Selection of endurance capabilities and the trade-off between pressure and volume in the evolution of the human heart.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
01 10 2019
Historique:
pubmed: 19 9 2019
medline: 9 4 2020
entrez: 19 9 2019
Statut: ppublish

Résumé

Chimpanzees and gorillas, when not inactive, engage primarily in short bursts of resistance physical activity (RPA), such as climbing and fighting, that creates pressure stress on the cardiovascular system. In contrast, to initially hunt and gather and later to farm, it is thought that preindustrial human survival was dependent on lifelong moderate-intensity endurance physical activity (EPA), which creates a cardiovascular volume stress. Although derived musculoskeletal and thermoregulatory adaptations for EPA in humans have been documented, it is unknown if selection acted similarly on the heart. To test this hypothesis, we compared left ventricular (LV) structure and function across semiwild sanctuary chimpanzees, gorillas, and a sample of humans exposed to markedly different physical activity patterns. We show the human LV possesses derived features that help augment cardiac output (CO) thereby enabling EPA. However, the human LV also demonstrates phenotypic plasticity and, hence, variability, across a wide range of habitual physical activity. We show that the human LV's propensity to remodel differentially in response to chronic pressure or volume stimuli associated with intense RPA and EPA as well as physical inactivity represents an evolutionary trade-off with potential implications for contemporary cardiovascular health. Specifically, the human LV trades off pressure adaptations for volume capabilities and converges on a chimpanzee-like phenotype in response to physical inactivity or sustained pressure loading. Consequently, the derived LV and lifelong low blood pressure (BP) appear to be partly sustained by regular moderate-intensity EPA whose decline in postindustrial societies likely contributes to the modern epidemic of hypertensive heart disease.

Identifiants

pubmed: 31527253
pii: 1906902116
doi: 10.1073/pnas.1906902116
pmc: PMC6778238
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

19905-19910

Subventions

Organisme : Medical Research Council
ID : MR/K02325X/1
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2019 the Author(s). Published by PNAS.

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Robert E Shave (RE)

Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Kelowna, BC V1V 1V7, Canada; rob.shave@ubc.ca danlieb@fas.harvard.edu ABAGGISH@mgh.harvard.edu.

Daniel E Lieberman (DE)

Department of Human Evolutionary Biology, Harvard University, Cambridge, MA 02138; rob.shave@ubc.ca danlieb@fas.harvard.edu ABAGGISH@mgh.harvard.edu.

Aimee L Drane (AL)

International Primate Heart Project, Cardiff Metropolitan University, CF23 6XD Cardiff, United Kingdom.

Marcel G Brown (MG)

Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.

Alan M Batterham (AM)

School of Health and Social Care, Teeside University, TS1 3BX Middlesbrough, United Kingdom.

Steven Worthington (S)

Institute for Quantitative Social Science, Harvard University, Cambridge, MA 02138.

Rebeca Atencia (R)

International Primate Heart Project, Cardiff Metropolitan University, CF23 6XD Cardiff, United Kingdom.
Jane Goodall Institute, Tchimpounga Chimpanzee Rehabilitation Centre, Republic of Congo.

Yedra Feltrer (Y)

International Primate Heart Project, Cardiff Metropolitan University, CF23 6XD Cardiff, United Kingdom.

Jennifer Neary (J)

Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.

Rory B Weiner (RB)

Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.

Meagan M Wasfy (MM)

Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.

Aaron L Baggish (AL)

Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; rob.shave@ubc.ca danlieb@fas.harvard.edu ABAGGISH@mgh.harvard.edu.

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