Mentioned in a previous post, exposure to heat stress has been demonstrated to cause a release of norepinephrine. This is interesting, mostly, because norepinephrine is the target of a line of drugs known as norepinephrine reuptake inhibitors. These drugs prevent the reuptake of norepinephrine, and thereby treat conditions such as ADHD, and depression. Likewise, some studies have hinted at the fact that sauna use may help with depression.
Here’s a study showing that heat acclimation actually increases the amount of norepinephrine stored within the hypothalamus, at least in rats:
The hypothesis that anterior hypothalamic (AH) sensitivity to norepinephrine (NE) is altered by chronic exercise in the heat was tested in male Sprague-Dawley rats. Treadmill exercise 6 days/wk for 3 wk at 21 m/min was performed at 23 degrees C (control; C) or at 35 degrees C (heat acclimated; HA), progressing from 20 to 50 min/day in 2 wk. Time for core temperature (Tco) to rise from 39.5 to 40.5 degrees C during a heat-tolerance test after conditioning increased (P less than 0.05) in the HA group. To test for a change in AH sensitivity, the change in Tco to 2-, 5-, 10-, 20-, and 40-micrograms doses of NE injected bilaterally into the AH was determined after conditioning. Dose-response regression lines showed that exercise in the heat increased the slope and shifted the Tco-NE dose relation to the left. In a separate series of experiments on 6 sedentary(s), 10 C, and 10 HA animals, the amounts of NE, dopamine, and 3,4-dihydroxyphenylglycol (DOPEG) were determined by high-pressure liquid chromatography in the AH, median preoptic area (PO), cortex, and cerebellum after 9 wk of conditioning. Results showed that in the PO there was a significant increase in NE and DOPEG in the HA vs. C group and a trend of increasing NE from the S to C to HA groups. The data indicate that exercise in the heat increases NE-induced peripheral heat-dissipating capacity and increases catecholamine storage in the PO. (via.)