Shibata M, Moritani T, Miyawaki T, Hayashi T, Nakao K
Laboratory of Health and Sports Science, Faculty of Nursing, College of Nursing Art and Science, Hyogo, Japan.
Int J Obes Relat Metab Disord. 2002 Oct;26(10):1356-62. doi: 10.1038/sj.ijo.0802131.
The purposes of this study were to examine a new method to determine exercise intensity for obese people based on the cardiac vagal activity and to determine the effect of this approach on myocardial stress.
Forty-three middle aged obese female volunteers (age 43.7+/-6.5 y; height 1.56+/-0.05 m; body mass 66.5+/-9.3 kg; body mass index 27.3+/-2.8 kg m(2); percentage body fat 40.7+/-5.9%).
In the first experiment, 43 subjects performed a ramp exercise test on a bicycle ergometer with measurement of ECG and gas exchange parameters. In the second experiment, 11 subjects performed 45 min of constant walking exercise on a treadmill at a level corresponding to exercise intensity determined by vagal activity obtained from a ramp bicycle test. Blood pressure, endothelin 1 (ET-1), catecholamine, atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) were measured before and after exercise.
The heart rate variability power decreased with increasing work rate, and changed little after reaching individual-specific work rate. We presumed that vagal activity disappeared at this point and that the heart rate at this exercise intensity was determined as the vagal activity threshold (T(VA)). The results showed a significant positive correlation (r=0.742, P<0.0001) between T(VA) and ventilatory threshold (VT) heart rates, although the mean heart rate of T(VA) (114.3+/-8.5 beats/min) was significantly lower (P<0.001) than that at VT (119.0+/-11.7), suggesting the cardiac vagal withdrawal occurred prior to the onset of lactate acidosis (lactic acid accumulation). Furthermore, exercise intervention experiment at T(VA) indicated that ET-1, catecholamine and BNP levels were not significantly different before and after exercise. However, ANP levels increased significantly after exercise (pre-exercise 18.6+/-5.38 vs post-exercise 44.0+/-24.87 pg/ml, P<0.001), which in turn brought about a significant post-exercise reduction in the blood pressure (SBP 117.6+/-13.7 vs 110.5+/-7.4 mmHg, P<0.05; DBP 78.6+/-6.7 vs 73.5+/-6.6 mmHg, P<0.01).
Our data suggest that it is possible to determine the exercise intensity (T(VA)) on the basis of cardiac vagal response. These results also suggest that exercise at T(VA) level is a safe exercise intensity in the light of cardiac stress, and that T(VA) may be recommended for obese people who might possess lower cardiac sympatho-vagal activity.
本研究的目的是检验一种基于心脏迷走神经活动来确定肥胖人群运动强度的新方法，并确定该方法对心肌应激的影响。
43名中年肥胖女性志愿者（年龄43.7±6.5岁；身高1.56±0.05米；体重66.5±9.3千克；体重指数27.3±2.8千克/米²；体脂百分比40.7±5.9%）。
在第一个实验中，43名受试者在自行车测力计上进行递增运动试验，同时测量心电图和气体交换参数。在第二个实验中，11名受试者在跑步机上以与从递增自行车试验获得的迷走神经活动所确定的运动强度相对应的水平进行45分钟的持续步行运动。在运动前后测量血压、内皮素1（ET-1）、儿茶酚胺、心钠素（ANP）和脑钠肽（BNP）。
心率变异性功率随工作率增加而降低，在达到个体特定工作率后变化不大。我们推测此时迷走神经活动消失，并且将该运动强度下的心率确定为迷走神经活动阈值（T(VA)）。结果显示T(VA)与通气阈值（VT）心率之间存在显著正相关（r = 0.742，P < 0.0001），尽管T(VA)的平均心率（114.3±8.5次/分钟）显著低于VT时的平均心率（119.0±11.7次/分钟，P < 0.001），这表明心脏迷走神经撤离发生在乳酸酸中毒（乳酸积累）发作之前。此外，在T(VA)水平进行的运动干预实验表明，运动前后ET-1、儿茶酚胺和BNP水平无显著差异。然而，运动后ANP水平显著升高（运动前18.6±5.38 vs运动后44.0±24.87 pg/ml，P < 0.001），这反过来导致运动后血压显著降低（收缩压117.6±13.7 vs 110.5±7.4 mmHg，P < 0.05；舒张压78.6±6.7 vs 73.5±6.6 mmHg，P < 0.01）。
我们的数据表明，基于心脏迷走神经反应来确定运动强度（T(VA)）是可行的。这些结果还表明，从心脏应激的角度来看，在T(VA)水平进行运动是一种安全的运动强度，并且对于可能具有较低心脏交感-迷走神经活动的肥胖人群，可能推荐采用T(VA)。
