Lack of β2 -adrenoceptors aggravates heart failure-induced skeletal muscle myopathy in mice.
Bottom Line: HF and other chronic degenerative diseases share a common feature of a stressed system: sympathetic hyperactivity.Considering that β2 -adrenoceptors mediate the activity of sympathetic nervous system in skeletal muscle, we presently evaluated the contribution of β2 -adrenoceptors for the morphofunctional alterations in skeletal muscle and also for exercise intolerance induced by HF.Ninety days after MI both WT and β2 KO mice presented to cardiac dysfunction and remodelling accompanied by significantly increased norepinephrine and epinephrine plasma levels, exercise intolerance, changes towards more glycolytic fibres and vascular rarefaction in plantaris muscle.
Affiliation: School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.Show MeSH
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Mentions: Functional capacity was assessed as maximal exercise performance in running test until exhaustion and ambulation test. Figure1 shows that β2KO SHAM mice displayed higher exercise tolerance than WT SHAM mice (Fig.1A) with no difference in step-to-body length ratio (Fig.1B). Myocardial infarction induced exercise intolerance in both β2KO MI and WT MI mice when compared with their respective SHAM control mice; however, the magnitude of distance run reduction was greater in β2KO than WT MI mice (49 ± 4 versus 30 ± 3%, P < 0.05; Fig.1A). Interestingly, only β2KO MI mice displayed decreased performance on ambulation test (Fig.1B), which suggests that β2-AR disruption aggravated MI-induced muscle strength loss.
Affiliation: School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.