Apolipoprotein E polymorphism and the relationships of physical fitness to plasma lipoprotein-lipid levels in men and women. Med. Sci. Sports Exerc., Vol. 31, No. 5, pp. 692-697, 1999.
Purpose: A high level of cardiovascular fitness is generally associated with a plasma lipoprotein-lipid profile predictive of a low cardiovascular disease risk. We have investigated whether apolipoprotein (apo) E polymorphism could alter the relationships of physical fitness to plasma lipoprotein-lipid levels in a sample of healthy untrained subjects (64 premenopausal women and 65 men).
Methods: Subjects were grouped according to gender and apo E phenotype determined by isoelectric focusing electrophoresis.
Results: In both genders, V̇O2max expressed in mL·kg−1·min−1 was negatively correlated with plasma triglyceride levels in apo E2 carriers and apo E3 homozygotes (−0.55 ≤ r ≤ − 0.31; P < 0.05), whereas these associations were not found in apo E4 groups. Plasma low-density lipoprotein (LDL)-C levels were negatively associated with V̇O2max (r = −0.39; P < 0.05) only in women homozygotes for apo E3 whereas V̇O2max was positively correlated with plasma high-density lipoprotein (HDL)2-C levels only in men (r = 0.51; P < 0.001) and women (r = 0.65; P < 0.001) who were apo E3 homozygotes. A control for concomitant association with body fat mass and glucose intolerance performed by partial correlation analyses revealed that, with the exception of the plasma HDL2-C levels in the apo E3 homozygotes, most of the significant associations between V̇O2max (mL·kg−1·min−1) and plasma lipoprotein-lipid levels were mediated by concomitant variation in body fatness and glucose tolerance.
Conclusions: These results suggest that the magnitude of the relationships between V̇O2max and plasma lipoprotein-lipid levels is influenced by the apo E polymorphism. Thus, apo E2 carriers may be particularly responsive to improved fitness, thereby preventing the development of hypertriglyceridemia and type III dyslipoproteinemia.
Lipid Research Center, Physical Activity Sciences Laboratory, and Diabetes Research Unit, Laval University, Québec, CANADA
Submitted for publication June 1997.
Accepted for publication October 1998.
The authors express their gratitude to the subjects for their excellent collaboration and to the staff of the Physical Activity Sciences Laboratory, the Lipid Research Center, and the Diabetes Research Unit for their dedicated work.
This work was supported by the Québec Heart and Stroke Foundation and by the Medical Research Council of Canada. J. St.-Amand is a FCAR and Promutuel-vie fellow.
Sital Moorjani is deceased.
Address correspondence to: Jean-Pierre Després, Ph.D., Director, Lipid Research Center, Laval University Medical Research Center, CHUL, 2705 Blvd Laurier, Ste-Foy, Québec, Canada G1V 4G2. E-mail: Jean-Pierre.Despres@crchul.ulaval.ca.