IntroductionRecent data from long-distance endurance participants suggest that cardiac function is impaired after completion. Existing data further indicate that right ventricular function is more affected than left ventricular function. The cellular mechanisms underpinning cardiac deterioration are limited and therefore the aim of this study was to examine cardiomyocyte and molecular responses of the right and left ventricle to an acute bout of exhaustive endurance exercise.Materials and methodsMale Sprague-Dawley rats were assigned to sedentary controls or acute exhaustive endurance exercise consisting of a 120 minutes long forced treadmill run. The contractile function and Ca2+ handling properties in isolated cardiomyocytes, protein expression levels of sarcoplasmic reticulum Ca2+-ATPase and phospholamban including two of its phosphorylated states (serine 16 and threonine 17), and the mitochondrial respiration in permeabilized cardiac muscle fibers were analyzed.ResultsThe exercise group showed a significant reduction in cardiomyocyte fractional shortening (right ventricle 1 Hz and 3 Hz p<0.001; left ventricle 1 Hz p<0.05), intracellular Ca2+ amplitude (right ventricle 1 and 3 Hz p<0.001; left ventricle 1 Hz p<0.01 and 3 Hz p<0.05) and rate of diastolic Ca2+ decay (right ventricle 1 Hz p<0.001 and 3 Hz p<0.01; left ventricle 1 and 3 Hz p<0.01). Cardiomyocyte relaxation during diastole was only significantly prolonged at 3 Hz in the right ventricle (p<0.05) compared to sedentary controls. We found an increase in phosphorylation of phospholamban at serine 16 and threonine 17 in the left (p<0.05), but not the right, ventricle from exhaustively exercised animals. The protein expression levels of sarcoplasmic reticulum Ca2+-ATPase and phospholamban was not changed. Furthermore, we found a reduction in maximal oxidative phosphorylation and electron transport system capacities of mitochondrial respiration in the right (p<0.01 and p<0.05, respectively), but not the left ventricle from rats subjected to acute exhaustive treadmill exercise.ConclusionAcute exhaustive treadmill exercise is associated with impairment of cardiomyocyte Ca2+ handling and mitochondrial respiration that causes depression in both contraction and diastolic relaxation of cardiomyocytes.
This study evaluated acute cardiac stress after a high-intensity interval training session in patients with type 2 diabetes (T2D) versus healthy controls. High intensity aerobic exercise was performed by 4 × 4-min intervals (90–95% of maximal heart rate), followed by a ramp protocol to peak oxygen uptake. Echocardiography was performed before and 30 min after exercise. Holter electrocardiography monitored heart rhythms 24 h before, during, and 24 h after the exercise. Left atrial end-systolic volume, peak early diastolic mitral annular velocity, and the ratio of peak early to late diastolic mitral inflow velocity were reduced by approximately 18%, 15%, and 31%, respectively, after exercise across groups. Left ventricular end-diastolic wall thickness was the only echo parameter that significantly differed between groups in response to exercise. The T2D group had a rate of supraventricular extrasystoles per hour that was 265% greater than that of the controls before exercise, which remained higher after exercise. A single exhaustive exercise session impaired left ventricular diastolic function in both groups. The findings also indicated impaired right ventricular function in patients with T2D after exercise.ClinicalTrials.gov Identifier: NCT02998008.
Regular aerobic exercise training has a wide range of beneficial cardiac effects, but recent data also show that acute very strenuous aerobic exercise may impose a transient cardiac exhaustion. The aim of this study was to assess the response to acute high-intensity aerobic exercise on properties of mitochondrial respiration, cardiomyocyte contractile function, Ca2+ handling and transcriptional changes for key proteins facilitating Ca2+ handling and endoplasmic reticulum (ER) stress responses in type 2 diabetic mice. Diabetic mice were assigned to either sedentary control or an acute bout of exercise, consisting of a 10×4 minutes high-intensity interval treadmill run. Mitochondrial respiration, contractile and Ca2+ handling properties of cardiomyocytes were analysed 1 hour after completion of exercise. Gene expression levels of key Ca2+ handling and ER stress response proteins were measured in cardiac tissue samples harvested 1 hour and 24 hours after exercise. We found no significant changes in mitochondrial respiration, cardiomyocyte contractile function or Ca2+ handling 1 hour after the acute exercise. However, gene expression of Atp2a2, Slc8a1 and Ryr2, encoding proteins involved in cardiomyocyte Ca2+ handling, were all significantly upregulated 24 hours after the acute exercise bout. Acute exercise also altered gene expression of several key proteins in ER stress response and unfolded protein response, including Grp94, total Xbp1, Gadd34, and Atf6. The present results show that despite no significant alterations in functional properties of cardiomyocyte function, Ca2+ handling or mitochondrial respiration following one bout of high intensity aerobic exercise training, the expression of genes involved in Ca2+ handling and key components in ER stress and the unfolded protein response were changed. These transcriptional changes may constitute important steps in initiating adaptive remodelling to exercise training in type 2 diabetes.
Purpose. The purpose of this study was to evaluate the acute stress on the heart following one session of high intensity interval training in patients with type 2 diabetes (T2D) versus healthy controls. Methods. High intensity aerobic exercise was performed by 4x4 minutes intervals (90-95% of maximal heart rate), followed by a ramp protocol to peak oxygen uptake (VO2peak). Echocardiography was performed before, and 30 minutes after exercise. Heart rhythm was monitored 24h pre-exercise, during and 24h post exercise by Holter electrocardiogram. Results. After exercise we report a reduction in in both groups in the early diastolic peak mitral annular velocity, the ratio of mitral peak early to late diastolic inflow. Further, left atrial end-systolic volume was reduced after exercise. The LV end-diastolic wall thickness increased in CG. T2D had significant more supraventricular extrasystoles per hour before and after exercise. Conclusion. One single session of exhaustive exercise induced acute cardiac alterations in both left- and right-sided cardiac chambers with reduction in volumes and indices of systolic and diastolic dysfunction in both T2D patients and controls. There was no indication of different stress response in T2D compared to controls. ClinicalTrials.gov Identifier: NCT02998008
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