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The purpose of this study was to clarify the effect one-sided skeletal muscle contraction has on the circulatory system, spinal α-motoneuron excitability, and somatosensory-system-evoked potential. Nine healthy males maintained tension at 10, 20, and 30% of maximal voluntary contraction in static gripping in right hand. Heart rate, ln high frequency (HF), blood pressure (BP), F-wave, and somatosensory-evoked potential (SEP) were recorded during gripping task. BP, F-wave and SEP were recorded from left hand (contralateral side from contracting side). There were significant main effects of contractions strength on heart rate (0%: 68.2 ± 6.8 bpm, 10%: 67.6 ± 7.4 bpm, 20%: 69.7 ± 8.5 bpm, 30%: 73.7 ± 9.3 bpm, F3.24=9.18, P

The present study was performed to test the hypothesis that the blood pressure (BP) response to resistance exercise in middle-aged men with stiffening arteries is greater than that in young men with compliant arteries. The BP responses to acute dynamic resistance exercise (leg press) at individual relative (low, moderate and high) and absolute intensities were investigated in both young and middle-aged men. A total of 21 sedentary healthy normotensive men, 21-25 years of age (young) and 41-59 years of age (middle-aged), were included in the study. At rest, the arterial compliance (simultaneous ultrasound and applanation tonometry) and muscle strength (leg press) were lower, and indices of arterial stiffness and BP were higher in the middle-aged men than in the young men (p < 0.05). There were no significant differences in height, body mass, or heart rate between the two groups. During exercise, the systolic BP of the middle-aged men at 80% one-repetition maximum (1RM) was significantly lower than that of the young men for the last half of the exercise period (p < 0.05). The amounts of change in systolic and diastolic BP from baseline to the end of resistance exercise were lower in the middle-aged men than in the young men at individual relative intensities (p < 0.05) and at individual absolute intensity. In contrast to our hypothesis, these findings indicated that the BP response during dynamic resistance exercise using large muscle groups may be attenuated in middle-aged men relative to young men.

This study examined the effects of low-intensity morning exercise (ME) on physiological response during unsteady workload evening exercise. Nine healthy men participated in the following 2 experimental conditions: 15 minutes of bicycle exercise at 40% maximum oxygen consumption (V[Combining Dot Above]O2max) in the morning (the ME condition) and rest (control [C] condition). Heart rate (HR), blood pressure (BP), temperature, oxygen uptake, and natural logarithm of high frequency, an index of cardiac parasympathetic modulation, were measured before evening exercises, which were performed for 32 minutes in 2 parts: The steady-state exercise test included three 4-min bouts of exercise at 20, 60, and 40% V[Combining Dot Above]O2max. The unsteady exercise test consisted of 4-min bouts of exercise with gradual increases and decreases in workload at 20 and 60% V[Combining Dot Above]O2max. Heart rate, BP, and oxygen uptake were measured in both experiments. Maximal and minimal values, amplitude, and phase lags were measured with each cycle of unsteady workload exercise. With steady-state exercise, HR and systolic BP at 60 and 40% V[Combining Dot Above]O2max were significantly lower in the ME condition than in the C condition. However, oxygen uptake was not significantly different between the 2 conditions. With unsteady exercise, the HR and oxygen uptake phase lags were significantly shorter and the amplitude of oxygen intake was significantly larger in the ME condition than in the C condition. There were no significant differences in physiological parameters between the conditions at rest or during recovery. The physiological response during evening exercise is enhanced by low-intensity ME, which might be an effective conditioning method on a sporting event day.

Aim: Fluctuations in autonomic nervous functions throughout the menstrual cycle and the underlying mechanism concerning them are not well known. This study was designed to test the hypothesis that fluctuations in cardiovagal baroreflex sensitivity (BRS) throughout the menstrual cycles of young women are due to fluctuations in carotid arterial distensibility. Methods: In eight eumenorrhoeic healthy young women (18–24 years), we determined the variations in the carotid arterial distensibility coefficient (DC; via simultaneous ultrasonography and applanation tonometry), cardiovagal BRS (phase IV of the Valsalva manoeuvre and the sequence method; up- or down-sequence spontaneous BRS), and serum oestradiol and progesterone concentrations at five points in the menstrual cycle (menstrual = M, follicular = F, ovulatory = O, early luteal = EL, and late luteal = LL). Results: Serum oestradiol and progesterone levels were consistent with the predicted cycle phases. Carotid arterial DC fluctuated cyclically, increasing significantly from the M (52.4 ± 4.9 × 10−3 kPa−1, mean ± SE) and F (52.7 ± 4.4) phases to the O (57.6 ± 4.4) phase and declining sharply in the EL (46.0 ± 4.0) and LL (45.1 ± 3.0) phases (F = 6.37, P

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 (V˙o 2 peak), 40 min/day, 4 days/wk] for 6 wk and detraining for another 6 wk. There were no significant differences in baseline one-leggedV˙o 2 peak and CSA of the common femoral artery and vein (via B-mode ultrasound) between experimental and control legs. In the experimental leg, one-leggedV˙o 2 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-leggedV˙o 2 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-leggedV˙o 2 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 inV˙o 2 peak was change in femoral arterial CSA, explaining ∼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.

To examine the possible age-related blood pressure (BP) deregulation in response to central hypervolemia, we measured spontaneous baroreflex sensitivity (SBRS), carotid arterial compliance (CC), and R-R interval coefficient of variation (RRICV) during basal and thermoneutral resting head-out-of-water immersion (HOWI) in 7 young (YG = 24.0 +/- 0.8 years) and 6 middle-aged/older (OL = 59.3 +/- 1.3 years) healthy men. Compared with basal conditions (YG = 19.6 +/- 4.0 vs OL = 6.1 +/- 1.5 ms/mmHg, P < 0.05), SBRS remained higher in YG than OL during rest HOWI (YG = 23.6 +/- 6.6 vs OL = 9.3 +/- 2.1 ms/mmHg, P < 0.05). The RRICV was significantly different between groups (YG = 6.5 +/- 1.4 vs OL = 2.8 +/- 0.4%, P < 0.05) under HOWI. The OL group had no increase in CC, but a significant increase in systolic BP (basal = 115.3 +/- 4.4 vs water = 129.3 +/- 5.3 mmHg, P < 0.05) under HOWI. In contrast, the YG group had a significant increase in CC (basal = 0.16 +/- 0.01 vs water = 0.17 +/- 0.02 mm(2)/mmHg, P < 0.05) with no changes in systolic BP. SBRS was positively related to CC (r = 0.58, P < 0.05 for basal vs r = 0.62, P < 0.05 for water). Our data suggest that age-related vagal dysfunction and reduced CC may be associated with SBRS differences between YG and OL groups, and with BP elevation during HOWI in healthy older men.

The aim of the present study was to determine non-invasively the effects of endurance training on both the size and blood flow of the arterial conductance vessels during exercise by men. Twelve healthy male subjects were assigned to either an exercise-trained group (ET, n = 7) or a sedentary control group (S, n = 5). The ET group underwent cycle-endurance training for 8 weeks (80% VO2max, 40 min day-1, 5 days week-1). The S group led normal lives during the 8-week period. Before and after the training period, cross-sectional areas (CSA) of the ascending and abdominal aorta were measured by echography. Measurements were taken in the semisupine position on a cycle ergometer fitted with a backrest, at rest and during 40, 60 and 80% VO2max of exercise. In addition, Doppler ultrasonographic velocity and flow in the ascending aorta were simultaneously measured. The CSA of the ascending and abdominal aorta after training were significantly larger than those before training in the ET group. Although there were no significant differences in the peak and mean velocities in the ascending aorta before and after the training in the ET group, the blood flow in the ascending aorta during exercise after training was significantly larger than that found before training at each relative intensity. There were no significant differences in any of the Doppler echographic parameters in the S group. These findings suggest that the arterial conductance vessels can be morphologically altered in an adaptive response to the endurance training. Furthermore, the dilation of the conductance vessels with endurance training contributes to an increase in blood flow to the exercising muscles without a rise in blood velocity. In other words, the arterial conductance vessels adapt to maintain adequate blood velocity and shear stress.

Endurance training induces reductions in both resting and postexercise heart rate (HR). If adaptation in cardiac autonomic regulation is a contributing factor in these reductions, changes in cardiac autonomic nervous system (ANS) should correspond to those in HR during an endurance-training program. We investigated the changes in resting and postexercise HR variabilities (both in the time and frequency domain) over a 6-wk training program.HR variability was measured five times in an endurance-training group (N = 7) and four times in a control group (N = 5) during the course of study.Endurance training decreased HR and increased indices of parasympathetic modulation measured both at rest and during postexercise recovery periods. Noteworthy is that no changes in either HR or indices of ANS modulation measured during postexercise recovery periods were detectable after the first 7 d of the study despite continued changes in resting HR and indices in ANS modulation measured between the 7th and 42nd days of the endurance-training program.The study demonstrates that with endurance-training changes in cardiac ANS modulation partly contribute to a decrease in HR at rest and during postexercise recovery period, and that adaptation of the cardiac autonomic control occurs sooner in immediate postexercise periods than at rest.