TY - JOUR
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
AU - Kavanagh, Justin
AU - KOERBIN, Gus
AU - Chan, Jonathan
AU - Sabapathy, Surendran
PY - 2015
Y1 - 2015
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.
KW - Cardiac function
KW - Endurance exercise
KW - Hemodynamics
KW - Strain
KW - Torsion
KW - strain
KW - endurance exercise
KW - torsion
KW - cardiac function
KW - hemodynamics
UR - http://www.scopus.com/inward/record.url?scp=84927921170&partnerID=8YFLogxK
UR - http://www.physiology.org/doi/10.1152/ajpheart.00917.2014
UR - http://www.mendeley.com/research/altered-ventricular-mechanics-after-60-min-highintensity-endurance-exercise-insights-exercise-speckl-2
U2 - 10.1152/ajpheart.00917.2014
DO - 10.1152/ajpheart.00917.2014
M3 - Article
SN - 0363-6135
VL - 308
SP - H875-H883
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 8
ER -