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71.
Gregory C. Bogdanis Mary E. Nevill Henryk K. A. Lakomy Carl M. Graham Gary Louis 《European journal of applied physiology》1996,74(5):461-469
The effects of active recovery on metabolic and cardiorespiratory responses and power output were examined during repeated
sprints. Male subjects (n = 13) performed two maximal 30-s cycle ergometer sprints, 4 min apart, on two separate occasions with either an active [cycling
at 40 (1)% of maximal oxygen uptake; mean (SEM)] or passive recovery. Active recovery resulted in a significantly higher mean
power output (
) during sprint 2, compared with passive recovery [
] 603 (17) W and 589 (15) W, P < 0.05]. This improvement was totally attributed to a 3.1 (1.0)% higher power generation during
the initial 10 s of sprint 2 following the active recovery (P < 0.05), since power output during the last 20 s sprint 2 was the same after both recoveries. Despite the higher power output
during sprint 2 after active recovery, no differences were observed between conditions in venous blood lactate and pH, but
peak plasma ammonia was significantly higher in the active recovery condition [205 (23) vs 170 (20) μmol · 1−1;P < 0.05]. No differences were found between active and passive recovery in terms of changes in plasma volume or arterial blood
pressure throughout the test. However, heart rate between the two 30-s sprints and oxygen uptake during the second sprint
were higher for the active compared with passive recovery [148 (3) vs 130 (4) beats · min−1;P < 0.01) and 3.3 (0.1) vs 2.8 (0.1) 1 · min−1;P < 0.01]. These data suggest that recovery of power output during repeated sprint exercise is enhanced when low-intensity
exercise is performed between sprints. The beneficial effects of an active recovery are possibly mediated by an increased
blood flow to the previously exercised muscle. 相似文献
72.
P. D. BALSOM K. S
DERLUND B. SJ
DIN B. EKBLOM 《Acta physiologica (Oxford, England)》1995,154(3):303-310
Seven male subjects performed repeated bouts of high-intensity exercise, on a cycle ergometer, before and after 6 d of creatine supplementation (20 g Cr H2O day-1). The exercise protocol consisted of five 6-s exercise periods performed at a fixed exercise intensity, interspersed with 30-s recovery periods (Part I), followed (40 s later) by one 10 s exercise period (Part II) where the ability to maintain power output was evaluated. Muscle biopsies were taken from m. vastus lateralis at rest, and immediately after (i) the fifth 6 s exercise period in Part I and (ii) the 10 s exercise period in Part II. In addition, a series of counter movement (CMJ) and squat (SJ) jumps were performed before and after the administration period. As a result of the creatine supplementation, total muscle creatine [creatine (Cr) + phosphocreatine (PCr)] concentration at rest increased from (mean + SEM) 128.7 (4.3) to 151.5 (5.5)mmolkg_1 dry wt (P < 0.05). This was accompanied by a 1.1 (0.5) kg increase in body mass (P < 0.05). After the fifth exercise bout in Part I of the exercise protocol, PCr concentration was higher [69.7 (2.3) vs. 45.6 (7.5) mmol kg“‘ dry wt, P < 0.05], and muscle lactate was lower [26.2 (5.5) vs. 44.3 (9.9) mmol kg”1 dry wt, P < 0.05] after vs. before supplementation. In Part II, after creatine supplementation, subjects were better able to maintain power output during the 10-s exercise period (P < 0.05). There was no change in jump performance as a result of the creatine supplementation (P > 0.05). These findings show that enhanced fatigue resistance during short duration high-intensity exercise following creatine supplementation is associated with a greater availability of PCr and a lower accumulation of lactate in the muscle. The finding that jump performance was not enhanced suggests that short-term creatine feeding does not influence peak power output. 相似文献
73.
Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses
Recently, it was reported that acute hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s–1 on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg (P<0.0001) at 30 s of maximal exertion, but further significant changes did not occur as exercise duration increased to 120 s [arterial oxygen tension 72.4 (2) mmHg]. A significant arterial hypoxemia also developed in galloping horses in the acute hypervolemia study [arterial oxygen tension at 30 and 120 s was 76.7 (1.7) and 71.9 (1.6) mmHg, respectively], but significant differences between treatments could not be demonstrated. In both treatments, a similar desaturation of arterial hemoglobin was also observed at 30 s of maximal exercise, which intensified with increasing exercise duration as hyperthermia, acidosis and hypercapnia intensified. Thus, acute expansion of plasma volume did not benefit arterial oxygenation in maximally exercising thoroughbred horses. 相似文献
74.
S. Stamatelopoulos A. Tsakiris S. Moulopoulos 《Medical & biological engineering & computing》1978,16(4):383-386
An implantable mechanical-chemical device was constructed to act as a feedback mechanism in controlling the blood pressure. It consisted of a balloon connected to a rubber catheter ending in a slit valve. Flow-pressure curves were derived fromin vitro testings for three valve thresholds (120, 140 and 170 mmHg). Five fast-acting hypotensive drugs subsequently filled the device during 40 noradrenaline infusions in 25 dogs, with the balloon in the abdominal aorta and the catheter in the inferior vena cava. The results were as follows: (i) Following a short initial increase in systolic aortic pressure, significantly lower (p<0·001) than in control experiments, the device prevented any pressure rise above its threshold. (ii) The time needed for pressure lowering at the device's threshold depended on the drug used being 3·34±0·84 (mean ± s.e. in minutes) for sodium nitroprusside, 5·99±0·96 for phentolamin, 11·63±2·97 for hydralazine, 14·54±2·43 for a-methyl-dopa and 23·32±2·07 for diazoxide. 相似文献
75.
Summary In 11 adult cats, lightly anesthetized with chloralose-urethane, blood from both common carotid arteries was led into a plastic chamber of 15–20 ml and returned to the carotids at a point 1.5 cm more cranial. By doing so arterial blood was assumed to pool within the chamber and lose itsP
CO
2 oscillations which are normally known to exist as a result of the respiratory cycle. In control periods blood bypassed the chamber, thus maintaining respiratoryP
CO
2 oscillations. Spontaneous ventilation was measured spirometrically. The animals were breathing pure O2.Results. 1. When the sinus (carotid) nerves were intact or sectioned there was no significant difference in ventilation before or after switching from non-oscillating to oscillatingPa
CO
2. 2. When the vertebral arteries were ligated a drop in ventilation occurred after turning to oscillatingPa
CO
2 which was followed by a slight rise above control values after 30–50 sec. This phenomenon was independent of sinus nerve integrity. Thus in hyperoxie condition the smallPa
CO
2 oscillations known to occur in phase with respiration do not seem to provide a respiratory stimulus to resting ventilation above that generated by the mean level ofPa
CO
2. The ventilatory depression after vertebral artery ligation must at this time remain unexplained. 相似文献
76.
The effects of two kinds of induction speed of sevoflurane anesthesia on the EEG pattern were compared in the same individual using medical student volunteers: a first exposure of 4% was given, followed after full recovery, by incremental doses of 1, 2 and 4% successively, each being administered for 10min. The arterial blood level of the anesthetic was measured using gaschromatograph. The changes of EEG pattern during fast induction with 4% were not represented by the abbreviation of those observed during the slow induction with the incremental doses. The administration of 4% induced a sudden appearance of high voltage, rhythmic slow waves of 2–3Hz at 1–3min when the arterial blood anesthetic level increased maximally, which was then followed by a pattern of faster activities of 10–14Hz mixed with 5–8Hz slow waves. In contrast, the administration of incremental doses induced an increase in frequency and amplitude of EEG activities in the light plane, followed by their decreases in deeper planes. The final EEG patterns were identical for both these methods of induction. These findings confirmed our previous hypothesis that not only the arterial blood level of anesthetics but the rate of its increase are important factors determining the EEG pattern of anesthesia.(Avramov MN et al.: Effects of different speeds of induction with sevoflurane on the EEG in man. J Anesth 1: 1–7, 1987) 相似文献
77.
T. Kubo M. Kihara H. Hata Y. Misu 《Naunyn-Schmiedeberg's archives of pharmacology》1987,335(3):274-277
Summary The cardiovascular effects of selective alpha1 and alpha2 agonists and antagonists injected into the nucleus tractus solitarii (NTS) were studied in urethane-anesthetized rats. Methoxamine (0.3–3 g) injected bilaterally into the NTS caused a dose-dependent increase in blood pressure and heart rate. Phenylephrine (6 g) and an imidazolidine derivative St 587 (3 g) similarly injected also produced an increase in blood pressure, whereas a-methylnoradrenaline and an azepine derivative B-HT 920 (1 and 3 g) caused a decrease in blood pressure and heart rate. The pressor response to methoxamine (1 g) was markedly inhibited by prazosin (0.3 pg) injected into the same sites or hexamethionum (25 mg/kg, i. v.). Prazosin (0.3 g) alone injected bilaterally into the NTS did not affect the blood pressure, while yohimbine (0.1 g) similarly injected increased the pressure. These results suggest that in the rat NTS there exist alpha1 adrenoceptors responsible for an increase in arterial pressure. The NTS alpha2 adrenoceptors seem to be involved in the tonic regulation of arterial pressure.
Send offprint requests to T. Kubo at the above address 相似文献
78.
We have studied the haemodynamic effects of the application of the medical anti-shock trouser (MAST) in 10 healthy subjects in the semi-upright position in order to simulate mild hypovolaemia. Left ventricular end diastolic dimension (EDD) was measured by M-mode echocardiography and cardiac output (CO) by the Doppler ultrasound technique. Forearm blood flow (FBF) was measured by plethysmography and blood pressure (BP) by the standard cuff technique. Systematic increases in MAST pressure of up to 80 mm Hg were applied. EDD increased to a maximum of 9.3% (p0.01) which was associated with a maximum increase in CO of 31.7% (p0.05). FBF increased by a maximum of 54.2% (p0.001) whilst BP increased by a maximum of 12% (p0.001). These results demonstrate that the application of the MAST is an effective means of transferring blood to the central circulation by compression of the capacitance vessels resulting in significant increases in cardiac output and tissue perfusion. At high pressures there was evidence of compression of resistance vessels, which may be useful in reducing blood loss. The ease and rapidity with which his suit can be applied suggests that it may be useful in the short term treatment of hypovolaemia. 相似文献
79.
A carotid end-to-end anastomosis was performed in 50 Wistar rats (mean weight 260 g) by means of a Coherent 900 argon laser. Laser pulses (average 19) of 300 mW power and 5 s exposure time were used, the beam being focused to form a spot of 150 m diameter. From day 0 to day 210, 13 specimens underwent scanning electron microscope examination. The results show that the laser impact produces a wall injury of 100 m in width with some coagulative necrosis of the media and adventitia. The line of anastomosis became re-endothelialized within four days, at which time collagen fusion was observed in the subendothelial layers. The longitudinal arrangement of the endothelial cells was restored by day 10. In the long term, a thick collagenous meshwork maintained the strength of the media, while normal endothelium covered the anastomosis. Complications such as disruption and aneurysm formation were attributed to technical problems.
Résumé Anastomoses micro-artérielles au laser argon: étude en microscopie électronique à balayage. Les auteurs réalisent au laser Argon (Coherent 900) une anastomose carotidienne terminoterminale sur une série de 50 rats Wistar de poids moyen de 260 g. Les impacts laser (en moyenne 19) sont de 300 mW de puissance et d'une durée de 5 s chacun, avec un point de focalisation de 150 m de diamètre. On réalise sur 13 spécimens un examen en microscopie électronique à balayage. L'impact laser induit sur la paroi artérielle une lésion de 100 m de large avec une légère nécrose de coagulation de la media et de l'adventice. La ligne de suture est re-endothélialisée dès le quatrième jour, alors qu'une fusion du collagène est observée dans les couches sousendothéliales. L'arrangement longitudinal des cellules endothéliales est retrouvé dés le dixième jour. A long terme, un réseau collagénique serré assure la résistance de la media et un endothélium normal recouvre la ligne de soudure. Les complications tel que lâchage ou anéurysmes doivent être attribuées aux inconvénients techniques du début de l'expérimentation.相似文献
80.
Kenneth A. Kesler MD Malcolm B. Herring MD Michael P. Arnold MD Howard M. Park MD Sally Baughman MD John L. Glover MD 《Annals of vascular surgery》1986,1(1):60-65
A fibronectin substrate will significantly enhance the strength of endothelial cell attachment on grafts constructed of polyester elastomer (PE) and polytetrafluoroethylene (e-PTFE). This experiment was undertaken to determine the short-termin vivo stability of endothellum on these fibronectin coated surfaces. Eight mongrel dogs underwent bilateral carotid artery replacement with both graft materlals. All grafts were inoculated with 2,000 cells/mm2 using cultured autogenous venous endothelium labelled with Indium-111-oxine. The Indium-111 label in the grafts was measured immediately prior to implantation, after 1 hour ofin vivo perfusion, and at explantation after 24 hours. The percentage of inoculated cells attached to the grafts before perfusion was simillar for both materials, 93.3±3.0% versus 92.2±7.2%, for PE and e-PTFE respectively. All grafts were patent at one hour after implantation. PE grafts were found to have 93.8±3.9 % of the attached cells present at one hour while e-PTFE grafts had only 54.5 ± 10.8 % remaining, p<.001. After 24 hours, 5/8 (62.5%) e-PTFE grafts and 2/8 (25.0 %) PE grafts remained patent, p=.13. Of the patent grafts however, endothelial cell retention was still superior on the PE grafts with 78.0±0.6% of the attached cells remaining compared to only 24.5±6.1% on e-PTFE, p<.001. Occluded PE grafts had fewer cells remaining at 24 hours than patent ones, 78.0±0.6% versus 31.1±32.8%, respectively, p=.13. Histologically, patent PE grafts demonstrated nearly confluent endothelial monolayers while e-PTFE had patches of endothelial cells surrounded by, a platelet-fibrin carpet. We conclude that short-term patency appears to be determined by the extent of endothelial retention on PE but not e-PTFE. 相似文献