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Updated: Aug 14, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
Effect of weightlifting upon left ventricular function and markers of cardiomyocyte damage
Claire Stephenson1, Jenny McCarthy, Elias Vikelis
1Research Institute for Sport and Exercise Sciences, Henry Cotton Campus, Liverpool John Moores University, Liverpool L3 2ET, UK. spscstep@livjm.ac.uk
Abstract:
The purpose of this study was to assess left ventricular (LV) function and biochemical markers of myocyte after prolonged weightlifting activity. Seventeen male subjects (age range 20-34 years) performed a 90-min bout of weightlifting exercise consisting of three sets of 8-10 repetitions at 70% one-repetition maximum. Body mass, heart rate, systolic blood pressure (SBP) and echocardiographically determined indices of LV loading (LV internal diameter during diastole, LV meridonial wall stress), systolic function (stroke volume (SV), ejection fraction (EF), end-systolic pressure volume relationship; SBP/ESV) and diastolic filling (ratio of early to late; E:A) were obtained pre-exercise, immediately after and 24 h post-exercise. A 5-ml venous blood sample was obtained for the assessment of cardiac troponin T (cTnT) via third generation electrochemiluminescence assay. Data were assessed via one-way ANOVA and Pearson's correlation. Although SV declined (80.9 +/- 18.3 vs. 66.9 +/- 17.2, p < 0.05) there was no alteration in LV contractility (EF 62 +/- 6 vs. 59 +/- 7; SBP/ESV 3.51 +/- 1.4 vs. 3.51 +/- 1.4, p > 0.05). The E:A ratio was significantly decreased following exercise (1.78 +/- 0.41 vs. 1.33 +/- 0.37, p < 0.05). This decrease was not fully explained by loading conditions (r2 = 0.05 to 0.24). All values returned to baseline 24 h post-exercise. No cTnT was reported in any of the blood samples. In conclusion, there was no significant evidence of any LV contractile depression and no cTnT was observed post exercise. The small reduction in diastolic filling could not be explained by changes in haemodynamic loading or the post-exercise elevation in heart rate.
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