The effects of exercise on LDL

The effects of exercise on LDL
The effects of exercise on LDL

The third guidelines from the of the National Cholesterol Education Program's (NCEP) Adult Treatment Panel (ATP III) have always placed an emphasis on therapeutic lifestyle changes (TLC) as an essential component in the management of cardiovascular disease (CVD) risk.1 In 2004, more aggressive LDL goals where put into place that reinforced TLC as an essential component in reaching lipid levels.2

TLC as proposed includes improved diet, weight reduction, and increased physical activity.1 The somewhat vague NCEP activity recommendation for moderate exercise is based on a 1996 Surgeon General's report3 and calls for 30 minutes or more of exercise at 45%-85% of capacity.1,3

Capacity can be determined by either directly measuring maximal aerobic capacity (VO2) or using heart rate (HR). Because it requires no testing and is a surrogate for VO2, HR may be more convenient for most people.

Either way, total energy expenditure per week should equal 1,000 kilocalories or more (Table 1). Emphasis is placed on aerobic exercise as lipid changes from resistance training have not shown consistent benefits, likely related to the comparatively fewer calories expended.4

Table 1. Energy expenditure of various activities

Activity Kcal/hour
150-lb person
220-lb person
Walking the dog /strolling at 2.5 mph 200 294
Brisk walk at 4 mph 335 490
Lap swimming moderate pace (crawl 50 yards/min) 536
Jogging 5 mph (12-min mile) 536 784
Running 7.5 mph (8-min mile) 838 1,225
Cycling at a leisure pace (<10 mph) 268 392
 Cycling at 15 mph 670 980

Adapted from Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc. 2000;32:S498-504.

Following NCEP advice with the goal of reducing LDL could lead to disappointing results. A 2006 meta-analysis of 49 randomized controlled trials involving 2,990 men showed an overall improvement in lipid profiles, with a 2% decrease in total cholesterol (TC), 3% decrease for LDL, 9% decrease in triglycerides (TG), and an increase of 2% for HDL.5

A 2004 meta-analysis of 1,715 women in 41 randomized controlled trials showed similar effects with 2% reductions in TC, 3% in LDL, 5% TG, with HDL increasing 3%.6 Of course, there are considerable individual variations, and generally those with less favorable lipid profiles benefit the most; studies that included dietary changes had even better outcomes.7 However, the benefits of dietary modification are beyond the scope of this review.

Given the aggressive goals recommended by ATP-III/NCEP, this amount of change in the lipid profile seems almost negligible. Still, even a 1% reduction in LDL is a powerful, as it reduces CVD risk by 2%-3%.1 Similarly, every 1 mg/dL increase in HDL reduces risk of CVD by 2%-3%. Although the absolute changes in the lipid profile may seem disheartening, there is no doubt that regular physical activity is cardioprotective.

There are a number of benefits to maintaining an active lifestyle above and beyond what shows up on a lipid profile. To better understand the beneficial effects of exercise, a short review of lipid metabolism and testing is required.

Lipid metabolism

A standard lipid panel does not directly measure LDL; instead, it is based on the Friedewald formula in which LDL=TC – HDL – very low density lipoprotein (VLDL) – 1/5 TG. Because it is an indirect measurement, the beneficial changes from exercise may be missed. Specifically those changes related to LDL-C particle size and number as well as those changes affecting apolipoproteins.

The primary role of cholesterol molecules is to transport cholesterol esters (CE) and TGs. Cells use CEs for the production and maintenance of cell walls, as well as hormone formation. TGs are used as fuel to meet the immediate energy needs of skeletal muscle or stored in adipose tissue. In a fed state, CEs and TGs are transported from the gut by chylomicrons; while fasting, TGs are packaged in VLDL by the liver.  Whether they enter the circulation directly from the gut or are produced by the liver, CEs contain Apo-B in their outer shell.

Once in circulation the molecules interact with HDL to receive further Apo-lipoproteins (primarily Apo-C 1, 2, and 3, and Apo-E). The addition of Apo-C is necessary as it acts as a cofactor to lipoprotein lipase (LPL). LPL is important in the cellular exchange of TGs and CEs as VLDL and chylomicrons circulate.

As the TG-rich core is depleted, VLDLs become smaller and are reclassified as intermediate density lipoprotein (IDL). Both IDL and chylomicron remnants return to the liver where they are either reabsorbed or, in the case of IDL, converted to LDL. Hepatic lipase (HL) plays a crucial role in this transformation. Unlike chylomicrons and VLDL, LDL contains mostly CE and is relatively low in TG.  In an environment of high TG, LDL take on less CE and more TG making them smaller and more dense.8

Small dense LDL (sdLDL) are thought to have less affinity to LDL receptors in the liver and therefore less likely than their larger counterparts to be cleared from circulation. Furthermore, sdLDL are thought to be more readily oxidized and bind easier to vessel walls, leading to arthrosclerosis.9 Even small changes in LDL particle size have been linked to cardiac disease.9-11 For example, in the Quebec Cardiovascular Study, a peak particle diameter <25.6 nm was associated with a 3.6 times greater risk of heart disease than a peak particle diameter >26.5 nm.12

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