mechanism(s) that account for the remaining variance are unclear but may involve exercise training-related changes in baroreflex control (12, 15), peripheral arterial structure and function (5), blood volume and/or hydration status (4). Further studies are required to explore these possibilities.
There are several limitations to the present study. First, because we used a cross-sectional study design, potential genetic influences cannot be completely ruled out. Additionally, correlational and regression analyses could not provide causation. Second, we did not measure either aerobic capacity (i.e., maximal oxygen uptake) or maximal muscle strength of subjects. The average length of exercise training was also different between endurance- and resistance-trained groups. However, as expected endurance-trained and resistance-trained groups exhibited distinct cardiovascular morphological adaptations (i.e., increased LV chamber vs. increased LV wall thickness, lower vs. higher large-conduit arterial PWV) as previously reported (13, 14), suggesting that the habitual exercise training regimes of our trained individuals were sufficient to test our hypothesis. Third, we measured steady-state BP responses to the short-term orthostatic stimulation because such measures could provide useful clinical and pathophysiological information (11, 16). However, it remains unclear if an individual's BP response to 5 min HUT is indicative of their tolerance to prolonged orthostatic stress.
In summary, we investigated the influence of chronic exercise training (e.g., endurance exercise training vs. resistance exercise training) on the BP responses to the orthostatic stimulation. Our findings suggest that the BP response to HUT varies as a function of habitual training modality, and that this is related to exercise training-induced morphological adaptations of the LV and large-conduit arteries.
This study was supported by the Uehara Memorial Foundation (J. Sugawara) and Mizuno Sports Promotion Foundation (J. Sugawara).
No conflicts of interest, financial or otherwise, are declared by the author(s).
Author contributions: J.S., H.K., and S.O. conception and design of research; J.S., H.K., T.M., T.I., and S.O. performed experiments; J.S., H.K., T.M., and T.I. analyzed data; J.S., H.K., T.M., T.I., J.P.F., and S.O. interpreted results of experiments; J.S. prepared figures; J.S. drafted manuscript; J.S., J.P.F., and S.O. edited and revised manuscript; J.S., H.K., T.M., T.I., J.P.F., and S.O. approved final version of manuscript.
- Copyright © 2012 the American Physiological Society