LIMITATION OF EXERCISE PERFORMANCE BY ACTIVITY OF INTRACEREBRAL DOPAMINERGIC SYNSPSES

Abstract

<p>Evidence from the literature suggests that a limiting factor to the performance of exhaustive exercise is the ability of the brain to maintain the stimulation of the alpha-motor neuron. This these examined the hypothesis that this "central fatigue" results from a deficit in the transfer of information across striatal dopaminergic synapses. Decreases in striatal dopaminergic activity should impair exercise capacity whereas increases in dopaminergic activity should therefor improve exercise capacity. The rat was chosen as the experimental animal because of the availability of techniques to alter dopaminergic activity and to quantify exercise capacity. Striatal dopaminergic activity was reduced by depletion of striatal dopamine by an intracerebroventricular injection of 200mg of 6-hydroxydopamine. Dopaminergic activity was increases by an intreperitoneal injection of the specific dopamine receptor agonist apormorphine. Exercise capacity was quantified with treadmill-grid system by measuring the time taken for a running rat to become exhausted. Striatal dopamine depletion decreased exercise capacity whereas apomorphine increased xercise capacity. In contras, striatal and hpothalmic norepinephrine depletion had no effect on exercise capacity.</p> <p>The limitation of exercise capacity by the activity of striatal dopaoinergic synapses was not due to a failure of these synapses to maintain the release of dopamine, but may be due to these synapses releasing amounts of dopamine which are insufficient to transmit all the information arriving at the presynaptic terminal to the postsynaptic neuron. I propose that the release of dopamine is limited in exhausted rats by the activitation of presynaptic dopamine receptors located on the terminal and that the purpose of these receptors is to maintain the concentration of dopamine in the functional pool of the terminal.</p>