Physical Activity and Plasma Lipids and Lipoproteins
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Epidemiological and clinical studies have suggested that physically active subjects have lower serum cholesterol and triglyceride concentration than individuals with sedentary lifestyle. Furthermore, the serum concentration of high density lipoprotein (HDL) cholesterol is increased in subjects with very high physical activity (Wood et al., 1976). A decrease in serum triglycerides and an increase in HDL has been demonstrated also during training programs consisting of mild to moderate exercise (Huttunen et al., 1979). The mechanism of the exercise-induced changes in serum lipids is not clear. The alterations are not due solely to weight reduction, although this factor contributes to the favourable development in some individuals. One explanation for the reciprocal changes in serum triglycerides and HDL cholesterol is the activation of the lipoprotein lipase, the enzyme responsible for catabolism of serum triglycerides. Thus, negative correlations are present between serum triglyceride concentration and the activities of postheparin plasma and adipose tissue lipoprotein lipase, whereas a positive relationship has been reported between HDL cholesterol level and the activity of adipose tissue lipase (Nikkilä et al., 1978). Furthermore, physical exercise increases the activity of lipoprotein lipase in the skeletal muscle and in the adipose tissue (Nikkilä et al., 1978). Chronic training may also lead to decreased production of very low density lipoproteins (VLDL) (Robinson et al., 1974) and to activation of the enzyme lecithin-cholesterol acyltransferase (LCAT) involved in the transfer of unesterified cholesterol from cells to nascent HDL (Lopez-S. et al., 1974). In summary, there is good evidence that regular physical activity lowers the concentration of plasma VLDL triglycerides and raises the concentration of plasma HDL cholesterol in man. Further studies are, however, needed to prove that these changes result in worthwhile reduction of atherosclerotic disease.
Farahati S, Attarzadeh Hosseini S, Moazzami M, Daloee M, Daloee S Int J Prev Med. 2020; 11:62.
PMID: 32577192 PMC: 7297415. DOI: 10.4103/ijpvm.IJPVM_524_18.
Ding M, Zeleznik O, Guasch-Ferre M, Hu J, Lasky-Su J, Lee I Am J Epidemiol. 2019; 188(11):1932-1943.
PMID: 31364705 PMC: 6825824. DOI: 10.1093/aje/kwz171.
Amagasa S, Machida M, Fukushima N, Kikuchi H, Takamiya T, Odagiri Y Int J Behav Nutr Phys Act. 2018; 15(1):65.
PMID: 29986718 PMC: 6038338. DOI: 10.1186/s12966-018-0695-z.
Raymond L, Strasser T, Oberhaensli I, POMETTA D, JEANNERET O Soz Praventivmed. 1984; 29(4-5):218-9.
PMID: 6485576 DOI: 10.1007/BF02075885.