Exercise training alters skeletal muscle mitochondrial morphometry in heart failure patients

被引:16
|
作者
Santoro, C
Cosmas, A
Forman, D
Morghan, A
Bairos, L
Levesque, S
Roubenoff, R
Hennessey, J
Lamont, L
Manfredi, T
机构
[1] Univ Rhode Isl, Energy metab Lab, Kingston, RI 02881 USA
[2] Univ Connecticut, Sch Allied Hlth, Storrs, CT 06269 USA
[3] Boston Univ, Med Ctr, Div Cardiol, Boston, MA 02215 USA
[4] Tufts Univ, USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA
[5] Rhode Isl Hosp, Dept Med, Div Endocrinol, Providence, RI 02903 USA
来源
JOURNAL OF CARDIOVASCULAR RISK | 2002年 / 9卷 / 06期
关键词
heart failure; skeletal muscle; mitochondria;
D O I
10.1097/00043798-200212000-00012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background Previous research has demonstrated that exercise intolerance in heart failure patients is associated with significant alterations in skeletal muscle ultrastructure and oxidative metabolism that may be more consequential than cardiac output. Design To examine the effect of exercise training on skeletal muscle mitochondrial size in chronic heart failure patients. Methods Six heart failure patients participated in 16-weeks of supervised upper and lower extremity exercise training. At the conclusion of training, percutaneous needle biopsies of the vastus lateralis were taken and electron microscopy was used to assess mitochondrial sizes. Results The exercise programme resulted in a significant increase in peak maximal oxygen consumption (P < 0.05) and anaerobic threshold (P < 0.04). Knee extension muscle force increased following training (P < 0.02). After exercise training, the average size of the mitochondria increased by 23.4% (0.036 to 0.046 P < 0.015) and the average shape was unaltered. Conclusion Exercise training with heart failure patients alters skeletal muscle morphology by increasing mitochondrial size, with no change in shape. This may enhance oxidative metabolism resulting in an increased exercise tolerance. (C) 2002 Lippincott Williams Wilkins.
引用
收藏
页码:377 / 381
页数:5
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