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.
Our previous study showed that relatively low-intensity (approximately 50% one-repetition maximum [1RM]) resistance training (knee extension) with slow movement and tonic force generation (LST) caused as significant an increase in muscular size and strength as high-intensity (approximately 80% 1RM) resistance training with normal speed (HN). However, that study examined only local effects of one type of exercise (knee extension) on knee extensor muscles. The present study was performed to examine whether a whole-body LST resistance training regimen is as effective on muscular hypertrophy and strength gain as HN resistance training. Thirty-six healthy young men without experience of regular resistance training were assigned into three groups (each n = 12) and performed whole-body resistance training regimens comprising five types of exercise (vertical squat, chest press, latissimus dorsi pull-down, abdominal bend, and back extension: three sets each) with LST (approximately 55-60% 1RM, 3 seconds for eccentric and concentric actions, and no relaxing phase); HN (approximately 80-90% 1RM, 1 second for concentric and eccentric actions, 1 second for relaxing); and a sedentary control group (CON). The mean repetition maximum was eight-repetition maximum in LST and HN. The training session was performed twice a week for 13 weeks. The LST training caused significant (p < 0.05) increases in whole-body muscle thickness (6.8 +/- 3.4% in a sum of six sites) and 1RM strength (33.0 +/- 8.8% in a sum of five exercises) comparable with those induced by HN training (9.1 +/- 4.2%, 41.2 +/- 7.6% in each measurement item). There were no such changes in the CON group. The results suggest that a whole-body LST resistance training regimen is as effective for muscular hypertrophy and strength gain as HN resistance training.
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.
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