Improving high-density lipoprotein function by exercise: Does workout intensity matter?

High-density lipoprotein (HDL) particles have a broad spectrum of antiatherogenic properties including efflux of cellular cholesterol, vasodilation, reduction of apoptosis, anti-inflammatory effects and diminishing platelet activation.1 Following a ‘the higher, the better’ view, clinical and scientific concepts strongly focused on the quantity of HDL for a long time. The U-shaped association between HDL concentrations and cardiovascular risk in the CANHEART study and the disappointing results of the Phase III trials of CETP inhibitors changed this view.2,3 Since that time the focus has moved from HDL quantity to HDL quality. Assessment of HDL quality, however, is hampered by several aspects: with regard to the broad spectrum of HDL properties, there is no generally accepted definition of HDL function. Initial approaches to measure HDL function comprised biological tests with a low grade of standardization and high technical challenges and were therefore not applicable to clinical practice. In an attempt to measure a HDL property in an automated, observer-independent manner, novel cell-free assays have been established that, for example, quantify the redox activity of HDL. To date, however, data on interventions that modify HDL function as measured by any of these approaches are rare. Interestingly, there are some anecdotal reports on the effects of exercise on HDL function.4,5 Whereas there are, for example, first comparative data on the effects of aerobic and isometric exercise on HDL function, data on the impact of training intensity are very limited.6,7–8 In the present issue of the European Journal of Preventive Cardiology, Rahmati-Ahmadabad9 investigates the effects of two aerobic exercise programmes on HDL function in a rodent model. HDL function was assessed by measuring the expression of genes of the ATP-binding cassette transporters (ABC family) in heart tissue. The corresponding proteins are main elements of the reverse cholesterol transport, a pathway regulating lipoproteins and HDL biosynthesis. The fact that exercise leads to increased expression of the ABC genes is of great interest and may represent one of the mechanisms by which aerobic exercise exerts its protective atherosclerotic benefits. Upregulation of ABCA1/G1 levels is directly associated with atheroprotective effects in the vessel wall.10 Another interesting aspect of the paper by Rahmati-Ahmadabad9 is the fact that high-intensity interval training was superior to moderate-intensity continuous training in improving proteins determining HDL mediated enzymatic pathways. Increasing exercise intensity led to increasing expression of ABC genes, indicating a dose–response relationship. In human studies a dose–response relationship between the amount of exercise and the cardiovascular benefits has been established as well.11 This association, however, appears to have a ceiling effect (thank God).12,13 If exercise would be a drug, it would be the ideal cardiovascular polypill. It reduces blood pressure, weight and low-density lipoprotein cholesterol and it improves glucose tolerance and endothelial function. The present work of Rahmati-Ahmadabad adds another piece in the puzzle of our understanding of the mechanisms underlying this multifaceted polypill. The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Preventive Cardiology or of the European Society of Cardiology. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article.