Näveri H K, Leinonen H, Kiilavuori K, Härkönen M
Department of Medicine, Helsinki University Central Hospital, Finland.
Eur Heart J. 1997 Dec;18(12):1937-45. doi: 10.1093/oxfordjournals.eurheartj.a015203.
To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure.
Muscle biopsy study.
Skeletal muscle metabolic response to maximal bicycle exercise was studied in 10 patients with chronic congestive heart failure (ejection fraction 0.22 +/- 0.05; peak oxygen consumption, VO2 15.1 +/- 4.9 ml.min-1.kg-1) and in nine healthy subjects (peak VO2 33.5 +/- 6.7 ml.min-1.kg-1). Activities of skeletal muscle enzymes were measured from the vastus lateralis muscle of 48 patients (ejection fraction 0.24 +/- 0.06, peak VO2 17.4 +/- 5.4 ml.min-1.kg-1) and 36 healthy subjects (peak VO2 38.3 +/- 8.4 ml.min-1.kg-1).
Although blood lactate levels were lower in patients than in healthy subjects (2.2 +/- 0.3 vs 5.2 +/- 0.6 mmol.l-1; P < 0.001) at peak exercise (96 +/- 11 W for patients and 273 +/- 14 W for controls), skeletal muscle lactate was similarly elevated (25.6 +/- 3.2 vs 22.7 +/- 2.7 mmol.kg-1) and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 mmol.kg-1). The muscle ATP decreased by 21% (P < 0.05) and 8% (P < 0.01) in the patients and controls, respectively. Activities of rate limiting enzymes of the citric acid cycle (alpha-ketoglutarate dehydrogenase) and oxidation of free fatty acids (carnitine palmitoyltransferase II) were 48% and 21% lower than in controls, but the mean phosphofructokinase activity was unchanged in congestive heart failure.
It seems that the main limiting factor of exercise performance during heavy exercise is the same in congestive heart failure and healthy subjects, a high rate of skeletal muscle lactate accumulation and high-energy phosphate depletion. In congestive heart failure, the low activity of aerobic enzymes is likely to impair energy production and lead to lactate acidosis at low workloads.
研究充血性心力衰竭男性患者运动能力受限及骨骼肌能量产生的机制。
肌肉活检研究。
对10例慢性充血性心力衰竭患者（射血分数0.22±0.05；峰值耗氧量，VO₂ 15.1±4.9 ml·min⁻¹·kg⁻¹）和9名健康受试者（峰值VO₂ 33.5±6.7 ml·min⁻¹·kg⁻¹）进行了骨骼肌对最大强度自行车运动的代谢反应研究。测量了48例患者（射血分数0.24±0.06，峰值VO₂ 17.4±5.4 ml·min⁻¹·kg⁻¹）和36名健康受试者（峰值VO₂ 38.3±8.4 ml·min⁻¹·kg⁻¹）股外侧肌的骨骼肌酶活性。
尽管在峰值运动时（患者为96±11 W，对照组为273±14 W）患者的血乳酸水平低于健康受试者（2.2±0.3 vs 5.2±0.6 mmol·L⁻¹；P<0.001），但骨骼肌乳酸同样升高（25.6±3.2 vs 22.7±2.7 mmol·kg⁻¹），磷酸肌酸同样降低至低水平（P<0.02）（7.0±1.9 vs 6.7±0.9 mmol·kg⁻¹）。患者和对照组的肌肉ATP分别下降了21%（P<0.05）和8%（P<0.01）。柠檬酸循环限速酶（α-酮戊二酸脱氢酶）的活性和游离脂肪酸氧化（肉碱棕榈酰转移酶II）比对照组分别低48%和21%，但充血性心力衰竭患者的磷酸果糖激酶平均活性未改变。
似乎在重度运动期间，充血性心力衰竭患者和健康受试者运动表现的主要限制因素相同，即骨骼肌乳酸积累率高和高能磷酸耗竭。在充血性心力衰竭中，有氧酶活性低可能会损害能量产生并导致低负荷时的乳酸酸中毒。
