The purpose of the present study was to examine the changes in maximum voluntary isometric contraction (MVC) in the contralateral untrained limb during unilateral resistance training and detraining, and to examine the factors inducing these changes by means of electrophysiological techniques. Nine healthy males trained their plantar flexor muscles unilaterally 4 day-s x week(-1) for 6 weeks using 3 sets of 10-12 repetitions at 70-75% of one-repetition maximum a day, and detrained for 6 weeks. Progressive unilateral resistance training significantly (P < 0.05) increased MVC, integrated electromyogram (iEMG), and voluntary activation in the trained and contralateral untrained limbs. The changes in MVC after training were significantly correlated with the changes in iEMG in both limbs. No significant changes occurred in MVC, voluntary activation, and iEMG in the contralateral limb after detraining. The changes in MVC after detraining did not correlate with the changes in voluntary activation or iEMG in either limb. Training and detraining did not alter twitch and tetanic peak torques in either limb. These results suggest that the mechanisms underlying cross education of muscular strength may be explained by central neural factors during training, but not solely so during detraining.
The purpose of the present study was to elucidate the influence of intermittent hypobaric hypoxia at rest on endurance performance and cardiorespiratory and hematological adaptations in trained endurance athletes. Twelve trained male endurance runners were assigned to either a hypoxic group (n = 6) or a control group (n = 6). The subjects in the hypoxic group were exposed to a simulated altitude of 4500 m for 90 min, three times a week for 3 weeks. The measurements of 3000 m running time, running time to exhaustion, and cardiorespiratory parameters during maximal exercise test and resting hematological status were performed before (Pre) and after 3 weeks of intermittent hypoxic exposure (Post). These measurements were repeated after the cessation of intermittent hypoxia for 3 weeks (Re). In the control group, the same parameters were determined at Pre, Post, and Re for the subjects not exposed to intermittent hypoxia. The athletes in both groups continued their normal training together at sea level throughout the experiment. In the hypoxic group, the 3000 m running time and running time to exhaustion during maximal exercise test improved. Neither cardiorespiratory parameters to maximal exercise nor resting hematological parameters were changed in either group at Post, whereas oxygen uptake (.V(O2)) during submaximal exercise decreased significantly in the hypoxic group. After cessation of intermittent hypoxia for 3 weeks, the improved 3000 m running time and running time to exhaustion tended to decline, and the decreased .V(O2) during submaximal exercise returned to Pre level. These results suggest that intermittent hypoxia at rest could improve endurance performance and submaximal exercise efficiency at sea level in trained endurance athletes, but these improvements are not maintained after the cessation of intermittent hypoxia for 3 weeks.
The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (Sa(O2)) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and Sa(O2) during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (VO2), expired minute ventilation (VE), and Sa(O2) were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2 (VE/VO2) and Sa(O2) during submaximal exercise. There were significant correlations among the changes in HVR at rest and in VE/VO2 and Sa(O2) during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.
GaN self-assembled quantum dots (QDs) with high quality and high density have been grown by low-pressure metalorganic chemical vapor deposition under very low V/III ratios. In depositing over a critical thickness of four monolayer GaN, we observed a transition from two-dimensional to three-dimensional growth mode. The density of the QDs could be changed between 109 and 1010 cm−2. The typical diameter and height of the QDs were 20 and 2 nm, respectively. The size of the QDs was controlled to a considerable extent by changing the growth temperature and V/III ratio. Moreover, we observed two photoluminescence peaks from both the QDs and the wetting layer at room temperature. This result clearly demonstrates that the GaN QDs were formed with the Stranski–Krastanow growth mode.
The purpose of the present study was to clarify the following: (1) whether steady state oxygen uptake (VO(2)) during exercise decreases after short-term intermittent hypoxia during a resting state in trained athletes and (2) whether the change in VO(2) during submaximal exercise is correlated to the change in endurance performance after intermittent hypoxia. Fifteen trained male endurance runners volunteered to participate in this study. Each subject was assigned to either a hypoxic group (n=8) or a control group (n=7). The hypoxic group spent 3 h per day for 14 consecutive days in normobaric hypoxia [12.3 (0.2)% inspired oxygen]. The maximal and submaximal exercise tests, a 3,000-m time trial, and resting hematology assessments at sea level were conducted before and after intermittent normobaric hypoxia. The athletes in both groups continued their normal training in normoxia throughout the experiment. VO(2) during submaximal exercise in the hypoxic group decreased significantly (P<0.05) following intermittent hypoxia. In the hypoxic group, the 3,000-m running time tended to improve (P=0.06) after intermittent hypoxia, but not in the control group. Neither peak VO(2) nor resting hematological parameters were changed in either group. There were significant (P<0.05) relationships between the change in the 3,000-m running time and the change in VO(2) during submaximal exercise after intermittent hypoxia. The results from the present study suggest that the enhanced running economy resulting from intermittent hypoxia could, in part, contribute to improved endurance performance in trained athletes.
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