中文摘要：

为考察鳊鱼（Parabramis pekinensis）幼鱼的匀加速游泳（Constant acceleration swimming）能力,将32尾实验鱼随机均分为4组,即对照组和3个处理组（每组样本量n=8）,驯养温度为（25±1）℃。处理组分别在0.1、0.2和0.4cm·s-2的加速度（a）条件下,测定实验鱼的最大匀加速游泳速度（Constant acceleration speed,Ucat）及游泳测定过程历时（t）;游泳力竭后,立即取血浆、白肌和肝脏,进行生化测定（对照组不经游泳直接取样进行生化测定）。实验结果显示：随着a的增大Ucat分别为62.85、73.66、75.62cm·s-1,其中0.2cm·s-2组及0.4cm·s-2组的Ucat无显著差异,但均显著大于0.1cm·s-2组（p〈0.05）;t显著下降（p〈0.05）,分别为：632、349、174s;肌乳酸含量和血乳酸浓度增大,当a为0.4cm·s-2时,肌乳酸含量和血乳酸浓度均显著高于对照组（p〈0.05）;4组之间的肝乳酸含量无显著差异;处理组的肌葡萄糖含量随着a的增大而显著增加（p〈0.05）,但0.1cm·s-2组的肌葡萄糖含量显著低于对照组（p〈0.05）;4组之间的肌糖原含量无显著差异。研究表明随着a的增大,鳊鱼幼鱼的Ucat增加,t缩短,肌乳酸含量增大,这应与鱼类无氧代谢参与程度的增加密切相关;血乳酸水平的提高应由＂乳酸泄露＂所致;而底物消耗与匀加速游泳能力及游泳路程有关。

英文摘要：

To investigate the constant acceleration swimming performance of juvenile Chinese bream （Parabramis pekinensis）, 32 Chinese bream juveniles were selected and divided into 4 groups （control group, n=8; treatment groups, n=3 × 8）, and reared at （25± 1） ℃. Then the constant acceleration speed （Ucat） and the duration of measurement process （t） of experiment fish under ac- celeration of 0. 1, 0. 2, 0. 4 cra · s-1 were measured. Then, the plasma, white muscle and liver were sampled for biochemical indi- cator measurements immediately after Uc, t tests （the fish in control group were sampled without swimming）. The Ucar were 62.85, 73. 66 and 75.62 cm · s-1 in 0. 1, 0. 2, 0.4 cm · s-2 acceleration groups. There was no significant difference in Ucar between 0. 2 and 0.4 cm · s-2 acceleration groups, but U~,t of both groups were significantly higher than that of 0.1 cm · s-2 acceleration group （p〈 0.05）. The t decreased significantly with the increase of acceleration rate （p〈0.05）, and the values were 632, 349 and 174 s, re- spectively, in 0. 1, 0.2, 0.4 cm · s-2 acceleration groups. The white muscle lactate content （[lactate]） and plasma [-lactate] in- creased with the increase of acceleration. The white muscle [lactate] and plasma [lactate】 were significant higher than that of con- trol group when acceleration rate was 0.4 cm · s-2. There were no significant difference in liver [lactate] among control and three treatment groups. The white muscle [glucose] of treatment groups significantly increased with the increase of acceleration. Whereas white muscle [glucose] of 0. 1 cm· s-2 was significantly lower than that of control group （p〈0.05）. There were no significant differences in white muscle [glycogen] among control and treatment groups. The results show that the Ucar and white muscle [lac- tate] increased, but t became shorter with the increase of acceleration rate possibly due to the increased recruitment of anaerobic me- tabolism. The plasma [lactate] increas