Exercise intolerance and impaired aerobic capacity in heart transplant recipients.
- 1School of Exercise and Nutritional Sciences, San Diego State University, San Diego, California, USA.
- 2Respiratory Research Center, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California, USA.
- 3Division of Respiratory and Critical Care Medicine, Department of Medicine, Harbor-UCLA Medical Center, Torrance, California, USA.
Abstract
Heart transplant recipients exhibit reduced exercise tolerance and persistently diminished aerobic capacity despite exercise training. Exercise tolerance depends on integrated oxygen transport and utilization, which are impaired in heart transplant recipients. We synthesize evidence supporting that the combined effects of impaired pulmonary gas exchange, reduced haemoglobin concentration, heart denervation, chronic calcineurin inhibition, decreased muscle capillary density, and detraining from limited physical activity contribute to: (1) reduced pulmonary diffusion and alveolar ventilation-perfusion mismatch that contribute to hypoxemia and increased ventilatory demand; (2) impaired convective oxygen delivery due to anaemia and to heart denervation that limits cardiac output; (3) deficits in endothelial function and reduced muscle capillarization that contribute to diminished convective and diffusive oxygen transport within skeletal muscle. Using Wagner's model, which describes oxygen transport from the atmosphere to muscle mitochondrion, we develop the hypothesis that the persistent reduction in aerobic capacity in heart transplant recipients reflects the combined and interactive effects of impaired convective oxygen transport and reduced muscle oxygen diffusive capacity, rather than a single dominant limitation. This basis generates testable physiological targets for interventions aimed at improving functional capacity after transplantation.
Related
- Impaired Erythropoietin Production in Liver Transplant Recipients: the Role of Calcineurin Inhibitors
- Cluster-Based Phenotyping in an HFpEF Population Identifies a Biomarker-High, Atrial-Dysfunction Phenotype with Impaired Quality of Life, Reduced Exercise Capacity and Higher Healthcare Utilization
- Configurational patterns associated with relatively higher recent home-based exercise behavior among lung transplant recipients: a fuzzy-set qualitative comparative analysis.
- Application effect of an evidence-based early functional exercise program in kidney transplant recipients
- Exercise training in kidney transplant recipients (EXTRA Trial): protocol for a randomized controlled trial
BibTeX
@article{kolkhorst2026exercise,
title = {{Exercise intolerance and impaired aerobic capacity in heart transplant recipients.}},
author = {Fred W Kolkhorst and Daniel T Cannon and Harry B Rossiter},
journal = {Experimental physiology},
year = {2026},
month = oct,
doi = {10.1113/ep093964},
url = {https://europepmc.org/article/MED/42852708},
note = {CC BY},
}
RIS
TY - JOUR
TI - Exercise intolerance and impaired aerobic capacity in heart transplant recipients.
AU - Fred W Kolkhorst
AU - Daniel T Cannon
AU - Harry B Rossiter
PY - 2026
DA - 2026/10/09
JO - Experimental physiology
DO - 10.1113/ep093964
UR - https://europepmc.org/article/MED/42852708
AB - Heart transplant recipients exhibit reduced exercise tolerance and persistently diminished aerobic capacity despite exercise training. Exercise tolerance depends on integrated oxygen transport and utilization, which are impaired in heart transplant recipients. We synthesize evidence supporting that the combined effects of impaired pulmonary gas exchange, reduced haemoglobin concentration, heart denervation, chronic calcineurin inhibition, decreased muscle capillary density, and detraining from limited physical activity contribute to: (1) reduced pulmonary diffusion and alveolar ventilation-perfusion mismatch that contribute to hypoxemia and increased ventilatory demand; (2) impaired convective oxygen delivery due to anaemia and to heart denervation that limits cardiac output; (3) deficits in endothelial function and reduced muscle capillarization that contribute to diminished convective and diffusive oxygen transport within skeletal muscle. Using Wagner's model, which describes oxygen transport from the atmosphere to muscle mitochondrion, we develop the hypothesis that the persistent reduction in aerobic capacity in heart transplant recipients reflects the combined and interactive effects of impaired convective oxygen transport and reduced muscle oxygen diffusive capacity, rather than a single dominant limitation. This basis generates testable physiological targets for interventions aimed at improving functional capacity after transplantation.
SN - 0958-0670
SN - 1469-445X
ER -