european college of sport science

PP-MB02 Molecular Biology 2
Discussion: Our aim was to compare the interference of the liver upon the systemic lipid metabolism using two different protocols: Intermittent
(around 100% of the VO2max) and continuous (60%VO2max) exercise training. Despite the different exercise stimuli, we found no
different adaptations between the groups. Therefore, we can speculate that the two protocols induce similar adaptation in regard to liver
lipid metabolism (Chilibeck et al., 1998; Chapados et al., 2008).
References:
Chapados NA, Seelaender M, Levy E, Lavoie JM. (2008). Horm Metab Res, 40, 1-7.
Chilibeck PD, Bell GJ, Farrar RP, Martin TP. (1998). Can J Physiol Pharmacol, 76(9), 891-4.
Glaister M. (2005). Sports Med, 35(9), 757-77.
Lima WP, Carnevali LC Jr, Eder R, Costa Rosa LF, Bacchi EM, Seelaender MC. (2005), Clin Nutr, 24(6), 1019-28.
TGF-β ISOFORMS INHIBIT IN VITRO MIGRATION AND FUSION OF MYOGENIC PROGENITOR CELLS
SCHABORT, E.J., VAN DER MERWE, M., NIESLER, C.U.
EXERCISE SCIENCE AND SPORTS MEDICINE UNIT, UNIVERSITY OF CAPE TOWN
Introduction: Following muscle injury, the damaged tissue and influx of inflammatory cells stimulate the secretion of various growth
factors and cytokines into the afflicted area to initiate repair processes. This release of chemotactic signaling factors activates resident
myogenic precursor cells (quiescent satellite cells, other local sources of myocytes) and precursors from external fibers to participate in
regeneration. These signaling molecules also control cellular responses required to stimulate the mobilization and migration of cells from
distant niches to the site of injury, where fusion can occur to form myofibers. Specifically, sports injuries (e.g. muscle contusions) are a
primary concern to athletes who cannot afford the time off to recuperate. While treatment options are limited and time-consuming, research
has shown administration of autologous conditioned serum, which stimulates the release of growth factors aiding regeneration,
to be a promising new approach by reducing recovery time (Wright-Carpenter et al, 2004). The three Transforming Growth Factor-ß (TGFß)
isoforms and Insulin-like Growth Factor-I (IGF-I) are among the known factors released following muscle damage. We investigated the
effect of TGF-ß1, -ß2, -ß3 and IGF-I on muscle progenitor cell migration and the effect of TGF-ß isoforms on myoblast fusion.
Methods: The C2C12 skeletal muscle satellite cell-line was used to determine the effect of recombinant active TGF-ß1, -ß2 and -ß3, IGF-I
and TGF-ß isoforms + IGF-I on the migration of myogenic precursor cells. In addition, the effect of 72 hr TGF-ß treatment was analysed on
C2C12 fusion.
Results: IGF-I significantly increased migration compared to TGF-ß isoforms which had no effect on the mobilization of C2C12 cells. Although
all isoforms decreased IGF-I-induced cell migration, the number of migrated cells was still significantly higher compared to control.
Myoblast fusion was significantly reduced in all TGF-ß-treated C2C12 cells.
Discussion: The ability to regulate cellular processes in response to injury could be of important therapeutic value (Smith et al., 2008). We
have previously shown that all three TGF-ß isoforms significantly increase C2C12 satellite cell proliferation (Schabort et al., 2009). We have
now gone on to show that both myocyte migration and fusion are negatively regulated by all three isoforms. By distinguishing the factors
involved in, and the molecular signals required for myoblast recruitment during repair processes, strategies can be developed towards
improved cell-mediated therapies for muscle injury. Future research should involve in vivo combined-effects studies using multiple
growth factors. These results highlight the importance of understanding the cytokine milieu of progenitor cells when determining viable
treatment options.
References
Smith C, Kruger M, Smith R, et al. (2008). Sports Med, 38(11), 947-969.
Wright-Carpenter T, Opolon P, Appell H, et al. (2004). Int J Sports Med, 25(8), 582-587.
Schabort E, Van der Merwe M, Loos B, et al. (2009). Exp Cell Res, 315(3), 373-384.
THE MODULATION OF LIPID METABOLISM-RELATED GENES IN THE LIVER OF TRAINED TUMOUR-BEARING RATS.
CARNEVALI JR, L.C., EDER, R., LIMA, W.P., LIRA, F.S., PAPESCHI, J.C., GONÇALVES, D.C., SEELAENDER, M.C.L.
UNIVERSITY OF SÃO PAULO
Introduction: Lipid metabolism in the liver is clearly altered by the syndrome of cancer cachexia. Previous studies by our group have
shown that, in one such model, liver capacity for the oxidation of long chain fatty acids and for ketone body production is decreased
(Seelaender et al., 1996). The activity of the CPT (carnitine palmitoyltransferase) enzyme complex, the main step in the control of mitochondrial
long chain fatty acid transport, is reduced in cachectic rats, aggravating cachexia Regular moderate exercise is known to contribute
for the prevention of cancer, enhancing resistance against tumour growth. (Lira et al., 2008). A previous study by our group showed that
moderate exercise training (60% VO2max, 60min per day, 5 day a week, for 8 weeks) may increase hepatic lipid oxidation and augment
very low density lipoprotein (VLDL) secretion in the trained tumour-bearing rats (Lira et al., 2008). Changes in lipid metabolism are closely
related with associated protein gene expression modification, which is in many cases, mediated by mechanisms dependent on the
activation of PPARs. Some studies show that training is able to induce gene expression of proteins such as CPT I, CPT II, PPARalpha, FABP.
Hence, we investigated whether 8 weeks of moderate training would promote changes in the liver lipid metabolism in tumour-bearing
rats.
Methods: Male adult Wistar rats were distributed in 4 groups: Sedentary control (SC), Sedentary tumour-bearing (ST), exercise-trained
control (EC) and exercise trained tumour-bearing (ET). The mRNA expression of fatty-acid binding protein (FABP), apoliprotein B (apoB),
microsomal triacylglycerol transfer protein (MTP), Carnitine Palmitoyltransferase I (CPT I), Carnitine Palmitoyltransferase II (CPT II), peroxisome
proliferator-activated- receptor alpha (PPAR alpha) were assessed by real time PCR.
Results: Cachexia (tumour vs control group) induced an increased gene expression of PPAR alpha (P