Acta physiologica
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Platelet-activating factor (PAF) triggers cardiac pre-conditioning against ischemia/reperfusion injury. The actual protection of ischaemic pre-conditioning occurs in the reperfusion phase. Therefore, we studied in this phase the kinases involved in PAF-induced pre-conditioning. ⋯ The cardioprotective effect exerted by PAF pre-treatment involves activation of PKC and PI3K in post-ischaemic phases and might be mediated by the prevention of mPTP opening in reperfusion via GSK-3beta inactivation.
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Myofascial trigger points (MTrPs) are a major cause of musculoskeletal pain. It has been reported that stimulation of a latent MTrP increases motor activity and facilitates muscle pain via activation of the sympathetic nervous system. However, the magnitude of the sympathetic vasoconstrictor response following stimulation of MTrP has not been studied in healthy volunteers. The aims of this study were to (1) evaluate the magnitude of the vasoconstrictor response following a nociceptive stimulation (intramuscular glutamate) of MTrPs and a breath-hold manoeuvre (activation of sympathetic outflow) and (2) assess whether the vasoconstrictor response can be further modulated by combining a nociceptive stimulation of MTrPs and breath-hold. ⋯ The combination of glutamate injection into latent MTrPs together with the breath-hold manoeuvre did not result in further decrease in skin temperature and blood flow, indicating that sympathetic vasoconstrictor activity is fully activated by nociceptive stimulation of MTrPs.
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Controlled Clinical Trial
Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockade.
Beta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. ⋯ Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity.
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The contributions of cardiac output (CO) and total peripheral resistance to changes in arterial blood pressure are debated and differ between dynamic and static exercise. We studied the role stroke volume (SV) has in mild supine exercise. ⋯ Our three major findings are, firstly, that SV decreases during both dynamic and static mild supine exercise due to an increase in mean arterial pressure. Secondly, femoral beat volume decreases during static hand grip, but FF is unchanged due to the increase in HR. Finally, anticipatory responses to exercise are apparent prior to both dynamic and static exercise. SV changes contribute to CO changes and should be included in studies of central haemodynamics during exercise.