DOES RELAXATION RESPONSE INHIBIT ACUTE STRESS?

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The relaxation response designates a set of integrated physiologic changes that includes states of perceived well-being with reduced cortical activation on electroencephalograms (EEG) and reductions in respiratory rate, blood pressure, oxygen consumption and arterial blood lactate. This Centers for Disease Control and Prevention supported study examines how the relaxation response inhibits the physiologic changes of acute stress. It tests the hypothesis that molecular mediators of the relaxation response will counteract the biochemical and cellular changes associated with acute psychosocial stress. An additional goal is to develop techniques for studying the effects of normal physiologic variation, such as changes in breathing rate and heart rate, on functional magnetic resonance images. The hypothesis is that in a subset of structures namely the medulla, hypothalamus, amygdala and rostral anterior cingulate cortex) the fMRI signal changes will strongly correlate temporally with changes in respiratory function. Another hypothesis is that activation in the insula and lateral hypothalamus will correlate with non-linear heart rate and respiration rate complexity. The effects of decreased respiratory rate without focused attention or mantra will activate only a subset of the regions activated by the relaxation response. Specifically, the prediction is that limbic structures will not be significantly activated by this task in either group, but that primary and secondary motor cortex regions involved in volitional control of breathing will be activated.