Details
| Original language | English |
|---|---|
| Pages (from-to) | H478-H487 |
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 301 |
| Issue number | 2 |
| Early online date | 1 Aug 2011 |
| Publication status | Published - 1 Aug 2011 |
| Externally published | Yes |
Abstract
During incremental exercise, stroke volume (SV) plateaus at 40-50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting ("LV twist mechanics") contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P ≤ 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P ≤ 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting (P ≤ 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.
Keywords
- Diastole, Torsion, Twist, Untwisting
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Physiology
- Medicine(all)
- Cardiology and Cardiovascular Medicine
- Medicine(all)
- Physiology (medical)
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In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 301, No. 2, 01.08.2011, p. H478-H487.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Left ventricular mechanical limitations to stroke volume in healthy humans during incremental exercise
AU - Stöhr, Eric J.
AU - González-Alonso, José
AU - Shave, Rob
PY - 2011/8/1
Y1 - 2011/8/1
N2 - During incremental exercise, stroke volume (SV) plateaus at 40-50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting ("LV twist mechanics") contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P ≤ 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P ≤ 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting (P ≤ 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.
AB - During incremental exercise, stroke volume (SV) plateaus at 40-50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting ("LV twist mechanics") contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P ≤ 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P ≤ 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting (P ≤ 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.
KW - Diastole
KW - Torsion
KW - Twist
KW - Untwisting
UR - http://www.scopus.com/inward/record.url?scp=79961041006&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.00314.2011
DO - 10.1152/ajpheart.00314.2011
M3 - Article
C2 - 21572016
AN - SCOPUS:79961041006
VL - 301
SP - H478-H487
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
SN - 0363-6135
IS - 2
ER -