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Details

Autor(en) / Beteiligte
Titel
Muscle metaboreflex control is diminished in normotensive obese women
Ist Teil von
  • American journal of physiology. Heart and circulatory physiology, 2001-08, Vol.281 (2), p.H469-H475
Ort / Verlag
United States
Erscheinungsjahr
2001
Quelle
MEDLINE
Beschreibungen/Notizen
  • 1  Heart Institute (InCor), 2  Department of Endocrinology, University of São Paulo Medical School, and 3  School of Physical Education and Sports, University of São Paulo, São Paulo, Cep 05403-000 Brazil There is no information about the muscle metaboreflex control in obese individuals. In 40 normotensive obese women (OW; body mass index 33.5 ± 0.4 kg/m 2 , age 32.4 ± 1.1 yr) and 15 age-matched, normotensive lean women (LW; body mass index 22.7 ± 0.8 kg/m 2 , age 34.4 ± 1.4 yr), we measured muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) in the nonexercising forearm during static exercise at 10 and 30% of maximal voluntary contraction (MVC). Baseline MSNA (38 ± 2 vs. 31 ± 1 bursts/min, P  = 0.001) and mean blood pressure were significantly higher in OW compared with LW. FBF was significantly lower, whereas forearm vascular resistance was significantly higher in OW. During 10% MVC, MSNA increased similarly in both groups, but during 30% MVC, MSNA was higher in LW. FBF and forearm vascular resistance responses during both 10 and 30% MVC were similar between groups. During posthandgrip circulatory arrest, MSNA remained significantly elevated compared with baseline in both groups, but this increase was significantly lower in OW (3.8 ± 0.82 vs. 9.4 ± 1.03 bursts/min, P  = 0.002). In conclusion, muscle metaboreflex control of MSNA is blunted in OW. MSNA responses are not augmented during selective activation of central command/mechanoreceptors and metaboreceptors, despite increased MSNA levels in OW. Muscle vasodilatory response during graded handgrip isometric exercise is preserved in OW. obesity; sympathetic nerve activity
Sprache
Englisch
Identifikatoren
ISSN: 0363-6135
eISSN: 1522-1539
DOI: 10.1152/ajpheart.2001.281.2.h469
Titel-ID: cdi_highwire_physiology_ajpheart_281_2_H469

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