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Plasticity in the Microvasculature of Conditioned Weight Lifters After Acute High Pressure Stress
Author(s) -
Durand Matthew J.,
Phillips Shane A.,
Gutterman David D.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1136.1
Subject(s) - dilator , vasodilation , chemistry , nitric oxide , acetylcholine , dilation (metric space) , medicine , endocrinology , catalase , cardiology , anesthesia , oxidative stress , mathematics , combinatorics
Transient hypertension evoked by exercise impairs endothelial function in sedentary (SED) subjects but not in weight lifters (WL). We hypothesized that nitric oxide (NO) mediated vasodilation is preserved in microvessels from WL after exposure to high pressure compared to microvessels from SED subjects. Adipose arterioles were obtained from volunteers by gluteal biopsy, cannulated for videomicroscopy in a heated chamber filled with Krebs solution, pressurized to 60 mmHg, constricted with endothelin‐1, and dilation to acetylcholine (Ach) was assessed in the presence or absence of L‐NAME, rotenone, PEG‐catalase or Mito‐TEMPO. ACh‐induced dilation was measured again after raising intraluminal pressure to 150 mmHg for 30 minutes. After exposure to high pressure, microvessels from WL maintained dilation to Ach (before: 92±1.4%; after: 89±1.3%), but dilation in SED was reduced (before: 97±2.9%; after: 39±9.2%). At 60 mmHg of pressure, L‐NAME reduced dilation in WL while PEG‐catalase did not. After exposure to 150 mmHg, PEG‐catalase significantly reduced dilation, while L‐NAME had no effect. Both rotenone and Mito‐TEMPO also inhibited the H 2 O 2 ‐mediated dilator response after high pressure. These results indicate that after expose to high pressure in WL, dilation to ACh is maintained by switching from an NO‐ mediated to a H 2 O 2 ‐mediated dilation. The mitochondria play a critical role in this adaptive process.