补充烟酸及耐力训练对急性酒精性肝损伤大鼠SirT1活性与表达的影响及机制研究

目的:研究补充烟酸及耐力训练对急性酒精性肝损伤大鼠SirT1表达、活性的影响及机制.研究方法:以Wistar大鼠建立急性酒精性肝损伤模型,以跑台运动为训练手段,并且给予大鼠补充烟酸,测定血清ALT和AS以及肝脏MnSOD活性、NAD+/NADH比值、MDA含量、SirT1活性、线粒体ATP合成活力、MnSOD和SirT1 mRNA表达.结果:急性酒精摄入导致血清ALT和AST水平、肝脏MDA含量均显著升高,线粒体ATP合成活力、肝脏NAD+/NADH比值、MnSOD及SirT1活性及mRNA表达均显著降低;耐力训练及补充烟酸再给予酒精摄入与只给予酒精摄入血清ALT和AST水平、肝脏MDA含量、线粒体ATP合成活力、肝脏NAD+/NADH比值、MnSOD及SirT1活性及mRNA表达变化规律一致,但变化幅度相对较小.结论:耐力训练及补充烟酸均能提高肝脏细胞内NAD+/NADH的比值,使SirT1活性及表达升高,进而提高肝脏细胞抗氧化能力,达到预防/改善急性酒精性肝损伤的目的.     

运动性疲劳状态下大鼠骨骼肌线粒体呼吸链还原酶活性的研究

目的:研究运动性疲劳状态下,大鼠骨骼肌线粒体呼吸链还原酶复合体活性的变化,进一步探讨骨骼肌运动性疲劳发生的可能机制。方法:以健康雄性Wister大鼠为实验对象,随机分为安静对照组、大强度运动组和中等强度运动组,分光光度法测定线粒体呼吸链酶复合体(Ⅰ~Ⅲ)活性。结果:与安静对照组相比,大强度运动组CⅠ和CⅡ的活性显著性升高(P<0.01),分别升高63.56%和66.64%;CⅢ的活性显著性下降(P<0.01),下降32.20%;中等强度运动组CⅠ和CⅡ的活性显著性升高(P<0.01),分别升高254.24%和59.29%;CⅢ的活性显著性下降(P<0.01),下降30.51%。与大强度运动组相比,中等强度运动组CⅠ的活性显著性上升(P<0.01),上升116.58%,CⅡ和CⅢ的活性无显著性差异。结论:无论是大强度运动还是中等强度运动,在疲劳状态下,骨骼肌线粒体呼吸链还原酶活性都发生不同程度的变化。CⅠ和CⅡ活性显著增加可能是由于运动时能量需求量大,机体代谢过程中底物NADH和琥珀酸量增多引起的,而CⅢ活性明显降低可能与电子漏,CoQ自氧化产生自由基,内膜流动性下降等因素有关。中等强度持续运动对CⅠ活性的影响程度比大强度间歇运动更深远,这可能是运动方式不同所致。     

不同强度运动对大鼠骨骼肌AMP/ATP比值和AMPK活性的影响

目的:研究不同强度运动大鼠腓肠肌AMP、ATP含量及AMPK活性,旨在阐明不同强度运动时AMP/ATP的比值和AMPK的变化特点及二者的关系.方法:将62只雄性SD大鼠分为4大组:安静对照组、小强度运动组、中强度运动组、大强度运动组,其中运动组又各分为3小组,分别在运动后即刻、1 h和6 h取材.小、中和大强度一次性跑台运动的速度分别为10 m/min、18 m/min、26 m/min,坡度10°,时间60 min.AMP、ATP含量测定采用高效液相色谱法(HPLC),AMPK活性测定采用放射性同位素法.结果:小强度运动后AMPK活性不变,中到大强度运动后即刻分别增加50%(P<0.01)和1.8倍(P<0.01)并持续至1h,6 h回到安静水平;中到大强度即刻AMP分别增加16%(P<0.05)和62%(P<0.01),AMP/ATP分别升高33%(P<0.05)和89%(P<0.01),均在1 h回到安静水平;不同强度运动后即刻AMPK与AMP/ATP呈显著正相关(r=0.89).结论:1)AMPK在小强度运动时未激活,中到大强度运动时呈强度依赖性升高;2)运动激活AMPK的机制主要受AMP/ATP比值升高调控,而比值的升高主要依赖于AMP的增加而不是ATP的减少;3)运动后AMPK活性的恢复滞后于AMP/ATP比值的恢复.     

乳酸阈强度运动对超重女大学生心肺机能和身体成分的影响

该研究旨在观察乳酸阈强度训练提升超重女大学生心肺机能和改善身体成分的效果。方法：通过递增负荷实验测定超重女大学生个体乳酸阈，绘制血乳酸-走跑强度动力曲线，依此确定运动干预强度及设计运动方案；受试者进行12周乳酸阈强度运动训练；测定实验前后身体成分、肺活量、最大摄氧量、超声心动等指标进行与对照组的对比分析。结果显示：超重女大学生个体乳酸阈为3.75±0.91mmol/L，乳酸阈强度为6.91±0.88km/h，乳酸阈强度训练靶心率为137±12.2次/min；实验组训练后，体脂%、腹部脂肪含量等非常显著的下降，最大摄氧量、肺活量、每博输出量、射血分数显著性提升；对照组无明显变化。结论：12周乳酸阈强度运动锻炼可显著改善超重女大学生的心肺机能和身体成分；本研究得出的乳酸阈强度可作为超重女大学生有氧健身的参考强度。     

运动对大鼠肝脏GSH、GSSG含量及GSH/GSSG的影响

本实验以游泳训练的大鼠为实验模型 ,观察雄性SD大鼠的肝脏GSH、GSSG的含量以及GSH/GSSG的比值 ,发现一次急性力竭运动后 ,肝脏的GSH含量显著下降 ,P <0 .0 0 1,GSSG的含量显著升高 ,肝脏的GSH/GSSG的比值降低 ,P <0 .0 5 ,GSH/GSSG氧化还原缓冲作用改变的可能性增加影响了细胞信号传递过程。通过对应激激酶富含半胱氨酸结构域的磷酸化作用 ,激活应激激酶 (JNK、p3 8) ,也可激活神经鞘氨醇酶传导途径以及激活转录因子AP -1和NF -κB .最终可能导致某些特定基因转录增加。经十周递增负荷的游泳训练后 ,大鼠肝脏中GSH含量增加 ,P <0 .0 5 ,P <0 .0 0 1。GSSG含量没有变化 ,GSH/GSSG有增加的趋势 ,但无统计学意义。本实验还观察了大鼠肝脏中巯基含量 ,发现巯基与GSH的变化相一致 ,从侧面反映运动导致机体活性氧产生增加 ,细胞氧化还原状态发生改变。     

不同训练程度青少年的血乳酸一强度曲线以及无氧阈的研究

(一) 随着人体工作强度的逐渐增加,体内乳酸也先慢后快地堆积起来,乳酸开始迅速增加时的运动强度我们称为无氧阈。wasserman1973年对无氧阈有过如下定义:“无氧阈即为在代谢酸中毒和伴随而来的气体交换发生变化时的工作水平或耗氧水平”。我们认为,无氧阈可以看作是引起血乳酸急剧升高的最小强度,它是体内有氧代谢向无氧代谢过渡的转折点。小于该强度,有氧代谢占优势;大于该强度则血乳酸急剧上升,无氧酵解占优势。金特曼认为,当血乳酸超过4 mM/L     

对不同强度和时间的运动血乳酸与血红蛋白变化特点的探讨

研究了在不同强度和时间运动时,血乳酸和血红蛋白的变化特点。结果表明：运动时血乳酸浓度和血红蛋白含量有明显升高（P＜0．01）。其变化特点与运动强度和时间有密切关系,但大强度短时间运动时,血乳酸浓度与血红蛋白的含量上升尤为显著（P＜0．01）。     

射箭运动员不同训练时期血液内分泌和氨基酸变化的研究

目的:观察射箭运动员在冬训期间不同训练时期的血液内分泌指标和氨基酸的变化。方法:用化学发光法测定运动员血清睾酮(T)和皮质醇(C),用高效液相色谱法测定血液中四种氨基酸天门冬氨酸(Asp)、谷氨酸(Glu)、甘氨酸(Gly)和r-氨基丁酸(GABA)的含量。结果:男运动员训练疲劳后血睾酮明显下降(P<0.01),与进行中等强度训练时比较也降低,具有显著性意义(P<0.05)。运动员在运动疲劳期,皮质醇显著升高(P<0.01),而T/C比值显著下降(P<0.01)。女运动员在大强度大运动量训练后,血睾酮、T/C比值明显下降(P<0.05),皮质醇明显升高。中等强度训练时,男、女皮质醇较训练前期明显升高(P<0.05)。在进行中等强度训练期和大强度训练期运动后1小时血浆中谷氨酸的血浆浓度明显升高(P<0.01),而在大强度训练期后明显下降,低于安静值。门冬氨酸在中等强度训练后血浆浓度也升高(P<0.05),在疲劳期则呈下降趋势,但仍高于安静值。在进行中等强度训练期和大强度训练期运动1小时后血浆中r-氨基丁酸、甘氨酸均上升,大强度训练期明显升高,与训练前期安静值相比有显著意义(P<0.01)。结论:射箭运动员在长时...     

无氧阈前后的血乳酸值及其代谢特点

人体在以较小强度运动时体内血乳酸水平是很低的,当运动强度增加到一定阈值时血乳酸开始迅速增加,这个阈值即为无氧阈。无氧阈时的血乳酸约为四毫克分子/升。这时的一切可以定量的生理指标都可以用来表示无氧阈值。比如强度,耗氧量、肌电图     

摄氧量动力学的指数函数方程及对工作能力的影响

摄氧量动力学反映的是运动开始后摄氧量逐渐增加至稳定状态过程的变化情况，其曲线在小于无氧阈强度时呈单因素指数函数方程特征，在大于无氧阈强度时呈双因素指数函数方程特征，即包含了乳酸成分。     

Effect of 6 weeks of endurance training on the lactate minimum speed

The aim of this study was to assess the sensitivity of the lactate minimum speed test to changes in endurance fitness resulting from a 6 week training intervention. Sixteen participants (mean +/- s :age 23 +/- 4 years;body mass 69.7 +/- 9.1 kg) completed 6 weeks of endurance training. Another eight participants (age 23 +/- 4 years; body mass 72.7 +/-12.5 kg) acted as non-training controls. Before and after the training intervention, all participants completed: (1) a standard multi-stage treadmill test for the assessment of VO 2max , running speed at the lactate threshold and running speed at a reference blood lactate concentration of 3 mmol.l -1 ; and (2) the lactate minimum speed test, which involved two supramaximal exercise bouts and an 8 min walking recovery period to increase blood lactate concentration before the completion of an incremental treadmill test. Additionally, a subgroup of eight participants from the training intervention completed a series of constant-speed runs for determination of running speed at the maximal lactate steady state. The test protocols were identical before and after the 6 week intervention. The control group showed no significant changes in VO 2max , running speed at the lactate threshold, running speed at a blood lactate concentration of 3 mmol.l -1 or the lactate minimum speed.In the training group, there was a significant increase in VO 2max (from 47.9 +/- 8.4 to 52.2 +/- 2.7 ml.kg -1 .min -1 ), running speed at the maximal lactate steady state (from 13.3 +/- 1.7 to 13.9 +/- 1.6 km.h -1 ), running speed at the lactate threshold (from 11.2 +/- 1.8 to 11.9 +/- 1.8 km.h -1 ) and running speed at a blood lactate concentration of 3 mmol.l -1 (from 12.5 +/- 2.2 to 13.2 +/- 2.1 km.h -1 ) (all P ? 0.05). Despite these clear improvements in aerobic fitness, there was no significant difference in lactate minimum speed after the training intervention (from 11.0 +/- 0.7 to 10.9 +/- 1.7 km.h -1 ). The results demonstrate that the lactate minimum speed,when assessed using the same exercise protocol before and after 6 weeks of aerobic exercise training, is not sensitive to changes in endurance capacity.     

Effect of 6 weeks of endurance training on the lactate minimum speed

The aim of this study was to assess the sensitivity of the lactate minimum speed test to changes in endurance fitness resulting from a 6 week training intervention. Sixteen participants (mean +/- s: age 23+/-4 years; body mass 69.7+/-9.1 kg) completed 6 weeks of endurance training. Another eight participants (age 23+/-4 years; body mass 72.7+/-12.5 kg) acted as non-training controls. Before and after the training intervention, all participants completed: (1) a standard multi-stage treadmill test for the assessment of VO2max, running speed at the lactate threshold and running speed at a reference blood lactate concentration of 3 mmol x l(-1); and (2) the lactate minimum speed test, which involved two supramaximal exercise bouts and an 8 min walking recovery period to increase blood lactate concentration before the completion of an incremental treadmill test. Additionally, a subgroup of eight participants from the training intervention completed a series of constant-speed runs for determination of running speed at the maximal lactate steady state. The test protocols were identical before and after the 6 week intervention. The control group showed no significant changes in VO2max, running speed at the lactate threshold, running speed at a blood lactate concentration of 3 mmol x l(-1) or the lactate minimum speed. In the training group, there was a significant increase in VO2max (from 47.9+/-8.4 to 52.2+/-2.7 ml x kg(-1) x min(-1)), running speed at the maximal lactate steady state (from 13.3+/-1.7 to 13.9+/-1.6 km x h(-1)), running speed at the lactate threshold (from 11.2+/-1.8 to 11.9+/-1.8 km x h(-1)) and running speed at a blood lactate concentration of 3 mmol x l(-1) (from 12.5+/-2.2 to 13.2+/-2.1 km x h(-1)) (all P < 0.05). Despite these clear improvements in aerobic fitness, there was no significant difference in lactate minimum speed after the training intervention (from 11.0+/-0.7 to 10.9+/-1.7 km x h(-1)). The results demonstrate that the lactate minimum speed, when assessed using the same exercise protocol before and after 6 weeks of aerobic exercise training, is not sensitive to changes in endurance capacity.     

下坡跑运动与重复运动对大鼠骨骼肌组织病理学影响研究

为探讨重复运动后大鼠骨骼肌损伤适应过程中组织病理改变,将大鼠分为正常对照组、下坡跑运动组、重复运动组并分别进行下坡跑运动及重复运动,观察下坡跑运动及一周后重复运动后即刻、24 h、48 h、72 h、168 h大鼠股四头肌病理切片的变化。结果表明：重复运动组各时间段形态学变化较一次大强度下坡跑运动组有所减轻,表现为下坡跑运动后24 h肌纤维不完全断裂,损伤处细胞溶解,48 h病灶开始逐步清除,至168 h后仍有部分病灶存在。重复运动后症状相应减轻,48h后病灶清除速度明显加快,168 h后基本恢复到正常水平。这可能是损伤修复后肌纤维再生重建、肌节长度趋于均等化、增强了抗损伤能力的结果,提示重复运动能有效加速骨骼肌损伤修复的速度,加速骨骼肌对运动训练刺激的适应性。     

The effect of intensive interval training on the anaerobic power of the rat quadriceps muscle

The effect of intensive interval training on the maximal anaerobic power of the rat quadriceps muscle was investigated. The anaerobic energy production was estimated from the changes in the concentrations of phosphocreatine, adenine nucleotides, inosine monophosphate and lactate in freeze-clamped muscle tissue after electrical stimulation for 2-30 s. The results showed that the maximal running speed of rats tested increased by 24%, the maximal force exerted increased by 13%, and the succinate dehydrogenase activity by 48%, while the adenylate kinase activity was the same before and after training. No difference could be observed between the maximal anaerobic power of the quadriceps muscles of trained and sedentary animals. It seems that trained muscles may be able to work with a higher degree of economy than untrained muscles.     

Reliability of near-infrared spectroscopy for determining muscle oxygen saturation during exercise

Near-infrared spectroscopy is currently used to assess changes in the oxygen saturation of the muscle during exercise. The primary purpose of this study was to assess the reliability of near-infrared spectroscopy in determining muscle oxygen saturation (StO2) in the vastus lateralis during cycling and the gastrocnemius during running for exercise intensities at lactate threshold and maximal effort. Test-retest reliability was determined from an intraclass correlation coefficient obtained from a one-way analysis of variance. Reliability of muscle StO2 for the gastrocnemius at lactate threshold was R = .87, and R = .88 at maximal effort. Reliability of muscle StO2 for the vastus lateralis at lactate threshold was R = .94 and R = .99 at maximal effort.     

Changes in blood lactate and pyruvate concentrations and the lactate-to-pyruvate ratio during the lactate minimum speed test

The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1 +/- 6.7 years, VO 2max 52.0 +/- 7.9 ml kg -1 min -1 ) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a ‘U-shaped’ blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0 +/- 1.4 km h -1 ) was significantly slower than running speed at the lactate threshold (12.4 +/- 1.7 km h -1 ) (P < 0.05), but there were no significant differences in VO 2 , heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-topyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.     

Changes in blood lactate and pyruvate concentrations and the lactate-to-pyruvate ratio during the lactate minimum speed test

The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1+/-6.7 years, VO2max 52.0+/-7.9 ml x kg(-1) x min(-1)) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a 'U-shaped' blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0+/-1.4 km x h(-1)) was significantly slower than running speed at the lactate threshold (12.4+/-1.7 km x h(-1)) (P < 0.05), but there were no significant differences in VO2, heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-to-pyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.     

The effects of prior incremental cycle exercise on the physiological responses during incremental running to exhaustion: relevance for sprint triathlon performance

It is common for the physiological working capacity of a triathlete when cycling and running to be assessed on two separate days. The aim of this study was to establish whether an incremental running test to exhaustion has a negative effect after a 5 h recovery from an incremental cycling test. Eight moderately trained triathletes (age, 26.2 +/- 3.4 years; body mass, 67.3 +/- 9.1 kg; VO2max when cycling, 59 +/- 13 ml x kg x min(-1); mean +/- s) completed an incremental running test 5 h after an incremental cycling test (fatigue) as well as an incremental running test without previous activity (control). Maximum running speed, maximal oxygen uptake (VO2max) and the lactate threshold were determined for each incremental running test and correlated with the average speed during a 5 km run, which was performed immediately after a 20 km cycling time-trial, as in a sprint triathlon. There were no significant differences in maximum running speed, VO2max or the lactate threshold in either incremental running test (control or fatigue). Furthermore, good agreement was found for each physiological variable in both the control and fatigue tests. For the fatigue test, there were significant correlations between the average speed during a 5 km run and both VO2max expressed in absolute terms (r = 0.83) and the lactate threshold (r = 0.88). However, maximum running speed correlated most strongly with the average speed during a 5 km run (r = 0.96). The results of this study indicate that, under controlled conditions, an incremental running test can be performed successfully 5 h after an incremental cycling test to exhaustion. Also, the maximum running speed achieved during an incremental running test is the variable that correlates most strongly with the average running speed during a 5 km run after a 20 km cycling time-trial in well-trained triathletes.     

Changes in running economy following downhill running

In this study, we examined the time course of changes in running economy following a 30-min downhill (-15%) run at 70% peak aerobic power (VO2peak). Ten young men performed level running at 65, 75, and 85% VO2peak (5 min for each intensity) before, immediately after, and 1 - 5 days after the downhill run, at which times oxygen consumption (VO2), minute ventilation, the respiratory exchange ratio (RER), heart rate, ratings of perceived exertion (RPE), and blood lactate concentration were measured. Stride length, stride frequency, and range of motion of the ankle, knee, and hip joints during the level runs were analysed using high-speed (120-Hz) video images. Downhill running induced reductions (7 - 21%, P < 0.05) in maximal isometric strength of the knee extensors, three- to six-fold increases in plasma creatine kinase activity and myoglobin concentration, and muscle soreness for 4 days after the downhill run. Oxygen consumption increased (4 - 7%, P < 0.05) immediately to 3 days after downhill running. There were also increases (P < 0.05) in heart rate, minute ventilation, RER, RPE, blood lactate concentration, and stride frequency, as well as reductions in stride length and range of motion of the ankle and knee. The results suggest that changes in running form and compromised muscle function due to muscle damage contribute to the reduction in running economy for 3 days after downhill running.