Acute Impact of Different Exercise Modalities on Arterial and Platelet Function.

PURPOSE: Acute coronary syndromes and ischemic stroke are associated with arterial events involving platelets, the endothelium and atherosclerosis. Whilst regular physical activity is associated with lower risk of cardiovascular events and mortality, risk is transiently increased during and immediately following participation in an acute bout of exercise. No previous study has investigated the acute impact of exercise on platelet activation and arterial function in the same participants; it is also unknown if responses are dependent on exercise modality. We hypothesised that commonly adopted, yet physiologically distinct, modalities of exercise ("aerobic" versus "resistance") have differing effects on in vivo platelet activation and conduit artery diameter. METHODS: Eight apparently healthy middle-aged (53.5±1.6yrs) male subjects took part in four, 30 min experimental interventions (aerobic AE, resistance RE, combined aerobic/resistance exercise CARE or no-exercise), in random order. Blood samples were collected and the measurement of brachial artery diameter by ultrasound was performed before, immediately after, and one hour after each intervention. Platelet activation was determined by the positive binding of antibodies to surface receptors exposed on activated platelets (anti-CD62P and PAC-1). RESULTS: Brachial artery diameter increased immediately following all three exercise modalities (P<0.001), and remained above pre-exercise levels 1hr post-RE and -CARE. No changes were observed in markers of in vivo platelet activation with any experimental protocol. CONCLUSION: These data suggest that post-exercise enhancement in arterial function may mitigate the acute impact of exercise on platelet activation

Postprandial effects of a high salt meal on serum sodium, arterial stiffness, markers of nitric oxide production and markers of endothelial function

The fulltext of this publication will be made publicly available after relevant embargo periods have lapsed and associated copyright clearances obtained.AIM: The aim of the study was to determine if a high salt meal containing 65 mmol Na causes a rise in sodium concentrations and a reduction in plasma nitrate/nitrite concentrations (an index of nitric oxide production). Secondary aims were to determine the effects of a high salt meal on augmentation index (AIx) a measure of arterial stiffness and markers of endothelial function. METHODS AND RESULTS: In a randomised cross-over study 16 healthy normotensive adults consumed a low sodium soup containing 5 mmol Na and a high sodium soup containing 65 mmol Na. Sodium, plasma nitrate/nitrite, endothelin-1 (ET-1), C-reactive protein (CRP), vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations before and every 30 min after the soup for 2 h. Blood pressure (BP) and AI were also measured at these time points. There were significant increases in serum sodium, osmolality and chloride in response to the high sodium meal. However plasma nitrate/nitrite concentrations were not different between meals (meal p = 0.812; time p = 0.45; meal × time interaction p = 0.50). Plasma ANP, AVP and ET-1 were not different between meals. AI was significantly increased following the high sodium meal (p = 0.02) but there was no effect on BP. CONCLUSIONS: A meal containing 65 mmol Na increases serum sodium and arterial stiffness but does not alter postprandial nitrate/nitrite concentration in healthy normotensive individuals. Further research is needed to explore the mechanism by which salt affects vascular function in the postprandial period. This trial was registered with the Australian and New Zealand Clinical Trials Registry Unique Identifier: ACTRN12611000583943http://www.anzctr.org.au/trial_view.aspx?ID=343019

Glucose and lactate turnover in adults with falciparum malaria: effect of complications and antimalarial therapy

Hypoglycaemia and lactic acidosis are potentially life-threatening, poorly understood sequelae of Plasmodium falciparum infections. We investigated relationships between clinical status, treatment, and glucose and lactate kinetics during management of falciparum malaria in 14 Vietnamese adults. Nine had severe malaria, of whom 4 were administered quinine (Group la) and 5 artesunate (Group 1b). Five uncomplicated cases received artesunate (Group 2). Glucose and lactate turnover were studied on 3 occasions: (i) immediately after initial antimalarial treatment, (ii) at parasite clearance a median of 3 days later, and (iii) at discharge from hospital a median of 9 days post-admission. Steady-state glucose and lactate kinetics were derived from plasma isotopic enrichment during a primed-continuous infusion of D-[6,6-D-2] glucose and a parallel infusion of L-[1-C-13]lactate. Group la patients had the lowest plasma glucose concentrations in the admission study (median [range] 3(.)9 [3(.)6-5(.)1] vs 6(.)3 [4-9(.)7-1] and 4(.)5 [4(.)3-5(.)5] mmol/L in Groups 1b and 2 respectively; P 0.17). This was also the case at parasite clearance and suggested an inappropriate beta cell response. Group la patients had the highest admission lactate production (60 [36-77] vs 26 [21-47] and 22 [4-31] mumol/kg.min in Groups lb and 2 respectively; P < 0.05 vs Group 2). Amongst the 9 severe cases, there was an inverse association between plasma glucose and lactate production at admission and parasite clearance (P < 0.05), but no correlation between admission lactate production and serum bicarbonate (P = 0(.)73). The present data confirm previous studies showing that quinine depresses plasma glucose through stimulation of insulin secretion. It is hypothesized that the low plasma glucose activates Na+,K+-ATPase through increased plasma catecholamine concentrations, leading to accelerated glycolysis and increased lactate production in well-oxygenated tissues. In some severely ill patients with falciparum malaria, a raised plasma lactate on its own may, therefore, be an unreliable index of a developing acidosis