Modest changes in high-density lipoprotein concentration and metabolism with prolonged exercise training.
Modest changes in high-density lipoprotein concentration and metabolism with prolonged exercise training.
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随着长时间的运动训练，高密度脂蛋白浓度和新陈代谢发生适度变化。
DOI：
10.1161/01.cir.78.1.25
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发表时间：
1988
期刊：
影响因子：
37.8
通讯作者：
Herbert,PN
中科院分区：
文献类型：
--
作者：
Thompson,PD;Cullinane,EM;Sady,SP;Flynn,MM;Bernier,DN;Kantor,MA;Saritelli,AL;Herbert,PN
研究了8名久坐男性在运动训练14周和32-48周前后的高密度脂蛋白（HDL）代谢。受试者每天骑固定自行车1小时，每周骑5天，持续14周（n = 8），此后每周骑4天，总共训练32-48周（n = 7）。HDL代谢进行了评估与125 I-放射性标记的自体HDL，而受试者消耗规定的饮食。14周后，最大摄氧量增加了26 +/- 7%（p <0.001），但随着训练时间的延长，最大摄氧量没有进一步增加。体重和估计的体脂没有变化。14周后，HDL胆固醇增加了5 +/- 3 mg/dl，甘油三酯降低了19 +/- 23 mg/dl（两者的p值均小于0.025），但继续训练没有额外的变化。运动14周（p <0.025）和32周或更长时间后，肝素后血浆脂蛋白脂酶活性比基线活性高22%。相比之下，每次测量时，肝甘油三酯脂肪酶活性分别比基线低16 +/- 8%和15 +/- 8%（两者的p均小于0.005）。静脉注射脂肪溶液后，甘油三酯的消失率在14周时高出24 +/- 24%，在更长时间的训练后高出49 +/- 18%（p <0.005）。研究结束时的总胆固醇和低密度脂蛋白胆固醇以及载脂蛋白A-I和A-II浓度与初始值无差异。在两次训练后测量中，血浆体积均高于初始值8%。载脂蛋白A-I的生物半衰期在14周时保持不变，但在研究结束时延长了10 +/- 13%（p = 0.07），除1例受试者外，所有受试者的生物半衰期均增加。在14周和32周或更长时间时，载脂蛋白A-II的半衰期分别为基线以上8 +/- 8%（p = 0.031）和11 +/- 14%（p = 0.06）。载脂蛋白A-I和A-II的合成速率与32-48周时的基线值无差异。我们的结论是，8-11个月的运动训练在以前久坐的男性提高脂肪耐受性和增加高密度脂蛋白胆固醇浓度，通过延长高密度脂蛋白生存。然而，HDL载脂蛋白存活率的变化并不接近先前在优秀耐力运动员和久坐男性之间注意到的差异。HDL胆固醇浓度的变化不大，表明在许多受试者中，HDL运动相关变化的可能性可能不大。
High-density lipoprotein (HDL) metabolism was studied in eight sedentary men before and after 14 and 32-48 weeks of exercise training. Subjects rode stationary bicycles 1 hour daily, 5 days each week for 14 weeks (n = 8), and 4 days each week thereafter for a total of 32-48 weeks (n = 7) of training. HDL metabolism was assessed with 125I-radiolabeled autologous HDL while subjects consumed defined diets. Maximal oxygen uptake increased 26 +/- 7% (p less than 0.001) after 14 weeks but did not increase further with more prolonged training. Body weight and estimated body fat did not change. HDL cholesterol increased 5 +/- 3 mg/dl, and triglycerides decreased 19 +/- 23 mg/dl after 14 weeks (p less than 0.025 for both), but there were no additional changes with continued training. Postheparin plasma lipoprotein lipase activity was 22% higher than baseline activity after both 14 (p less than 0.025) and 32 or more weeks of exercise. In contrast, hepatic triglyceride lipase activity was 16 +/- 8% and 15 +/- 8% lower than baseline at each measurement (p less than 0.005 for both). The disappearance rate of triglycerides after an intravenously administered fat solution was 24 +/- 24% higher at 14 weeks and 49 +/- 18% (p less than 0.005) higher after more prolonged training. Total and low-density lipoprotein cholesterol and apolipoprotein A-I and A-II concentrations at the end of study were not different from initial values. Plasma volume was 8% above initial values at both post-training measurements. The biological half-life of apolipoprotein A-I was unchanged at 14 weeks but was 10 +/- 13% longer (p = 0.07) and increased in all but one subject at the end of the study. Half-life for apolipoprotein A-II was 8 +/- 8% (p = 0.031) and 11 +/- 14% (p = 0.06) above baseline at 14 and 32 or more weeks, respectively. The synthetic rates for apolipoproteins A-I and A-II were not different from baseline values at 32-48 weeks. We conclude that 8-11 months of exercise training in previously sedentary men enhances fat tolerance and increases HDL cholesterol concentrations by prolonging HDL survival. The changes in HDL apolipoprotein survival, however, do not approximate the differences previously noted between elite endurance athletes and sedentary men. Changes in HDL cholesterol concentration were not large and suggest that the potential for exercise-related changes in HDL may be modest in many subjects.
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作者：
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影响因子：
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作者：
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作者：
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影响因子：
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