Altered ventricular mechanics after 60 min of high-intensity endurance exercise

Insights from exercise speckle-tracking echocardiography

Glenn Stewart, Akira Yamada, Luke Haseler, Justin Kavanagh, Gus KOERBIN, Jonathan Chan, Surendran Sabapathy

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported after prolonged exercise (>180 min). However, it is unknown if 1) shorter-duration exercise (60 min) can perturb cardiac function or 2) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left ventricular (LV) and right ventricular global longitudinal strain (GLS), LV torsion, and high-sensitivity cardiac troponin T were measured in 15 competitive cyclists (age: 28 ± 3 yr, peak O2 uptake: 4.8 ± 0.6 l/min) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60), strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96 ± 8 W) in a semirecumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60(mean arterial pressure: 96 ± 1 vs. 86 ± 2 mmHg, P <0.001), and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge, hemodynamic conditions were unchanged from pre- to post-CRIT60 (mean arterial pressure: 98 ± 1 vs. 97 ± 1 mmHg, not significant), but strain decreased (left ventricular GLS: -20.3 ± 0.5% vs. -18.5 ± 0.4%, P <0.01; right ventricular GLS: -26.4 ± 1.6% vs. -22.4 ± 1.5%, P <0.05), whereas LV torsion remained unchanged. Serum high-sensitivity cardiac troponin T increased by 345% after the CRIT60 (6.0 ± 0.6 vs. 20.7 ± 6.9 ng/l, P <0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultraendurance sporting events and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study.
Original languageEnglish
Pages (from-to)H875-H883
Number of pages9
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume308
Issue number8
DOIs
Publication statusPublished - 2015

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Mechanics
Echocardiography
Exercise
Troponin T
Hemodynamics
Arterial Pressure
Athletes
Biomarkers
Serum

Cite this

Stewart, Glenn ; Yamada, Akira ; Haseler, Luke ; Kavanagh, Justin ; KOERBIN, Gus ; Chan, Jonathan ; Sabapathy, Surendran. / Altered ventricular mechanics after 60 min of high-intensity endurance exercise : Insights from exercise speckle-tracking echocardiography. In: American Journal of Physiology - Heart and Circulatory Physiology. 2015 ; Vol. 308, No. 8. pp. H875-H883.
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Altered ventricular mechanics after 60 min of high-intensity endurance exercise : Insights from exercise speckle-tracking echocardiography. / Stewart, Glenn; Yamada, Akira; Haseler, Luke; Kavanagh, Justin; KOERBIN, Gus; Chan, Jonathan; Sabapathy, Surendran.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 308, No. 8, 2015, p. H875-H883.

Research output: Contribution to journalArticle

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T1 - Altered ventricular mechanics after 60 min of high-intensity endurance exercise

T2 - Insights from exercise speckle-tracking echocardiography

AU - Stewart, Glenn

AU - Yamada, Akira

AU - Haseler, Luke

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AU - KOERBIN, Gus

AU - Chan, Jonathan

AU - Sabapathy, Surendran

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N2 - Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported after prolonged exercise (>180 min). However, it is unknown if 1) shorter-duration exercise (60 min) can perturb cardiac function or 2) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left ventricular (LV) and right ventricular global longitudinal strain (GLS), LV torsion, and high-sensitivity cardiac troponin T were measured in 15 competitive cyclists (age: 28 ± 3 yr, peak O2 uptake: 4.8 ± 0.6 l/min) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60), strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96 ± 8 W) in a semirecumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60(mean arterial pressure: 96 ± 1 vs. 86 ± 2 mmHg, P <0.001), and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge, hemodynamic conditions were unchanged from pre- to post-CRIT60 (mean arterial pressure: 98 ± 1 vs. 97 ± 1 mmHg, not significant), but strain decreased (left ventricular GLS: -20.3 ± 0.5% vs. -18.5 ± 0.4%, P <0.01; right ventricular GLS: -26.4 ± 1.6% vs. -22.4 ± 1.5%, P <0.05), whereas LV torsion remained unchanged. Serum high-sensitivity cardiac troponin T increased by 345% after the CRIT60 (6.0 ± 0.6 vs. 20.7 ± 6.9 ng/l, P <0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultraendurance sporting events and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study.

AB - Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported after prolonged exercise (>180 min). However, it is unknown if 1) shorter-duration exercise (60 min) can perturb cardiac function or 2) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left ventricular (LV) and right ventricular global longitudinal strain (GLS), LV torsion, and high-sensitivity cardiac troponin T were measured in 15 competitive cyclists (age: 28 ± 3 yr, peak O2 uptake: 4.8 ± 0.6 l/min) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60), strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96 ± 8 W) in a semirecumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60(mean arterial pressure: 96 ± 1 vs. 86 ± 2 mmHg, P <0.001), and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge, hemodynamic conditions were unchanged from pre- to post-CRIT60 (mean arterial pressure: 98 ± 1 vs. 97 ± 1 mmHg, not significant), but strain decreased (left ventricular GLS: -20.3 ± 0.5% vs. -18.5 ± 0.4%, P <0.01; right ventricular GLS: -26.4 ± 1.6% vs. -22.4 ± 1.5%, P <0.05), whereas LV torsion remained unchanged. Serum high-sensitivity cardiac troponin T increased by 345% after the CRIT60 (6.0 ± 0.6 vs. 20.7 ± 6.9 ng/l, P <0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultraendurance sporting events and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study.

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