Exercise and hypertension: a model for central neural plasticity.

1. Physical movement is accompanied by coordinated changes in respiratory and cardiovascular activity proportional to the metabolic demands of the locomotor task. Cardiorespiratory changes include increases in ventilation, blood pressure and heart rate, as well as altered regional sympathetic nerve activity and blood flow. 2. The posterior hypothalamic area, a periventricular region in the caudal-most diencephalon, has been shown to play a role in mediating the coupling of locomotion and cardiorespiratory activity. Stimulation of this brain region produces locomotor behaviour and simultaneous increases in cardiorespiratory activity that are independent of peripheral feedback from contracting muscles. Posterior hypothalamic neurons are also activated by exercise and exercise-related stimuli, such as muscle contraction. 3. In spontaneously hypertensive rats (SHR), a deficiency in the inhibitory GABA neurotransmitter system within the posterior hypothalamic area contributes to tonically elevated levels of arterial blood pressure. We previously identified a reduction in the GABA synthesizing enzyme glutamic acid decarboxylase (GAD) within the posterior hypothalamus of SHR. 4. We have recently demonstrated that exercise can upregulate GABA-mediated caudal hypothalamic control of cardiovascular function in SHR. Similarly, exercise increases GAD gene transcript levels in the posterior hypothalamus. Thus, we have identified a model to study exercise-related central neural plasticity in GABAergic neurotransmitter function. Moreover, we suggest that exercise may increase cardiovascular health through changing central neural regulation of blood pressure.