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Thursday, June 25th, 2009<br />

dilatation and sympatholysis by binding to endothelial ATP selective P2Y2 purinergic receptors and stimulating the vascular endothelium<br />

to release vasodilator-sympatholytic substances, including nitric oxide, prostaglandins and endothelium-derived hyperpolarization<br />

factors.<br />

Support: Copenhagen Hospital System, Novo Nordisk Foundation and Lundbeck Foundation.<br />

ROLE OF ENDOTHELIUM AND SKELETAL MUSCLE DERIVED VASODILATORS<br />

HELLSTEN, Y.<br />

UNIVERSITY OF COPENHAGEN<br />

Role <strong>of</strong> endothelium and skeletal muscle derived vasodilators<br />

in exercise hyperaemia<br />

Ylva Hellsten<br />

Copenhagen Muscle Research Centre, Department <strong>of</strong> Exercise and Sport Science, University <strong>of</strong> Copenhagen, Universitetsparken 13, DK-<br />

2100 Copenhagen Denmark<br />

In skeletal muscle, blood flow may increase more than 30-fold from rest to exercise, with a close match between the rate <strong>of</strong> flow and<br />

oxygen demand. The precise regulation is achieved by a balance between sympathetic vasoconstriction and locally formed vasodilators,<br />

but also vasoconstrictors and compounds that induce sympatholysis are involved . Studies using pharmacological inhibition <strong>of</strong> single or<br />

multiple vasodilator systems in humans have revealed that the compounds nitric oxide (NO), prostaglandins (PG’s), 11, 12 eicosatrienoic<br />

acid (11, 12 EETs), adenosine and ATP are regulators <strong>of</strong> muscle blood flow. Such studies have also demonstrated that there is interaction<br />

between vasodilators where a specific vasodilator can compensate for the impaired release <strong>of</strong> another, i.e. redundancy. Evidence for<br />

redundancy exists between NO and PG’s and between NO and 11, 12 EETs. In addition, some compounds exert or extend their vasoactive<br />

effects by inducing the release <strong>of</strong> vasodilators. Examples <strong>of</strong> this are the effects <strong>of</strong> ATP and adenosine in causing the release <strong>of</strong> NO and<br />

PG’s. In fact, evidence point at that release <strong>of</strong> nitric oxide and prostaglandins is the primary mechanism by which adenosine regulates<br />

exercise hyperaemia and that a direct effect <strong>of</strong> adenosine on adenosine receptors on smooth muscle cells appear to be <strong>of</strong> less importance.<br />

Thus, several vasodilators <strong>of</strong> importance for muscle blood flow control have been identified and evidence point at that the precise<br />

regulation <strong>of</strong> flow is the result <strong>of</strong> a close interplay between these vasodilators. Nevertheless, simultaneous inhibition <strong>of</strong> multiple known<br />

vasodilator systems has only been found to reduce exercise hyperemia in humans by ~30%, which could suggest the existence <strong>of</strong> yet<br />

unidentified vasodilators.<br />

Support: Danish Medical Research Council, Novo Nordisk Foundation, Lundbeck Foundation<br />

08:30 - 10:00<br />

Invited symposia<br />

IS-BM08 Laterality and assymetries in <strong>sport</strong>s<br />

MECHANISMS UNDERLYING FUNCTIONAL CHANGES IN THE PRIMARY MOTOR CORTEX IPSILATERAL TO AN ACTIVE<br />

ARM<br />

PEREZ, M.A.<br />

UNIVERSITY OF PITTSBURGH<br />

Performance <strong>of</strong> a unimanual motor task results in functional changes in both primary motor cortices (M1s). The neuronal mechanisms<br />

controlling the corticospinal output originating in the M1 ipsilateral to a moving arm remain poorly understood (1). Gaining insight into<br />

these mechanisms may contribute to a better understanding <strong>of</strong> how unimanual and bimanual movements are controlled (2,3,4,5).<br />

During this presentation I will review several electrophysiological markers <strong>of</strong> motor cortical function measured at rest and during different<br />

levels <strong>of</strong> unilateral and bilateral finger, wrist and elbow voluntary movements by using transcranial magnetic stimulation (TMS). These<br />

electrophysiological markers include: motor-evoked potential (MEP) recruitment curves, short-interval intracortical inhibition (SICI), interhemispheric<br />

inhibition measured by a paired-pulse TMS paradigm and by the ipsilateral cortical silent period (iSP), and the influence <strong>of</strong><br />

interhemispheric inhibition over SICI.<br />

Our results have shown activity-dependent changes in SICI in M1 ipsilateral, interhemispheric inhibition from M1 contralateral to M1<br />

ipsilateral, and in the influence <strong>of</strong> interhemispheric inhibition over SICI. Differences are observed between responses evoked from distal<br />

and proximal representations in the primary motor cortex (4,5). Altogether our findings indicate that interactions between GABAergic<br />

intracortical circuits mediating SICI and interhemispheric glutamatergic projections between M1s partly contribute to control activitydependent<br />

changes in corticospinal output in the M1 ipsilateral to a moving arm during voluntary movement by the opposite arm.<br />

1. Carson RG. Brain Res Brain Res Rev 49:641–662, 2005<br />

2. Hortobágyi et al. J Neurophysiol 90: 2451-2459, 2003<br />

3. Muellbacher W et al. Clin Neurophysiol 111: 344-349, 2000<br />

4. Perez and Cohen. J Neurosci 28: 5631-5640, 2008<br />

5. Perez and Cohen. Cortex (in press), 2009<br />

OSLO/NORWAY, JUNE 24-27, 2009 121

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