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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Exerc Sport Sci Rev. 2018 Jan;46(1):48–55. doi: 10.1249/JES.0000000000000130

Figure 3. Cellular microenvironment at rest and during high pressure in the exercise trained vasculature.

Figure 3

Activation of local RAS results in increased NOX II activity and subsequent production of O2−. Increased SOD expression allows the exercised vasculature to convert this superoxide to H2O2 which can be used for vasodilation when NO bioavailability is reduced. Regular exercise results in several beneficial adaptions to the mitochondria (40, 41). Mitochondrial H2O2 appears to play a significant role in this maintained dilation as blockade of SOD I and SOD III does not reduce dilation to same extent as catalase which scavenges H2O2 from all three SOD isozymes (7).