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Skeletal muscle microvascular oxygenation dynamics in heart failure: exercise training and nitric oxide-mediated function
- Source :
- American Journal of Physiology-Heart and Circulatory Physiology. 306:H690-H698
- Publication Year :
- 2014
- Publisher :
- American Physiological Society, 2014.
-
Abstract
- Chronic heart failure (CHF) impairs nitric oxide (NO)-mediated regulation of skeletal muscle O2 delivery-utilization matching such that microvascular oxygenation falls faster (i.e., speeds PO2 mv kinetics) during increases in metabolic demand. Conversely, exercise training improves (slows) muscle PO2 mv kinetics following contractions onset in healthy young individuals via NO-dependent mechanisms. We tested the hypothesis that exercise training would improve contracting muscle microvascular oxygenation in CHF rats partly via improved NO-mediated function. CHF rats (left ventricular end-diastolic pressure = 17 ± 2 mmHg) were assigned to sedentary (n = 11) or progressive treadmill exercise training (n = 11; 5 days/wk, 6–8 wk, final workload of 60 min/day at 35 m/min; −14% grade downhill running) groups. PO2 mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1-Hz twitch contractions under control (Krebs-Henseleit solution), sodium nitroprusside (SNP; NO donor; 300 μM), and NG-nitro-l-arginine methyl ester (L-NAME, nonspecific NO synthase blockade; 1.5 mM) superfusion conditions. Exercise-trained CHF rats had greater peak oxygen uptake and spinotrapezius muscle citrate synthase activity than their sedentary counterparts ( p < 0.05 for both). The overall speed of the PO2 mv fall during contractions (mean response time; MRT) was slowed markedly in trained compared with sedentary CHF rats (sedentary: 20.8 ± 1.4, trained: 32.3 ± 3.0 s; p < 0.05), and the effect was not abolished by L-NAME (sedentary: 16.8 ± 1.5, trained: 31.0 ± 3.4 s; p > 0.05). Relative to control, SNP increased MRT in both groups such that trained CHF rats had slower kinetics (sedentary: 43.0 ± 6.8, trained: 55.5 ± 7.8 s; p < 0.05). Improved NO-mediated function is not obligatory for training-induced improvements in skeletal muscle microvascular oxygenation (slowed PO2 mv kinetics) following contractions onset in rats with CHF.
- Subjects :
- Male
medicine.medical_specialty
Physiology
Vascular Biology and Microcirculation
Nitric Oxide
Ventricular Function, Left
Nitric oxide
Microcirculation
Rats, Sprague-Dawley
chemistry.chemical_compound
Oxygen Consumption
Physiology (medical)
Internal medicine
Ventricular Pressure
medicine
Animals
Nitric Oxide Donors
Myocardial infarction
Enzyme Inhibitors
Muscle, Skeletal
Heart Failure
biology
business.industry
Skeletal muscle
Stroke Volume
Oxygenation
medicine.disease
Adaptation, Physiological
Exercise Therapy
Rats
Oxygen
Nitric oxide synthase
Disease Models, Animal
Kinetics
Endocrinology
medicine.anatomical_structure
chemistry
Heart failure
Physical Endurance
biology.protein
Nitric Oxide Synthase
medicine.symptom
Cardiology and Cardiovascular Medicine
business
Biomarkers
Muscle Contraction
Muscle contraction
Subjects
Details
- ISSN :
- 15221539 and 03636135
- Volume :
- 306
- Database :
- OpenAIRE
- Journal :
- American Journal of Physiology-Heart and Circulatory Physiology
- Accession number :
- edsair.doi.dedup.....c17d791e3f9f53909603a6194f671220