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1 Center for Genetic Medicine Research, Children's National Medical Center, Washington, District of Columbia, United States
2 Center for Genetic Medicine Research, Children's National Medical Center, Washington, District of Columbia, United States; Department of Pediatrics, George Washington University, Washington, District of Columbia, United States
3 Department of Medicine, University of Dundee, Dundee, United Kingdom
4 School of Kinesiology, University of Illinois, Chicago, Illinois, United States
5 School of Biomedical Scinces, University of Nottingham, Derby, United Kingdom
* To whom correspondence should be addressed. E-mail: ychen{at}cnmcresearch.org.
Resistance training using lengthening (eccentric) contractions induces greater increases in muscle size than shortening (concentric) contractions but the underlying molecular mechanisms are not clear. Using temporal expression profiling, we compared changes in gene expression within 24 h of an acute bout of each type of contractions conducted simultaneously in the quadriceps of different legs. Five healthy young men performed shortening contractions with one leg while the contralateral leg performed lengthening contractions. Biopsies were taken from both legs before exercise and 3, 6, and 24 h afterwards, in the fed state. Expression profiling (n=3) was performed using a custom-made Affymetrix MuscleChip containing probesets of approximately 3,300 known genes and ESTs expressed in skeletal muscle. We identified 51 transcripts differentially regulated between the two exercise modes. Using unsupervised hierarchical clustering, we identified four distinct clusters, three of which corresponded to unique functional categories (protein synthesis, stress response/early growth, and sarcolemmal structure). Using quantitative RT-PCR (n=5), we verified expression changes (lengthening/shortening) in SIX1 (3h, -1.9 fold, p<0.001), CSRP3 (6h, 2.9 fold, p<0.05), and MUSTN1 (24h, 4.3 fold, p<0.05). We examined whether FBXO32/atrogin-1/MAFbx, a known regulator of protein breakdown and of muscle atrophy was differentially expressed: the gene was down-regulated after lengthening contractions (3h, 2.7 fold, p<0.05; 6h, 3.3 fold, p<0.05; 24 h, 2.3 fold, p<0.05). The results suggested that lengthening and shortening contractions activated distinct molecular pathways as early as 3 hour post-exercise. The molecular differences might contribute to mechanisms underlying the physiological adaptations seen with training using the two modes of exercise.
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