Stroke volume response during prolonged exercise depends on left ventricularfilling

evidence from a beta-blockade study

Fabio Giuseppe Laginestra, Ole Kristian Berg, Stian Kwak Nyberg, Massimo Venturelli, Eivind Wang, and Jan Helgerud


Prolonged moderate-intensity exercise (>15 min) leads to a progressive upward drift in heart rate (HR) that may compromise stroke volume of the heart (SV). Early studies proposed that this phenomenon was driven by the decrease in central blood volume due to blood pooling in the periphery. However, later studies demonstrated that the increased HR were likely not driven by such responses. Alternatively, the HR drift may be related to reduced SV due to impaired ventricular function. It is unclear whether HR increases to compensate for decreased SV caused by impaired ventricular function or if SV declines because of increased HR.


The aim of this study was to assess the effects of cardiovascular drift on left ventricular volumes and in turn SV during prolonged moderate-intensity exercise. To this aim a novel approach, combining ultrasonography of the heart with conditions of normal cardiovascular drift and prevention of HR drift by a small dose of beta-blockers, was used. By comparing the two conditions, we sought to shed light on how cardiac drift is related to left ventricular function. We hypothesized that left ventricular function would be preserved during continuous moderate-intensity exercise and that changes in SV would be secondary to changes in HR.


Thirteen healthy young males (average age 24 years) completed two 60-min cycling bouts on a cycle ergometer at about 60 % maximal oxygen consumption either under placebo condition or after ingesting a small dose of beta-blockers. HR drift was successfully prevented when using beta-blockers from min 10 to min 60 (average: 128 to 126 beats/min) but not in the placebo group (average: 134 to 148 beats min).


Conclusion: Blocking HR drift enhances SV during prolonged exercise. These findings suggest that SV behavior is tightly related to loading conditions of the left ventricle. The increased HR may be sympathetically driven but not due to impairments in left ventricular function.


Read the full study: https://pubmed.ncbi.nlm.nih.gov/37306400/