Nightingale Angus K, Crilley Jenifer G, Pegge Nicholas C, Boehm Ernie A, Mumford Catherine, Taylor Doris J, Styles Peter, Clarke Kieran, Frenneaux Michael P
Bristol Heart Institute, Bristol University, Bristol, UK.
Eur J Heart Fail. 2007 Mar;9(3):287-91. doi: 10.1016/j.ejheart.2006.06.006. Epub 2006 Oct 4.
Chronic heart failure (CHF) is associated with abnormalities of skeletal muscle metabolism. This may be due to impaired oxygen delivery as a result of endothelial dysfunction.
We postulated that ascorbic acid would improve oxygen delivery to exercising muscle and improve skeletal muscle metabolism.
We studied skeletal muscle metabolism using (31)P magnetic resonance spectroscopy in 39 CHF patients. Endothelial function was assessed by changes in pulse wave velocity. Subjects were randomised to receive 4 g ascorbic acid daily for 4 weeks in a placebo-controlled double-blind study.
Ascorbic acid significantly increased phosphocreatine utilization during exercise. In addition, glycolytic ATP synthesis increased in the ascorbic acid group (change in rate of ATP synthesis at 1 min -0.21+/-0.76 with placebo, 2.06+/-0.60 following ascorbic acid; p<0.05). Phosphocreatine and ADP recovery after exercise were not changed. The fall in pulse wave velocity during reactive hyperaemia was increased by ascorbic acid from -6.3+/-2.6% to -12.1+/-2.0% (p<0.05).
These findings suggest that ascorbic acid increased both phosphocreatine utilization and glycolytic ATP synthesis during exercise in patients with CHF implying worsened skeletal muscle metabolism despite improvements in endothelial function.
慢性心力衰竭（CHF）与骨骼肌代谢异常有关。这可能是由于内皮功能障碍导致氧输送受损所致。
我们推测，抗坏血酸可改善运动肌肉的氧输送并改善骨骼肌代谢。
我们使用磷-31磁共振波谱研究了39例CHF患者的骨骼肌代谢。通过脉搏波速度变化评估内皮功能。在一项安慰剂对照的双盲研究中，受试者被随机分配，每天接受4g抗坏血酸，持续4周。
抗坏血酸显著增加运动期间磷酸肌酸的利用。此外，抗坏血酸组糖酵解ATP合成增加（1分钟时ATP合成速率变化，安慰剂组为-0.21±0.76，抗坏血酸组为2.06±0.60；p<0.05）。运动后磷酸肌酸和ADP的恢复未改变。抗坏血酸使反应性充血期间脉搏波速度的下降从-6.3±2.6%增加到-12.1±2.0%（p<0.05）。
这些发现表明，抗坏血酸增加了CHF患者运动期间的磷酸肌酸利用和糖酵解ATP合成，这意味着尽管内皮功能有所改善，但骨骼肌代谢仍恶化。
