No abstract

Background-Reductions in the compliance of central arteries exert a number of adverse effects on cardiovascular function and disease risk. Endurance training is efficacious in increasing arterial compliance in healthy adults. We determined the effects of resistance training on carotid arterial compliance using the intervention study design. Methods and Results-Twenty-eight healthy men 20 to 38 years old were randomly assigned to the intervention group (nϭ14) and the control group (nϭ14). Control subjects were instructed not to alter their normal activity levels throughout the study period. Intervention subjects underwent 3 supervised resistance training sessions per week for 4 months and detraining for a subsequent 4 months. The resistance training increased maximal strength in all muscle groups tested (PϽ0.001). There were no significant differences in baseline arterial compliance and ␤-stiffness index between the intervention and control groups. In the intervention group, carotid arterial compliance decreased 19% (PϽ0.05), and ␤-stiffness index increased 21% (PϽ0.01) after resistance training. These values returned completely to the baseline levels during the detraining period. Arterial compliance did not change in the control group. In both groups, there were no significant changes in brachial and carotid blood pressure, carotid intima-media thickness, lumen diameter, and femoral arterial compliance. Changes in carotid artery compliance were significantly and negatively related to corresponding changes in left ventricular mass index (rϭϪ0.56, PϽ0.001) and left ventricular hypertrophy index (rϭϪ0.68, PϽ0.001). Conclusions-In marked contrast to the beneficial effect of regular aerobic exercise, several months of resistance training "reduces" central arterial compliance in healthy men.

Aims: The Modelflow method can estimate cardiac output from arterial blood pressure waveforms using a three-element model of aortic input impedance (aortic characteristic impedance, arterial compliance, and systemic vascular resistance). We tested the reliability of a non-invasive cardiac output estimation during submaximal exercise using the Modelflow method from finger arterial pressure waveforms collected by Portapres in healthy young humans. Methods: The Doppler echocardiography method was used as a reference method. Sixteen healthy young subjects (nine males and seven females) performed a multi-stage cycle ergometer exercise at an intensity corresponding to 70, 90, 110 and 130% of their individual ventilatory threshold for 2 min each. The simultaneous estimation of cardiac output (15 s averaged data) using the Modelflow and Doppler echocardiography methods was performed at rest and during exercise. Results and Conclusion: The Modelflow-estimated cardiac output correlated significantly with the simultaneous estimates by the Doppler method in all subjects (r ¼ 0.87, P < 0.0001) and the SE of estimation was 1.93 L min )1 . Correlation coefficients in each subject ranged from 0.91 to 0.98. Although the Modelflow method overestimated cardiac output, the errors between two estimates were not significantly different among the exercise levels. These results suggest that the Modelflow method using Portapres could provide a reliable estimation of the relative change in cardiac output non-invasively and continuously during submaximal exercise in healthy young humans, at least in terms of the relative changes in cardiac output. Keywords cardiac output, Doppler echocardiography, finger arterial pressure waveform.Cardiac output (CO) is one indicator of cardiac function. A non-invasive estimation of CO with high time resonance is favourable in exercise physiological research. The Modelflow method involves the measurement of beat-by-beat aortic flow volume from arterial pressure waveforms (Wesseling et al.

Reductions in the compliance of central arteries exert a number of adverse effects on systemic cardiovascular function and disease risk. Using the cross-sectional study design, we determined the relation between chronic resistance training and carotid arterial compliance. A total of 62 healthy normotensive men, 20 to 39 years of age (young) and 40 to 60 years of age (middle-aged), who were either sedentary or resistance-trained, were studied. In both activity groups, carotid arterial compliance (simultaneous ultrasound and applanation tonometry) was lower (P<0.05) in the middle-aged compared with the young men. There was no significant difference between young sedentary and resistance-trained men. In the middle-aged group, carotid arterial compliance in the resistance-trained men was approximately 30% lower (P<0.01) than their sedentary peers. Femoral artery compliance and arm pulse wave velocity (measures of peripheral artery stiffness) were not different among any groups. Left ventricular hypertrophy index (echocardiography) was greater (P<0.05) in resistance-trained compared with sedentary men and was associated with carotid arterial compliance (r=-0.35; P<0.01). We concluded that (1) resistance training is associated with the smaller central arterial compliance in healthy middle-aged men; (2) age-related reductions in arterial compliance was greater in resistance-trained men than in sedentary men; and (3) the lower arterial compliance in the resistance-trained men is associated with left ventricular hypertrophy. In marked contrast to the beneficial effect of regular aerobic exercise, the present findings are not consistent with the idea that resistance training exerts beneficial influences on arterial wall buffering functions.

The cross-sectional area (CSA) of large-conductance arteries increases in response to endurance training in humans. To determine whether training-induced changes in arterial structure are systemic in nature or, rather, are confined to the arteries supplying exercising muscles, we studied 10 young men who performed one-legged cycle training [80% of one-legged peak O2 uptake (VO2 peak)), 40 min/day, 4 days/wk] for 6 wk and detraining for another 6 wk. There were no significant differences in baseline one-legged VO2 peak) and CSA of the common femoral artery and vein (via B-mode ultrasound) between experimental and control legs. In the experimental leg, one-legged VO2 peak) increased 16% [from 3.0 +/- 0.1 to 3.4 +/- 0.1 (SE) l/min], arterial CSA increased 16% (from 84 +/- 3 to 97 +/- 5 mm2), and venous CSA increased 46% (from 56 +/- 5 to 82 +/- 5 mm2) after endurance training. These changes returned to baseline during detraining. There were no changes in one-legged VO2 peak) and arterial CSA in the control leg, whereas femoral venous CSA in the control leg significantly increased 24% (from 54 +/- 5 to 67 +/- 4 mm2) during training. Changes in femoral arterial and venous CSA in the experimental leg were positively and significantly related to corresponding changes in one-legged VO2 peak) (r = 0.86 and 0.76, respectively), whereas there were no such relations in the control leg (r = 0.10 and 0.17). When stepwise regression analysis was performed, a primary determinant of change in VO2 peak) was change in femoral arterial CSA, explaining approximately 70% of the variability. These results support the hypothesis that the regional increase in blood flow, rather than systemic factors, is associated with the training-induced arterial expansion. Femoral arterial expansion may contribute, at least in part, to improvement in efficiency of blood transport from the heart to exercising muscles and may facilitate achievement of aerobic work capacity.