TY - JOUR

T1 - Adaptation of myocardial twist in the remodelled athlete's heart is not related to cardiac output

AU - Cooke, Samuel

AU - Samuel, T. Jake

AU - Cooper, Stephen Mark

AU - Stöhr, Eric J.

N1 - Funding Information: The authors would like to extend their gratitude to James Thie, lecturer in sport coaching and performance in the Cardiff School of Sport & Health Sciences (Sport) (CSS&HS), for his contribution towards participant recruitment. The authors are also grateful to Chris Sandom, William Rees-Jones and James Rigby, undergraduate students in the CSS&HS (Sport), for their effort towards participant recruitment and contribution during data collection. Finally, appreciation is also acknowledged to Dr Phil Assheton, subject librarian at the University of Lincoln, for his additional advice and guidance regarding statistical analyses. We thank the reviewers and editors for excellent suggestions and critical, yet constructive peer-review. The idea of a mitigating effect of exercise on biological age, and therefore on the age-related increase in LV twist, was proposed by reviewer 1, and we think this is an exciting concept that should be evaluated in the future. E.J.S. conceived the experiment. E.J.S. and T.J.S. designed the experiment. E.J.S., T.J.S. and S.C. collected the data. All authors analysed data, drafted the manuscript and critically reviewed it for intellectual content. All authors have read and approved the final version of this manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. The authors have declared that no conflict of interest exist.

PY - 2018/10/31

Y1 - 2018/10/31

N2 - New Findings: What is the central question of this study? What is the role of heart muscle function in the increased output of remodelled, larger hearts? What is the main finding and its importance? The greater stroke volume of endurance athletes is not associated with enhanced function of the heart muscle (i.e. left ventricular twist, torsion and twist-to-shortening) in normal and low-oxygen environments. These data indicate that, in the process of cardiac adaptation, left ventricular twist may play an important role that is not related to generating a larger output. Since enlarged hearts with low output can develop in disease, the present findings may influence the future interpretation of heart muscle function in patients. Abstract: Despite increased stroke volume (SV), ‘athlete's heart’ has been proposed to have a similar left ventricular (LV) muscle function – as represented by LV twist – compared with the untrained state. However, the underpinning mechanisms and the associations between SV/cardiac output and LV twist during exercise are unknown. We hypothesised that endurance athletes would have a significantly lower twist-to-shortening ratio (TwSR, a parameter that relates twist to the shortening of heart muscle layers) at rest, but significantly greater LV muscle function during exercise. Eleven endurance trained male runners and 13 untrained males were tested at rest and during supine cycling exercise in normoxia and hypoxia (increased cardiac output but unaltered SV). Despite the expected cardiac remodelling in endurance athletes, LV twist, torsion, TwSR, strain and strain rate (‘LV systolic mechanics’) did not differ significantly between groups (P > 0.05). Structural remodelling, as per relative wall thickness, and LV twist did not correlate (r2 = 0.04, P = 0.33). In normoxia and hypoxia, exercise increased LV systolic mechanics in both groups (P < 0.001), but with different relationships to SV and cardiac output. Conversely to our hypothesis, hearts of different size had similar LV systolic mechanics, suggesting that similar twist, torsion and TwSR at rest and during exercise irrespective of cardiac output may be an important mechanism in healthy hearts. We hypothesise that the regulatory ‘purpose’ of LV twist may be related to the sensing of maximal cardiac myofibre stress, which may act as a biologically purposeful limiter to contraction.

AB - New Findings: What is the central question of this study? What is the role of heart muscle function in the increased output of remodelled, larger hearts? What is the main finding and its importance? The greater stroke volume of endurance athletes is not associated with enhanced function of the heart muscle (i.e. left ventricular twist, torsion and twist-to-shortening) in normal and low-oxygen environments. These data indicate that, in the process of cardiac adaptation, left ventricular twist may play an important role that is not related to generating a larger output. Since enlarged hearts with low output can develop in disease, the present findings may influence the future interpretation of heart muscle function in patients. Abstract: Despite increased stroke volume (SV), ‘athlete's heart’ has been proposed to have a similar left ventricular (LV) muscle function – as represented by LV twist – compared with the untrained state. However, the underpinning mechanisms and the associations between SV/cardiac output and LV twist during exercise are unknown. We hypothesised that endurance athletes would have a significantly lower twist-to-shortening ratio (TwSR, a parameter that relates twist to the shortening of heart muscle layers) at rest, but significantly greater LV muscle function during exercise. Eleven endurance trained male runners and 13 untrained males were tested at rest and during supine cycling exercise in normoxia and hypoxia (increased cardiac output but unaltered SV). Despite the expected cardiac remodelling in endurance athletes, LV twist, torsion, TwSR, strain and strain rate (‘LV systolic mechanics’) did not differ significantly between groups (P > 0.05). Structural remodelling, as per relative wall thickness, and LV twist did not correlate (r2 = 0.04, P = 0.33). In normoxia and hypoxia, exercise increased LV systolic mechanics in both groups (P < 0.001), but with different relationships to SV and cardiac output. Conversely to our hypothesis, hearts of different size had similar LV systolic mechanics, suggesting that similar twist, torsion and TwSR at rest and during exercise irrespective of cardiac output may be an important mechanism in healthy hearts. We hypothesise that the regulatory ‘purpose’ of LV twist may be related to the sensing of maximal cardiac myofibre stress, which may act as a biologically purposeful limiter to contraction.

KW - contractility

KW - exercise

KW - hypertrophy

KW - LV twist

KW - remodelling

KW - ‘athlete's heart’

UR - http://www.scopus.com/inward/record.url?scp=85054906872&partnerID=8YFLogxK

U2 - 10.1113/ep087165

DO - 10.1113/ep087165

M3 - Article

C2 - 30204274

AN - SCOPUS:85054906872

VL - 103

SP - 1456

EP - 1468

JO - Experimental physiology

JF - Experimental physiology

SN - 0958-0670

IS - 11

ER -