Interaction of contractile activity and training history on mRNA abundance in skeletal muscle from trained athletes.
Skeletal muscle displays enormous plasticity to respond to contractile activity with muscle from strength- (ST) and endurance-trained (ET) athletes representing diverse states of the adaptation continuum. Training adaptation can be viewed as the accumulation of specific proteins. Hence, the altered gene expression that allows for changes in protein concentration is of major importance for any training adaptation. Accordingly, the aim of the present study was to quantify acute subcellular responses in muscle to habitual and unfamiliar exercise. After 24-h diet/exercise control, 13 male subjects (7 ST and 6 ET) performed a random order of either resistance (8 x 5 maximal leg extensions) or endurance exercise (1 h of cycling at 70% peak O2 uptake). Muscle biopsies were taken from vastus lateralis at rest and 3 h after exercise. Gene expression was analyzed using real-time PCR with changes normalized relative to preexercise values. After cycling exercise, peroxisome proliferator-activated receptor-gamma coactivator-1alpha (ET approximately 8.5-fold, ST approximately 10-fold, P < 0.001), pyruvate dehydrogenase kinase-4 (PDK-4; ET approximately 26-fold, ST approximately 39-fold), vascular endothelial growth factor (VEGF; ET approximately 4.5-fold, ST approximately 4-fold), and muscle atrophy F-box protein (MAFbx) (ET approximately 2-fold, ST approximately 0.4-fold) mRNA increased in both groups, whereas MyoD (approximately 3-fold), myogenin (approximately 0.9-fold), and myostatin (approximately 2-fold) mRNA increased in ET but not in ST (P < 0.05). After resistance exercise PDK-4 (approximately 7-fold, P < 0.01) and MyoD (approximately 0.7-fold) increased, whereas MAFbx (approximately 0.7-fold) and myostatin (approximately 0.6-fold) decreased in ET but not in ST. We conclude that prior training history can modify the acute gene responses in skeletal muscle to subsequent exercise.
Coffey
Vernon G
VG
School of Medical Sciences, RMIT University, Melbourne, Australia.
Shield
Anthony
A
Canny
Benedict J
BJ
Carey
Kate A
KA
Cameron-Smith
David
D
Hawley
John A
JA
D000328:Adult; D001642:Bicycling / Q000502:physiology; D018592:Cross-Over Studies; D015870:Gene Expression / Q000235:genetics; D006360:Heat-Shock Proteins / Q000235:genetics; D006801:Humans; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D009124:Muscle Proteins / Q000235:genetics; D018482:Muscle, Skeletal / Q000502:physiology*; D017570:MyoD Protein / Q000235:genetics; D018008:Myogenin / Q000235:genetics; D055435:Myostatin; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D011494:Protein Kinases / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D044843:SKP Cullin F-Box Protein Ligases / Q000235:genetics; D013177:Sports / Q000502:physiology*; D014157:Transcription Factors / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics; D014891:Weight Lifting / Q000502:physiology
D006360:Heat-Shock Proteins; C525911:MSTN protein, human; D009124:Muscle Proteins; D017570:MyoD Protein; D018008:Myogenin; D055435:Myostatin; C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D012333:RNA, Messenger; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D042461:Vascular Endothelial Growth Factor A; C440907:FBXO32 protein, human; D044843:SKP Cullin F-Box Protein Ligases; D011494:Protein Kinases; C403287:pyruvate dehydrogenase kinase 4