Premium
Exercise training‐induced mitochondrial biogenesis is impaired in skeletal muscle‐specific LKB1 knockout mice
Author(s) -
Hallowell David M.,
Tanner Colby B.,
Nuttall Megan R.,
Anderson Stephen K.,
Bradshaw Jared M.,
Madsen Steven R.,
Thomson David M.
Publication year - 2012
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.26.1_supplement.1142.46
Subject(s) - skeletal muscle , mitochondrial biogenesis , sed , endocrinology , citrate synthase , medicine , endurance training , knockout mouse , mitochondrion , treadmill , biology , chemistry , biochemistry , enzyme , receptor
Regular exercise training leads to increased mitochondrial protein content in skeletal muscle. The necessity of liver kinase B1 (LKB1) for this adaptation is unknown. Our purpose here was to determine whether skeletal muscle LKB1 is required for exercise training‐induced increases in mitochondrial protein content. To test this, skeletal muscle‐specific LKB1 knockout (KO) and littermate control (C) mice (n=8–9) were either sedentary (SED) or treadmill trained (TRN) 4 days/week, twice per day for 3 weeks. Exercise intensity and duration for both WT and KO mice were determined as tolerated by the KO mice such that the training stimulus was identical for both genotypes. Gastrocnemius (GAST) of TRN C mice had a significant (p ≤ 0.05) increase in the content of the mitochondrial proteins cytochrome‐C and complex I of the electron transport chain (ETC) as well as a trend (p=0.14) for an increase in core 2 of complex III of the ETC. vs. SED C mice. These training adaptations did not occur in TRN KO GAST. We conclude that LKB1 is necessary for increases in some mitochondrial proteins after moderate intensity exercise training. This work was funded by NIAMSD Grant AR‐51928.