Key result
Endurance athletes exhibited reduced untwisting rates (20.3 degrees/s) in response to lower body negative pressure compared to normally active individuals (-16.2 degrees/s; P<0.05).
Why the study?
Does lower body negative pressure alter ventricular twist and untwisting differently in endurance athletes compared to normally active individuals?
Cross-Sectional (n=16)
Does lower body negative pressure alter ventricular twist and untwisting differently in endurance athletes compared to normally active individuals?
Endurance athletes exhibit a decreased untwisting rate during orthostatic stress, which may explain their larger reductions in stroke volume and susceptibility to orthostatic intolerance.
Answers are grounded in this paper and cite their sources.
May explain orthostatic intolerance in athletes; leaves open causal role of untwisting in stroke volume regulation.
Endurance-trained individuals exhibit larger reductions in left ventricular (LV) end-diastolic volume in response to lower body negative pressure (LBNP) compared with normally active individuals. However, the relationship between LV torsion and untwisting and the LV volume response to LBNP in endurance athletes is unknown. Eight endurance-trained athletes [maximal oxygen consumption (VO2max): 66.4+/-7.2 ml.kg(-1).min(-1)] and eight normally active individuals (VO2max: 41.9+/-9.0 ml.kg(-1).min(-1)) (all men) underwent two cardiac magnetic resonance imaging (MRI) assessments, the first during supine rest and the second during -30 mmHg LBNP. Right ventricular (RV) and LV volumes were assessed, myocardial tagging was applied in order to quantify LV peak torsion and peak untwisting rate, and filling rates were measured with phase-contrast MRI. In response to LBNP, endurance-trained individuals had greater reductions in RV and LV end-diastolic volume and stroke volume (P<0.05). Endurance athletes had reduced untwisting rates (20.3+/-8.7 degrees/s), while normally active individuals had increased untwisting rates (-16.2+/-32.1 degrees/s) in response to LBNP (P<0.05). Changes in peak untwisting rate were significantly correlated with change in peak torsion (R=-0.87, P<0.05), with the change in early filling rate and VO2max, but not with changes in end-diastolic or end-systolic volume (P>0.05). We conclude that increased untwisting rates in normally active subjects may mitigate the drop in early filling rate with LBNP and thus may be a compensatory mechanism for the reduction in stroke volume with volume unloading. The opposite response in athletes, who showed a decreased untwisting rate, may contribute to their larger reductions in LV end-diastolic and stroke volumes with volume unloading and their orthostatic intolerance.
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Esch et al. (2010) conducted a cross-sectional in Healthy individuals (endurance athletes and normally active) (n=16). Lower body negative pressure (LBNP) vs. Normally active individuals undergoing LBNP was evaluated on Change in untwisting rate in response to LBNP (p=<0.05). Endurance athletes exhibited reduced untwisting rates (20.3 degrees/s) in response to lower body negative pressure compared to normally active individuals (-16.2 degrees/s; P<0.05).
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