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.Male WT and β2 -adrenoceptor knockout mice on a FVB genetic background (β2 KO) were submitted to myocardial infarction (MI) or SHAM surgery.Skeletal muscle atrophy of infarcted β2 KO mice was paralleled by reduced levels of phosphorylated Akt at Ser 473 while increased levels of proteins related with the ubiquitin--proteasome system, and increased 26S proteasome activity.
Affiliation: School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.Show MeSH
Related in: MedlinePlus
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.