Wilson L B, Dyke C K, Parsons D, Wall P T, Pawelczyk J A, Williams R S, Mitchell J H
Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235-9034, USA.
J Appl Physiol (1985). 1995 Nov;79(5):1744-52. doi: 10.1152/jappl.1995.79.5.1744.
The purpose of this study was to determine whether the reflex hemodynamic responses to static contraction of predominately glycolytic muscle are greater than the changes elicited by primarily oxidative muscle. Low-frequency electrical stimulation (continuous 21 days) of the tibial nerve of one hindlimb of adult rabbits converted the metabolic characteristics of the predominately glycolytic gastrocnemius to a muscle that was primarily oxidative. After 21 days of stimulation, the rabbits were decerebrated, and static contraction of the glycolytic muscle (unstimulated gastrocnemius) initially decreased heart rate (HR; -16 +/- 3 beats/min) and mean arterial pressure (MAP; -17 +/- 3 mmHg). Thereafter, MAP increased 13 +/- 3 mmHg above baseline. Static contraction of the oxidative muscle (stimulated gastrocnemius) produced similar decreases in HR and MAP (-12 +/- 4 beats/min and -12 +/- 3 mmHg, respectively). However, the subsequent increase in MAP (8 +/- 3 mmHg; above baseline) was less than that evoked by contraction of the glycolytic muscle. The responses evoked by stretch of each muscle and high-intensity electrical stimulation were the same, indicating that the afferents from the muscle were not destroyed by the chronic-stimulation technique. These results support the hypothesis that metabolic by-products play a role in the pressor response to static contraction of skeletal muscle. In addition, these data confirm that contraction of predominately oxidative muscle can evoke a reflex pressor response, albeit smaller than the change elicited from primarily glycolytic muscle.
本研究的目的是确定对主要进行糖酵解的肌肉静态收缩的反射性血流动力学反应是否大于主要进行氧化代谢的肌肉所引发的变化。对成年兔一侧后肢的胫神经进行低频电刺激（持续21天），可使主要进行糖酵解的腓肠肌的代谢特征转变为主要进行氧化代谢的肌肉。刺激21天后，对兔子进行去大脑处理，糖酵解肌肉（未受刺激的腓肠肌）的静态收缩最初使心率（HR；-16±3次/分钟）和平均动脉压（MAP；-17±3 mmHg）降低。此后，MAP比基线升高13±3 mmHg。氧化代谢肌肉（受刺激的腓肠肌）的静态收缩使HR和MAP产生类似程度的降低（分别为-12±4次/分钟和-12±3 mmHg）。然而，随后MAP的升高（8±3 mmHg；高于基线）小于糖酵解肌肉收缩所引起的升高。每种肌肉的拉伸和高强度电刺激所引发的反应相同，表明慢性刺激技术并未破坏肌肉的传入神经。这些结果支持了以下假设，即代谢副产物在骨骼肌静态收缩的升压反应中起作用。此外，这些数据证实，主要进行氧化代谢的肌肉收缩可引发反射性升压反应，尽管其小于主要进行糖酵解的肌肉所引发的变化。
