Finley J P, Bonet J F, Waxman M B
J Appl Physiol Respir Environ Exerc Physiol. 1979 Dec;47(6):1218-22. doi: 10.1152/jappl.1979.47.6.1218.
The autonomic pathways mediating the bradycardia response to facial immersion (FI) have not been fully elaborated in man. By means of parasympathetic and sympathetic blockade we studied the heart rate response to FI in nine highly trained young swimmers, at rest and during dynamic cycle exercise. With no blockade, heart rate at rest declined with FI 36 +/- 18%. Under beta-blockade with propranolol or alpha-blockade with phentolamine FI produced a similar decrement. Atropine reduced the response. During exercise FI produced 48 +/- 9% decline without blockade. The response was similar with beta-blockade, but was completely abolished with atropine. Systolic blood pressure responses to FI measured by cuff in three subjects were small and bore no relation to the heart rate response. The results are compatible with parasympathetic efferent mediation of the heart rate response to FI. They are incompatible with a role for sympathetic mediation except as a complex interaction between parasympathetic and sympathetic influences. Hypertension and other sympathetic responses to FI do not play a role in production of bradycardia, but are apparently incidental effects. The heart rate decrement produced by FI increases with greater steady-state heart rate.
介导面部浸入（FI）所致心动过缓反应的自主神经通路在人体中尚未完全阐明。我们通过副交感神经和交感神经阻滞，研究了9名训练有素的年轻游泳运动员在静息状态和动态循环运动期间对FI的心率反应。在未进行阻滞时，静息心率随FI下降36±18%。使用普萘洛尔进行β受体阻滞或使用酚妥拉明进行α受体阻滞时，FI产生的心率下降相似。阿托品可降低该反应。运动期间，未进行阻滞时FI使心率下降48±9%。β受体阻滞时反应相似，但阿托品可完全消除该反应。通过袖带测量的3名受试者对FI的收缩压反应较小，且与心率反应无关。结果表明，心率对FI的反应由副交感神经传出介导。这与交感神经介导的作用不相符，除非是副交感神经和交感神经影响之间的复杂相互作用。高血压和其他对FI的交感神经反应在心动过缓的产生中不起作用，显然是附带效应。FI引起的心率下降随稳态心率升高而增加。
