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Cardiac hypertrophy impairs cardiac receptor control of circulation in man
C Giannattasio1, G Seravalle, G Bolla
1Centro Auxologico Italiano, Università di Milano, Italy.
Insights
Cardiopulmonary reflex control is impaired in athletes with left ventricular hypertrophy. This suggests heart structural changes, not hypertension, cause this reflex impairment.
Area of Science:
- Cardiovascular physiology
- Exercise physiology
- Autonomic nervous system
Background:
- Cardiopulmonary reflex control of circulation is vital for maintaining blood pressure.
- This reflex is known to be impaired in hypertensive individuals with left ventricular hypertrophy.
- The specific cause of this impairment (hypertension vs. cardiac hypertrophy) remains unclear.
Purpose of the Study:
- To investigate whether hypertension or left ventricular hypertrophy itself impairs cardiopulmonary reflex control.
- To differentiate the effects of physiological cardiac hypertrophy from pathological hypertrophy.
Main Methods:
- Studied normotensive sedentary individuals and normotensive weight-lifters with left ventricular hypertrophy.
- Manipulated left ventricular end-diastolic diameter (LVEDD) to stimulate cardiac receptors.
- Assessed reflex responses via forearm vascular resistance and plasma noradrenaline levels.
Main Results:
- Both increasing and decreasing LVEDD elicited reflex responses in forearm vascular resistance and noradrenaline.
- Weight-lifters showed significantly blunted reflex responses compared to sedentary individuals for a given LVEDD change.
- Hemodynamic responses to a cold pressor test were similar between groups.
Conclusions:
- Cardiopulmonary reflex impairment occurs in normotensive individuals with exercise-induced left ventricular hypertrophy.
- This suggests that structural alterations in the heart, independent of hypertension, are responsible for impaired cardiopulmonary reflex control.
Abstract:
The cardiopulmonary reflex control of circulation (which, in man, depends largely on cardiac receptors) is impaired in hypertensive subjects who have left ventricular hypertrophy. To determine whether hypertension or cardiac hypertrophy per se is responsible for this, we studied nine sedentary normotensive subjects aged 23 +/- 1 years and nine age-matched normotensive weight-lifters with echocardiographic signs of left ventricular hypertrophy (left ventricular mass index for the weight-lifters: 134 +/- 7; for the sedentary subjects: 99 +/- 7 g/m2; P less than 0.01). Cardiac receptors were manipulated by increasing and decreasing the left ventricular end-diastolic diameter (LVEDD) by raising the leg and by reducing the lower-body negative pressure, respectively, and the reflex responses were assessed from the changes in forearm vascular resistance and plasma noradrenaline (high performance liquid chromatography assay). Forearm vascular resistance and the noradrenaline concentration were reduced by increasing the LVEDD, and were increased when the LVEDD was reduced. For a given change in the LVEDD, the responses were markedly less in the weight-lifters than in the non-athletes. In contrast, the haemodynamic effects of a cold pressor test were similar in both groups. Thus, the cardiopulmonary reflex is impaired in normotensive subjects in whom intense physiological training has led to an increase in left ventricular hypertrophy. This suggests that structural alteration of the heart per se is responsible for the phenomenon.