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Effect of chronic treadmill running on apoptotic protein expression in soleus muscle of normotensive and hypertensive rats
Author(s) -
Quadrilatero Joe,
Graham Drew A.,
Rush James W.E.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1344-d
Subject(s) - skeletal muscle , medicine , endocrinology , xiap , soleus muscle , apoptosis , sed , muscle hypertrophy , dna fragmentation , myocyte , caspase , biology , programmed cell death , biochemistry
Augmented apoptotic signaling in skeletal muscle has been well documented in several conditions including aging, chronic heart failure, disuse, and neuromuscular disorders. Recently, we have found increased DNA fragmentation and altered apoptotic protein levels in skeletal muscle of spontaneously hypertensive rats (SHR) relative to normotensive controls (WKY). Current evidence suggests that exercise may alter apoptosis‐related proteins in skeletal muscle; however, the effect of exercise on skeletal muscle apoptosis in hypertensive animals is unclear. Male WKY (n=24) and SHR (n=24) rats were assigned to a sedentary (SED) condition or exercise (EX) consisting of progressive treadmill running 5 days/wk for 6 wks. Compared to WKY controls, soleus muscle of SHR had decreased anti‐apoptotic Bcl‐2, XIAP and ARC protein levels as well as elevated pro‐apoptotic caspase 3 activity. Further, the levels of Bcl‐2, MnSOD and Hsp70 protein in soleus muscle were significantly elevated following EX compared to the SED condition. In contrast, EX training had no effect on ARC, XIAP and CuZnSOD protein levels as well as caspase 3 activity. These results suggest that exercise can alter the expression of several proteins which may provide protection against skeletal muscle apoptosis in both SHR and WKY rats; however, exercise may not influence caspase signaling. Research supported by the Heart and Stroke Foundation of Ontario.