european college of sport science

Thursday, June 25th, 2009
certain degree can attenuate the age-associated loss in muscle function. Young control (YC), exercised (YE) and old, control (OC) and
exercise (OE) rats were used, with six weeks of treadmill running program at the 60% of VO2max. Aging resulted in increased level of
SIRT1 in cytoplasm and nuclear extracts, while exercise training significantly increased the relative activity of SIRT1 in both age groups. The
levels of nicotinamide phosphoribosyltransferase (NAMPT) and NAD+ significantly degreased with aging, which were prevented by
exercise training. Both, aging and exercise training modified the level of acetylation in number of proteins. The oxidative challenge was
evaluated by accumulation of carbonyl groups, which increased at OC, and 8-oxydeoxyguanosine level of nuclear extracts, which did not
change. On the other hand, the content of SIRT6, which suggest to influence base excision repair increased with aging in parallel with the
content of 8-oxoguanine DNA glycosylase (OGG1). Aging resulted in massive increase in the content of hypoxia inducible factor alpha
(HIF-1alpha) and vascular endothelial factor (VEGF), which was prevented by exercise training.
Aging of the skeletal muscle is associated with inadequate production of NAD+ because of impaired synthesis via NAMPT, although the
activity of SIRT1 does not change with aging.
Hence, NAMPT emerged as possible therapeutic target to attenuate aging process in skeletal muscle, suggesting metabolic and partly
reversible consequences of aging, as regular exercise, decreased the gap in all between young and old groups.
ESTROGEN REGULATES SATELLITE CELL ACTIVATION FOLLOWING A NOTEXIN-INDUCED SKELETAL MUSCLE INJURY
VELDERS, M., FRITZEMEIER, K.H., DIEL, P.
GERMAN SPORTS UNIVERSITY COLOGNE, INSTITUTE OF CARDIOVASCULA
Skeletal muscle repair processes are mediated by the coordinated response of inflammatory immune cells and satellite cells. It has been
reported that estrogen activates satellite cells in skeletal muscle damaged by high intensity downhill running exercise and that this process
is ER-mediated (Tiidus, Holden et al. 2001; Tiidus, Deller et al. 2005; Enns, Iqbal et al. 2008; Enns and Tiidus 2008). To prove that
estrogen may also activate satellite cell activity in a skeletal muscle injury model relevant to pathological processes involved in inflammatory
dystrophic skeletal muscle diseases or sarcopenia, we analyzed the effects of estrogen in a myotoxin (Notexin) based skeletal muscle
injury model. This model is known to cause an early inflammatory reaction followed by a satellite cell driven repair period. Female
Wistar rats were divided into three experimental groups: intact (SHAM), ovariectomized (OVX) and ovariectomized E2 substituted animals
(E2). We investigated the effects of subcutaneous (E2) replacement for 7 days on immune and satellite cell activation. Results show that
protein expression levels detected by western blot analysis of the proliferating cell nuclear antigen (PCNA) are highest in the toxindamaged
m.Gastrocnemius (m.GAS) of OVX rats compared to control (Sham) and E2-substitued groups, 24-h following the injury. A
different PCNA expression pattern was detected 3-d after Notexin injections into the right m.GAS. Here, PCNA expression was highest in
the right m.GAS of Sham and E2 animals compared to OVX animals. This differential expression pattern of PCNA could be due to the
proliferation and infiltration of inflammatory immune cells into the injured m.GAS after 24-h. The increased expression of PCNA in the right
m.GAS of Sham and E2 animals after 3-days may be the result of increased satellite cell proliferation. Gene expression data confirms that
the expression of the satellite cell marker Pax-7 is highest in the right m.GAS of Sham and E2 treated groups compared to OVX. Protein
expression levels of the inflammatory cytokine tumor necrosis factor alpha (TNFα) are elevated 24-h post-injury in the right m.GAS of all
treatment groups and are below detection levels after 3 days. In summary, our results show that estrogen replacement increases satellite
cell numbers following a toxin-induced skeletal muscle injury. Based on this information we speculate that normal E2 serum levels may
provide protection against inflammatory dystrophic diseases and sarcopenia, whereas reduced E2 serum levels may promote the development
of these diseases. Further studies are in progress to investigate whether these mechanisms are estrogen receptor alpha or beta
mediated.
COMBINED TREATMENT WITH INSULIN AND EXERCISE TRAINING AMELIORATES EXPRESSION OF CALCIUM SIGNAL-
LING PROTEINS IN STREPTOZOTOCIN-INDUCED DIABETIC RAT HEARTS.
LE DOUAIRON LAHAYE, S., MALARDÉ, L., ZGUIRA, M.S., VINCENT, S., LEMOINE MOREL, S., ZOUHAL, H., DELAMARCHE, P.,
CARRÉ, F., RANNOU BEKONO, F.
LABORATORY MOUVEMENT SPORT SANTÉ
Background – Insulin therapy and regular exercise activity have positive impact on the diabetic cardiomyopathy, where impaired contractile
responsiveness to β-adrenergic stimulation results in part from alterations in the Ca2+ regulatory systems. If the cellular and
molecular mechanisms involved in insulin or exercise training myocardial adaptations have been partially explained, the concomitant
effects of these 2 approaches remains incompletely characterized. So, the present study was undertaken to assess the combined effects
of insulin treatment and exercise training on Ca2+ signalling proteins expression on heart of diabetic rats.
Methods – Type 1 diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ, 45 mg/kg, in citrate buffer) in adult
male Wistar rats. One week after STZ injection, diabetic rats were randomly divided into 3 groups: non-treated diabetic, insulin-treated
diabetic, and trained insulin-treated diabetic animals. Exercise training consisted of progressive running at speeds to 25 m/min, 60
minutes/day, 5 days/week for 8 weeks on a rodent treadmill set at 10°. A group of normal sedentary rats served as control. Abundance
of Ca2+ signalling proteins was assessed using Western blots. Langendorff left ventricular performance was also determined.
Results – After nine weeks of diabetes, SERCA2, RyR2 and NCX1 protein expression were significantly reduced by 32, 44, 23%, respectively,
whereas PLB expression was significantly elevated (46%) and FKBP 12 unchanged. Intrinsic contractile parameters were also significantly
reduced. Insulin treatment initiated after 1 week of diabetes normalized the expression of SERCA2, RyR2, and NCX1, and attenuated
the loss in cardiac relaxation and contraction as assessed by ±dP/dt. Moreover, training accentuated positive insulin-treatment effects
because trained insulin-treated diabetic animals exhibited significantly higher SERCA2, RyR2, and NCX1 protein expression and
RyR2/FKBP12 ratio than insulin-treated diabetic animals. Although the difference were not significant, positive and negative dP/dt were
increased (19 and 8%, respectively), by the association exercise training-insulin compared with insulin alone.
Conclusion – Taken collectively, these data suggest that the beneficial effect of insulin treatment in the expression of the main Ca2+
signalling proteins could be potentiated by exercise training. Moreover, these adaptations might lead to normalise cardiac contractile
efficiency. So this study provides additional funding as to the beneficial role of exercise in the management of diabetes.
OSLO/NORWAY, JUNE 24-27, 2009 197