Skip Navigation LinksHome > April 2007 - Volume 39 - Issue 4 > Exercise-Induced Decrease in Insular Cortex rCBF during Post...
Medicine & Science in Sports & Exercise:
doi: 10.1249/mss.0b013e31802f04e0
BASIC SCIENCES: Original Investigations

Exercise-Induced Decrease in Insular Cortex rCBF during Postexercise Hypotension


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The insular cortex (IC), a region of the brain involved in blood pressure (BP) modulation, shows decreases in regional cerebral blood flow (rCBF) during postexercise hypotension (PEH).

Purpose: To determine whether changes in IC neural activity were caused by prior exercise or by changes in BP, this investigation compared patterns of rCBF during periods of hypotension, which was induced by prior exercise (i.e., PEH) and sodium nitroprusside (SNP) infusion and a cold pressor (CP), to restore BP.

Methods: Ten subjects were studied on three different days with randomly assigned conditions: i) resting baseline; ii) PEH; and iii) SNP-induced hypotension (matched to the PEH BP decrease). Data were collected for heart rate (HR) and mean BP, and rCBF was assessed using single-photon emission computed tomography (SPECT) as an index of brain activation.

Results: Using ANOVA across conditions, there were differences (P < 0.05; mean ± SD) from baseline during PEH for HR (+12 ± 3 bpm) and mean BP (−8 ± 2 mm Hg) and during SNP-induced hypotension (HR = +15 ± 4 bpm; MBP = −9 ± 2 mm Hg), with no differences between PEH and SNP. After exercise, there were decreases (P < 0.05) in the leg sensorimotor area, anterior cingulate, and the right and left inferior thalamus, right inferior insula, and left anterior insular regions. During SNP-induced hypotension, there were significant increases in the right and left inferior thalamus and the right and left inferior anterior IC. CP during PEH increased BP and IC activity.

Conclusions: Data show that reductions in IC neural activity are not caused by acute BP decreases. Findings suggest that exercise can lead to a temporary decrease in IC neural activity, which may be a significant neural factor contributing to PEH.

©2007The American College of Sports Medicine


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