Objectives To study the effect of exercise and a high fat meal (HFM) on endothelial function. Background Postprandial lipemia and exercise oppose each other in terms of cardiovascular risk, however the mechanism of their interaction is not well understood. Methods Endothelial function was assessed by brachial artery flow mediated dilation (FMD), in eight healthy men before and after a HFM preceded (16–18 hrs) by rest, a single bout of continuous moderate intensity exercise (CME), and high intensity interval exercise (HIIE). Results Before the HFM, initial brachial artery diameters were similar in all trials (0.43±0.04 cm), but after the HFM basal diameter decreased only in the control (0.39±0.03) and CME (0.38±0.04) trials. Prior to the HFM, FMD/shear was improved by a single bout of CME (+20%, p<0.01) and HIIE (+45%, p<0.01, group differences, p<0.01), with no effect in the control trial. After the HFM (30, 120, and 240 mins), FMD decayed to a lesser extent with CME, but in a similar fashion to the control trial. In contrast FMD in the HIIE trial remained elevated following the exercise despite a clear meal-induced lipemia. Although, there were no correlations between vascular function and food-induced markers of cardiovascular risk, antioxidant status was strongly correlated with FMD (r=0.9, p<0.001). Conclusion These findings reveal a clinically relevant protective effect of acute exercise upon the vasculature that is clearly exercise intensity dependent and tightly related to exercise-induced antioxidant capacity.

Graft flow is highly dependent on the degree of competitive flow. High competitive flow was found to produce unfavourable WSS consistent with endothelial dysfunction and subsequent graft narrowing and failure. Partial competitive flow, however, may be better tolerated as it was found to be similar to the ideal condition of no competitive flow.

Improving reduced skeletal muscle function is important for optimising exercise tolerance and quality of life in chronic obstructive pulmonary disease (COPD) patients. By applying high-intensity training to a small muscle group, we hypothesised a normalisation of muscle function.Seven patients with COPD performed 6 weeks (3 days?week -1 ) of high-intensity interval aerobic knee extensor exercise training. Five age-matched healthy individuals served as a reference group. Muscle oxygen uptake and mitochondrial respiration of the vastus lateralis muscle were measured before and after the 6-week training programme. Initial peak work and maximal mitochondrial respiration were reduced in COPD patients and improved significantly after the training programme. Peak power and maximal mitochondrial respiration in vastus lateralis muscle increased to the level of the control subjects and were mainly mediated via improved complex I respiration. Furthermore, when normalised to citrate synthase activity, no difference in maximal respiration was found either after the intervention or compared to controls, suggesting normal functioning mitochondrial complexes.The present study shows that high-intensity training of a restricted muscle group is highly effective in restoring skeletal muscle function in COPD patients.

Significantly more HSP70 was released into the circulation following conventional than following off-pump CABG. Circulating HSP70 may indicate cellular stress or damage. Furthermore, HSPs are suggested as immunoregulatory agents, and may be important in the host defence postoperatively.

Correct positioning of the venous cannula draining blood to the cardiopulmonary bypass circuit is important. Intraoperative transesophageal echocardiography allows satisfactory determination of the cannula position in nearly all patients. Ten percent of venous cannulae are primarily positioned in the right hepatic vein and not in the inferior vena cava as intended.

Patients with CABG exhibit a marked desaturation during early postoperative mobilization. Preoperative ejection fraction did not affect S(v)O(2) during exercise. The clinical consequences and underlying mechanism require further investigation.

AimsCellular processes in the heart rely mainly on studies from experimental animal models or explanted hearts from patients with terminal end‐stage heart failure (HF). To address this limitation, we provide data on excitation contraction coupling, cardiomyocyte contraction and relaxation, and Ca2+ handling in post‐myocardial‐infarction (MI) patients at mid‐stage of HF.Methods and resultsNine MI patients and eight control patients without MI (non‐MI) were included. Biopsies were taken from the left ventricular myocardium and processed for further measurements with epifluorescence and confocal microscopy. Cardiomyocyte function was progressively impaired in MI cardiomyocytes compared with non‐MI cardiomyocytes when increasing electrical stimulation towards frequencies that simulate heart rates during physical activity (2 Hz); at 3 Hz, we observed almost total breakdown of function in MI. Concurrently, we observed impaired Ca2+ handling with more spontaneous Ca2+ release events, increased diastolic Ca2+, lower Ca2+ amplitude, and prolonged time to diastolic Ca2+ removal in MI (P < 0.01). Significantly reduced transverse‐tubule density (−35%, P < 0.01) and sarcoplasmic reticulum Ca2+ adenosine triphosphatase 2a (SERCA2a) function (−26%, P < 0.01) in MI cardiomyocytes may explain the findings. Reduced protein phosphorylation of phospholamban (PLB) serine‐16 and threonine‐17 in MI provides further mechanisms to the reduced function.ConclusionsDepressed cardiomyocyte contraction and relaxation were associated with impaired intracellular Ca2+ handling due to impaired SERCA2a activity caused by a combination of alteration in the PLB/SERCA2a ratio and chronic dephosphorylation of PLB as well as loss of transverse tubules, which disrupts normal intracellular Ca2+ homeostasis and handling. This is the first study that presents these mechanisms from viable and intact cardiomyocytes isolated from the left ventricle of human hearts at mid‐stage of post‐MI HF.

Early mobilization after cardiac surgery induces a marked reduction in mixed venous oxygen saturation (Svo2). Using pulmonary artery catheters and indirect calorimetry, we investigated the effects of exercise and postural change on cardiac index (CI) and Svo2 before and on the first morning after coronary artery bypass surgery. Sixteen patients with an ejection fraction >0.50 were studied at rest, during supine bicycle exercise, and during passive standing. Supine cycling at 30 W increased CI by 1.5 +/- 0.8 L x min(-1) x m(-2) before and 0.9 +/- 0.7 L x min(-1) x m(-2) after surgery (P < 0.05), whereas Svo2 was reduced from 80% +/- 4% at rest to 63 +/- 6% preoperatively (P < 0.05) and from 71% +/- 5% to 46% +/- 11% postoperatively (P < 0.05). Passive standing reduced CI by 0.8 +/- 0.5 L x min(-1) x m(-2) before and 0.3 +/- 0.4 L x min(-1) x m(-2) after surgery (P < 0.05). Svo2 was reduced from 79% +/- 5% to 64% +/- 7% preoperatively (P < 0.05) and from 72% +/- 6% to 60% +/- 6% postoperatively (P < 0.05). The exercise challenge revealed an altered cardiovascular response after surgery, causing a larger reduction in Svo2 for the same workload. Passive standing significantly reduced Svo2 both days, but this effect was less pronounced after surgery. The response to postural change and exercise was altered after surgery and may both contribute to the reduction in Svo2 during postoperative mobilization.