Exercise and weight loss effects on cardiovascular risk factors in overweight men
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Exercise and weight loss effects on cardiovascular risk factors in overweight men. / Rosenkilde, Mads; Rygaard, Lisbeth; Nordby, Pernille; Nielsen, Lars Bo; Stallknecht, Bente.
In: Journal of Applied Physiology, Vol. 125, No. 3, 01.09.2018, p. 901–908.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Exercise and weight loss effects on cardiovascular risk factors in overweight men
AU - Rosenkilde, Mads
AU - Rygaard, Lisbeth
AU - Nordby, Pernille
AU - Nielsen, Lars Bo
AU - Stallknecht, Bente
PY - 2018/9/1
Y1 - 2018/9/1
N2 - Exercise training and weight loss both reduce cardiovascular risk, but the independent importance of the two strategies is unclear. We aimed to investigate independent and combined effects of exercise training and weight loss on lipoproteins and dyslipidemia in overweight sedentary men. Sixty individuals were randomized to 12 weeks of endurance training (T), energy-reduced diet (D), training and energy increased diet (T-iD), or control (C). Equal energetic deficits (-600 kcal/day) were prescribed by exercise for T and caloric restriction for D. T-iD completed similar exercise but remained in energy balance due to the dietary replacement of calories expended during exercise. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein B and A1, preβ-HDL, and susceptibility of LDL-C to oxidation were measured. Body weight was reduced similarly between T (-5.9{plus minus}0.7 kg) and D (-5.2{plus minus}0.8 kg) while T-iD (-1.0{plus minus}0.5 kg) and C (0.1{plus minus}0.6 kg) remained weight stable. Plasma TC, LDL-C, and apolipoprotein B were reduced in T compared to C (P<0.001 for both), but this was not observed for D (P>0.17). Changes in TC and LDL-C were associated with changes in body weight and body fat (P<0.01). In T-iD, increases in HDL-C and apolipoprotein A1 were observed (P<0.001). In conclusion, an exercise-induced decline in body weight reduces pro-atherogenic apoB-containing lipoproteins, whereas exercise compensated by energy intake increases the key component of reverse cholesterol transport, i.e. ApoA1-containing HDL-C.
AB - Exercise training and weight loss both reduce cardiovascular risk, but the independent importance of the two strategies is unclear. We aimed to investigate independent and combined effects of exercise training and weight loss on lipoproteins and dyslipidemia in overweight sedentary men. Sixty individuals were randomized to 12 weeks of endurance training (T), energy-reduced diet (D), training and energy increased diet (T-iD), or control (C). Equal energetic deficits (-600 kcal/day) were prescribed by exercise for T and caloric restriction for D. T-iD completed similar exercise but remained in energy balance due to the dietary replacement of calories expended during exercise. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein B and A1, preβ-HDL, and susceptibility of LDL-C to oxidation were measured. Body weight was reduced similarly between T (-5.9{plus minus}0.7 kg) and D (-5.2{plus minus}0.8 kg) while T-iD (-1.0{plus minus}0.5 kg) and C (0.1{plus minus}0.6 kg) remained weight stable. Plasma TC, LDL-C, and apolipoprotein B were reduced in T compared to C (P<0.001 for both), but this was not observed for D (P>0.17). Changes in TC and LDL-C were associated with changes in body weight and body fat (P<0.01). In T-iD, increases in HDL-C and apolipoprotein A1 were observed (P<0.001). In conclusion, an exercise-induced decline in body weight reduces pro-atherogenic apoB-containing lipoproteins, whereas exercise compensated by energy intake increases the key component of reverse cholesterol transport, i.e. ApoA1-containing HDL-C.
U2 - 10.1152/japplphysiol.01092.2017
DO - 10.1152/japplphysiol.01092.2017
M3 - Journal article
C2 - 29543138
VL - 125
SP - 901
EP - 908
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 3
ER -
ID: 198408598