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Galectin-3 increase in endurance athletes.

Robert Hättasch¹, Sebastian Spethmann², Rudolf A de Boer³

¹Charité Campus Mitte, Berlin, Germany.

European Journal of Preventive Cardiology

|June 1, 2013

Summary

This summary is machine-generated.

Plasma galectin-3 levels significantly increase after endurance exercise in athletes but do not correlate with heart function or fibrosis. The elevation in galectin-3 originates mainly from skeletal muscle, not the heart.

Keywords:

Athletes biomarker endurance exercise galectin-3 heart failure

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Area of Science:

Cardiology
Exercise Physiology
Biomarker Research

Background:

Galectin-3 is a promising biomarker for heart failure and myocardial fibrosis.
The impact of endurance exercise on plasma galectin-3 levels and its relation to myocardial fibrosis is not well understood.

Purpose of the Study:

To investigate the relationship between endurance exercise and plasma galectin-3 levels.
To determine if endurance exercise affects myocardial fibrosis or cardiac function in relation to galectin-3.

Main Methods:

Examined 21 male marathon runners before and after a 30km run, measuring plasma galectin-3, echocardiography, and cardiac MRI.
Analyzed galectin-3 mRNA in skeletal muscle and cardiac tissue of mice undergoing voluntary wheel running versus sedentary controls.

Main Results:

Plasma galectin-3 increased significantly post-exercise in athletes (12.8 to 19.9 ng/ml), without changes in cardiac function.
Baseline galectin-3 was higher in athletes than controls, but not correlated with myocardial fibrosis detected by CMR.
Mice studies showed significantly higher galectin-3 mRNA in skeletal muscle (98%) and moderately in the left ventricle (19.9%) after exercise.

Conclusions:

Plasma galectin-3 is substantially elevated post-endurance exercise but is not linked to cardiac function or myocardial fibrosis.
The increase in galectin-3 during endurance exercise primarily originates from skeletal muscle, not the myocardium.