scholarly journals Adaptation to exercise-induced stress is not dependent on cardiomyocyte α1A-adrenergic receptors

2021 ◽  
Vol 155 ◽  
pp. 78-87
Author(s):  
Xenia Kaidonis ◽  
Wenxing Niu ◽  
Andrea Y. Chan ◽  
Scott Kesteven ◽  
Jianxin Wu ◽  
...  
2021 ◽  
pp. 2001219
Author(s):  
Ajmol Ali ◽  
Sunali Mehta ◽  
Carlene Starck ◽  
Marie Wong ◽  
Wendy J. O'Brien ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0157704 ◽  
Author(s):  
Laurence Bal-Theoleyre ◽  
Alain Lalande ◽  
Frank Kober ◽  
Roch Giorgi ◽  
Frederic Collart ◽  
...  

2019 ◽  
Vol 51 (09) ◽  
pp. 608-617 ◽  
Author(s):  
Lucia Balagova ◽  
Jan Graban ◽  
Agnesa Puhova ◽  
Daniela Jezova

AbstractCatecholamine effects via β3-adrenergic receptors are important for the metabolism of the adipose tissue. Physical exercise is a core component of antiobesity regimens. We have tested the hypothesis that voluntary wheel running results in enhancement of β3-adrenergic receptor gene expression in the white and brown adipose tissues. The secondary hypothesis is that dietary tryptophan depletion modifies metabolic effects of exercise. Male Sprague-Dawley rats were assigned for sedentary and exercise groups with free access to running wheels for 3 weeks. All animals received normal control diet for 7 days. Both groups were fed either by low tryptophan (0.04%) diet or by control diet (0.2%) for next 2 weeks. The β3-adrenergic receptor mRNA levels in response to running increased in the retroperitoneal and epididymal fat pads. The gene expression of uncoupling protein-1 (UCP-1) was increased in the brown, while unchanged in the white fat tissues. Unlike control animals, the rats fed by low tryptophan diet did not exhibit a reduction of the white adipose tissue mass. Tryptophan depletion resulted in enhanced concentrations of plasma aldosterone and corticosterone, but had no influence on exercise-induced adrenal hypertrophy. No changes in β3-adrenergic receptor and cell proliferation measured by 5-bromo-2′-deoxyuridine incorporation in left heart ventricle were observed. The reduced β3-adrenergic receptor but not enhanced uncoupling protein-1 gene expression supports the hypothesis on hypoactive brown adipose tissue during exercise. Reduction in dietary tryptophan had no major influence on the exercise-induced changes in the metabolic parameters measured.


2020 ◽  
Vol 319 (1) ◽  
pp. H192-H202
Author(s):  
Alexander B. Hansen ◽  
Gilbert Moralez ◽  
Steven A. Romero ◽  
Christopher Gasho ◽  
Michael M. Tymko ◽  
...  

Sympathetic restraint of vascular conductance to inactive skeletal muscle is critical to maintain blood pressure during moderate- to high-intensity whole body exercise. This investigation shows that cycle exercise-induced restraint of inactive skeletal muscle vascular conductance occurs primarily because of activation of α-adrenergic receptors. Furthermore, exercise-induced vasoconstriction restrains the subsequent vasodilatory response to hand-grip exercise; however, the restraint of active skeletal muscle vasodilation was in part due to nonadrenergic mechanisms. We conclude that α-adrenergic receptors are the primary but not exclusive mechanism by which sympathetic vasoconstriction restrains blood flow in humans during whole body exercise and that metabolic activity modulates the contribution of α-adrenergic receptors.


2002 ◽  
Vol 282 (2) ◽  
pp. H508-H515 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Michel Lavallée

We hypothesized that nitric oxide (NO), in addition to β-adrenergic effects, may contribute to exercise-induced coronary responses after α-adrenergic receptor blockade. Data were analyzed as relationships between coronary sinus (CS) O2 saturation (CS O2sat) or coronary blood flow (CBF) and myocardial O2 consumption (MV˙o 2). As MV˙o 2 increased, CS O2sat fell more ( P < 0.05) after N ω-nitro-l-arginine methyl ester (l-NAME; slope = −2.9 ± 0.4 × 10−2 %saturation · μl O2 · min−1 · g−1) than before (slope = −2.1 ± 0.3 × 10−2%saturation · μl O2 · min−1 · g−1). The slope of CBF versus MV˙o 2 was not altered. After blockade of α-adrenergic receptors alone (phentolamine), CS O2sat failed to decrease as MV˙o 2 increased (slope = −0.1 ± 0.5 × 10−2 %saturation · μl O2 · min−1 · g−1).l-NAME given after phentolamine led to substantial decreases in CS O2sat ( P < 0.01) as MV˙o 2 increased (slope = −2.1 ± 0.4 × 10−2 percent saturation · μl O2 −1 · min−1 · g−1). CBF responses to exercise were smaller ( P < 0.01) after phentolamine + l-NAME (slope = 6.1 ± 0.1 × 10−3 ml/μl O2) than after phentolamine alone (slope = 6.9 ± 0.2 × 10−3 ml/μl O2). Thus a significant portion of exercise-induced coronary responses after α-adrenergic receptor blockade involves NO formation.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Aneta Otocka-Kmiecik ◽  
Marek Lewandowski ◽  
Urszula Szkudlarek ◽  
Dariusz Nowak ◽  
Monika Orlowska-Majdak

The aim of the study was to compare the effect of maximal exercise (ME) on paraoxonase (PON) and arylesterase (ARE) activity depending on lifestyle in respect to physical activity. The study was performed on 46 young men divided into two groups: sedentary (S) and physically active (PA). All participants performed ME on a treadmill. PON1 activities, FRAP, uric acid, bilirubin, TBARS, and lipid profile were determined in their blood before, at the bout of, and after ME. No significant differences in PON1 activities were found between S and PA subjects at baseline. Nearly all biochemicals increased at ME in both groups. Both PON and ARE activity increased at the bout of ME in PA subjects and only ARE activity in S subjects. ARE/HDL-C ratio increased at the bout of ME in PA and S subjects. The difference in PON1 activity response to ME between study groups may be a result of adaptation of PA subjects to regular physical activity. We suggest that PON1 activity may be a marker of antioxidant protection at ME and an indicator of adaptation to exercise.


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