Details
| Original language | English |
|---|---|
| Pages (from-to) | 507-518 |
| Number of pages | 12 |
| Journal | Experimental physiology |
| Volume | 100 |
| Issue number | 5 |
| Early online date | 12 Mar 2015 |
| Publication status | Published - 1 May 2015 |
| Externally published | Yes |
Abstract
New Findings: What is the central question of this study? Regulation of cardiac function is typically achieved by changes in heart rate (HR) and cardiac shortening velocity (strain rate; SR), but their interdependence in vivo remains poorly understood. What is the main finding and its importance? Using resistance exercise to increase heart rate and arterial resistance physiologically in humans and measuring regional cardiac SR (at the base and apex), we found that HR and SR were not strictly coupled because SR at the base and apex responded differently, despite the same HR. Importantly, our data show that the region-averaged 'longitudinal' SR, which is currently popular in the clinical setting, markedly underestimates the contribution of the apex. The fundamental importance of cardiac shortening and lengthening velocity (i.e. strain rate; SR) has been demonstrated in vitro. Currently, the interdependence between in vivo SR and HR is poorly understood because studies have typically assessed region-averaged 'longitudinal' strain rate, which is likely to underestimate the apical contribution, and have used non-physiological interventions that may also have been influenced by multicollinearity caused by concomitant reductions in arterial resistance. Resistance exercise acutely raises HR, blood pressure and arterial resistance and transiently disassociates these cardiovascular factors following exercise. Therefore, we measured SR, HR, blood pressure and arterial resistance in nine healthy men (aged 20 ± 1 years) immediately before, during and after double-leg-press exercise at 30 and 60% of maximal strength. Resistance exercise caused a disproportionate SR response at the left ventricular base and apex (interaction effect, P < 0.05). Consequently, associations between HR and regional peak SR were inconsistent and mostly very weak (r2 = 0.0004-0.24). Likewise, the areas under the curve for systolic and diastolic SR and their relationship with systolic and diastolic duration were variable and weak. Importantly, region-averaged 'longitudinal' SR was identical to basal SR, thus, markedly underestimating the apical contribution. In conclusion, in vivo HR and SR are not strictly coupled in healthy humans, which is explained by the region-specific responses of SR that are not captured by 'longitudinal SR'. This novel observation emphasizes the independent role of in vivo SR in overall cardiac function during stress and may cause a 'revival' of SR as a marker of regional left ventricular (dys)function.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Physiology
- Nursing(all)
- Nutrition and Dietetics
- Medicine(all)
- Physiology (medical)
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In: Experimental physiology, Vol. 100, No. 5, 01.05.2015, p. 507-518.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - In vivo human cardiac shortening and lengthening velocity is region dependent and not coupled with heart rate
T2 - 'longitudinal' strain rate markedly underestimates apical contribution
AU - Stöhr, Eric J.
AU - Stembridge, Mike
AU - Esformes, Joseph I.
PY - 2015/5/1
Y1 - 2015/5/1
N2 - New Findings: What is the central question of this study? Regulation of cardiac function is typically achieved by changes in heart rate (HR) and cardiac shortening velocity (strain rate; SR), but their interdependence in vivo remains poorly understood. What is the main finding and its importance? Using resistance exercise to increase heart rate and arterial resistance physiologically in humans and measuring regional cardiac SR (at the base and apex), we found that HR and SR were not strictly coupled because SR at the base and apex responded differently, despite the same HR. Importantly, our data show that the region-averaged 'longitudinal' SR, which is currently popular in the clinical setting, markedly underestimates the contribution of the apex. The fundamental importance of cardiac shortening and lengthening velocity (i.e. strain rate; SR) has been demonstrated in vitro. Currently, the interdependence between in vivo SR and HR is poorly understood because studies have typically assessed region-averaged 'longitudinal' strain rate, which is likely to underestimate the apical contribution, and have used non-physiological interventions that may also have been influenced by multicollinearity caused by concomitant reductions in arterial resistance. Resistance exercise acutely raises HR, blood pressure and arterial resistance and transiently disassociates these cardiovascular factors following exercise. Therefore, we measured SR, HR, blood pressure and arterial resistance in nine healthy men (aged 20 ± 1 years) immediately before, during and after double-leg-press exercise at 30 and 60% of maximal strength. Resistance exercise caused a disproportionate SR response at the left ventricular base and apex (interaction effect, P < 0.05). Consequently, associations between HR and regional peak SR were inconsistent and mostly very weak (r2 = 0.0004-0.24). Likewise, the areas under the curve for systolic and diastolic SR and their relationship with systolic and diastolic duration were variable and weak. Importantly, region-averaged 'longitudinal' SR was identical to basal SR, thus, markedly underestimating the apical contribution. In conclusion, in vivo HR and SR are not strictly coupled in healthy humans, which is explained by the region-specific responses of SR that are not captured by 'longitudinal SR'. This novel observation emphasizes the independent role of in vivo SR in overall cardiac function during stress and may cause a 'revival' of SR as a marker of regional left ventricular (dys)function.
AB - New Findings: What is the central question of this study? Regulation of cardiac function is typically achieved by changes in heart rate (HR) and cardiac shortening velocity (strain rate; SR), but their interdependence in vivo remains poorly understood. What is the main finding and its importance? Using resistance exercise to increase heart rate and arterial resistance physiologically in humans and measuring regional cardiac SR (at the base and apex), we found that HR and SR were not strictly coupled because SR at the base and apex responded differently, despite the same HR. Importantly, our data show that the region-averaged 'longitudinal' SR, which is currently popular in the clinical setting, markedly underestimates the contribution of the apex. The fundamental importance of cardiac shortening and lengthening velocity (i.e. strain rate; SR) has been demonstrated in vitro. Currently, the interdependence between in vivo SR and HR is poorly understood because studies have typically assessed region-averaged 'longitudinal' strain rate, which is likely to underestimate the apical contribution, and have used non-physiological interventions that may also have been influenced by multicollinearity caused by concomitant reductions in arterial resistance. Resistance exercise acutely raises HR, blood pressure and arterial resistance and transiently disassociates these cardiovascular factors following exercise. Therefore, we measured SR, HR, blood pressure and arterial resistance in nine healthy men (aged 20 ± 1 years) immediately before, during and after double-leg-press exercise at 30 and 60% of maximal strength. Resistance exercise caused a disproportionate SR response at the left ventricular base and apex (interaction effect, P < 0.05). Consequently, associations between HR and regional peak SR were inconsistent and mostly very weak (r2 = 0.0004-0.24). Likewise, the areas under the curve for systolic and diastolic SR and their relationship with systolic and diastolic duration were variable and weak. Importantly, region-averaged 'longitudinal' SR was identical to basal SR, thus, markedly underestimating the apical contribution. In conclusion, in vivo HR and SR are not strictly coupled in healthy humans, which is explained by the region-specific responses of SR that are not captured by 'longitudinal SR'. This novel observation emphasizes the independent role of in vivo SR in overall cardiac function during stress and may cause a 'revival' of SR as a marker of regional left ventricular (dys)function.
UR - http://www.scopus.com/inward/record.url?scp=84929657946&partnerID=8YFLogxK
U2 - 10.1113/EP085081
DO - 10.1113/EP085081
M3 - Article
C2 - 25772470
AN - SCOPUS:84929657946
VL - 100
SP - 507
EP - 518
JO - Experimental physiology
JF - Experimental physiology
SN - 0958-0670
IS - 5
ER -