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DOI 10.14814/phy2.13673

Медицинская библиотека · Physiological reports · 2018

Esmolol acutely alters oxygen supply-demand balance in exercising muscles of healthy humans.

Proctor David N, Luck J Carter, Maman Stephan R, Leuenberger Urs A, Muller Matthew D

СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Beta-adrenoreceptor antagonists (β blockers) reduce systemic O2 delivery and blood pressure (BP) during exercise, but the subsequent effects on O2 extraction within the active limb muscles are unknown. In this study, we examined the effects of the fast-acting, β1 selective blocker esmolol on systemic hemodynamics and leg muscle O2 saturation (near infrared spectroscopy, NIRS) during submaximal leg ergometry. Our main hypothesis was that esmolol would augment exercise-induced reductions in leg muscle O2 saturation. Eight healthy adults (6 men, 2 women; 23-67 year) performed light and moderate intensity bouts of recumbent leg cycling before (PRE), during (β1 -blocked), and 45 min following (POST) intravenous infusion of esmolol. Oxygen uptake, heart rate (HR), BP, and O2 saturation (SmO2 ) of the vastus lateralis (VL) and medial gastrocnemius (MG) muscles were measured continuously. Esmolol attenuated the increases in HR and systolic BP during light (-12 ± 9 bpm and -26 ± 12 mmHg vs. PRE) and moderate intensity (-20 ± 10 bpm and -40 ± 18 mmHg vs. PRE) cycling (all P < 0.01). Exercise-induced reductions in SmO2 occurred to a greater extent during the β1 -blockade trial in both the VL (P = 0.001 vs. PRE) and MG muscles (P = 0.022 vs. PRE). HR, SBP and SmO2 were restored during POST (all P < 0.01 vs. β1 -blocked). In conclusion, esmolol rapidly and reversibly increases O2 extraction within exercising muscles of healthy humans.

Для цитирования: Proctor David N, Luck J Carter, Maman Stephan R, Leuenberger Urs A, Muller Matthew D. Esmolol acutely alters oxygen supply-demand balance in exercising muscles of healthy humans.. Physiological reports. 2018. DOI: 10.14814/phy2.13673.

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