Sports Med (2014) 44:211–221

DOI 10.1007/s40279-013-0110-5

REVIEW ARTICLE

Differential Effects of Aerobic Exercise, Resistance Training

and Combined Exercise Modalities on Cholesterol and the Lipid
Profile: Review, Synthesis and Recommendations
Steven Mann • Christopher Beedie • Alfonso Jimenez

Published online: 31 October 2013

Ó The Author(s) 2013. This article is published with open access at [Link]

Abstract There is a direct relationship between chroni- 1 Introduction

cally elevated cholesterol levels (dyslipidaemia) and cor-
onary heart disease. A reduction in total cholesterol is The term ‘lipid profile’ describes the varying levels of
considered the gold standard in preventative cardiovascular lipids in the blood, the most commonly reported ones being
medicine. Exercise has been shown to have positive low-density lipoprotein (LDL) cholesterol, high-density
impacts on the pathogenesis, symptomatology and physical lipoprotein (HDL) cholesterol and triglycerides. High lev-
fitness of individuals with dyslipidaemia, and to reduce els of LDL cholesterol indicate surplus lipids in the blood,
cholesterol levels. The optimal mode, frequency, intensity which in turn increase the risk of cardiovascular compli-
and duration of exercise for improvement of cholesterol cations. HDL cholesterol transports lipids back to the liver
levels are, however, yet to be identified. This review for recycling and disposal; consequently, high levels of
assesses the evidence from 13 published investigations and HDL cholesterol are an indicator of a healthy cardiovas-
two review articles that have addressed the effects of aer- cular system [1]. Triglycerides in plasma are derived from
obic exercise, resistance training and combined aerobic and fats eaten in foods or from other energy sources. An excess
resistance training on cholesterol levels and the lipid pro- of triglycerides in plasma is positively and independently
file. The data included in this review confirm the beneficial associated with cardiovascular disease [2]. Very-low-den-
effects of regular activity on cholesterol levels and describe sity lipoprotein (VLDL) cholesterol—which is generally
the impacts of differing volumes and intensities of exercise less frequently reported in the literature—has been shown
upon different types of cholesterol. Evidence-based exer- to positively correlate with triglycerides and to be inde-
cise recommendations are presented, aimed at facilitating pendently associated with cardiovascular risk, even in
the prescription and delivery of interventions in order to individuals who express normal LDL cholesterol levels [3].
optimize cholesterol levels. The most commonly used measure of cholesterol is
arguably ‘total cholesterol’, a measure that includes LDL
cholesterol and HDL cholesterol. However, given the dif-
ferent effects of LDL cholesterol and HDL cholesterol on
health, total cholesterol can be a misleading metric. More
S. Mann (&)
UKActive Research Institute, Centre for Sports Science and sensitive measures report, for example, the total:HDL
Human Performance, University of Greenwich, Chatham cholesterol ratio, or non-HDL cholesterol levels (i.e. all
Maritime, Kent ME4 4TB, UK cholesterol variables that are positively associated with
e-mail: stevemann480@[Link]
cardiovascular disease [4]).
C. Beedie There is a direct relationship between chronically ele-
Department of Sport and Exercise Sciences, Aberystwyth vated cholesterol levels (dyslipidaemia) and coronary heart
University, Aberystwyth, Wales, UK disease (CHD) [5]. In a meta-analysis of 170,000 partici-
pants [6], it was reported that reductions in LDL choles-
A. Jimenez
Institute of Sports, Exercise and Active Living (ISEAL), Victoria terol decreased the incidence of heart attacks and ischaemic
University, Melbourne, VIC, Australia strokes. It has also been reported that individuals with
212 S. Mann et al.

elevated total cholesterol levels ([200 mg/dL/5.172 mmol/ physical activity and improvements in total cholesterol
L) have approximately twice the CHD risk of those with (p = 0.006), LDL cholesterol (p = 0.007), triglycerides
optimal levels (\180 mg/dL/4.66 mmol/L) [7]. The US (p = 0.02) and HDL cholesterol (p = 0.01) among 4,039
Centers for Disease Control and Prevention have suggested participants aged 30–60 years, although significant
that this is the case for 71 million US adults, equating to improvements in HDL cholesterol levels were found only
33.5 % of the population [8]. The prevalence of elevated in men.
total cholesterol is even higher in Europe, where 54 % of While the mechanisms underlying the effect of exercise
adults aged C25 years have total cholesterol levels above on the lipid profile are unclear, exercise appears to
the recommended levels [9]. enhance the ability of skeletal muscles to utilize lipids as
For over 10 years, the link between high cholesterol and opposed to glycogen, thus reducing plasma lipid levels
ischaemic heart disease has been evident. Data from 2003 [18]. The mechanisms may include increases in lecithin-
[10] attributed one third of all ischaemic heart disease cholesterol acyltrans (LCAT)—the enzyme responsible for
globally to high cholesterol levels. While the age-adjusted ester transfer to HDL cholesterol [19], which has been
prevalence of high cholesterol in the USA decreased from shown to increase following exercise training [20]—and
26.6 % (in 1988–1994) to 25.3 % (in 1994–2004), recent increases in lipoprotein lipase activity, although the data
data [11] have suggested that the proportion of the adult in this instance are inconsistent [21] and may depend
population using pharmacological cholesterol-lowering upon the energy expenditure that is elicited. Ferguson
substances increased from 11.7 to 40.8 % during this per- et al. [22] reported that 1,100 kcal of energy expenditure
iod. It has long been recognised that reductions in serum is required to elicit increases in HDL cholesterol that
cholesterol can reduce CHD risk—for example, reductions coincide with significant increases in lipoprotein lipase
of around 0.6 mmol/L can reduce the incidence of activity. The process of cholesterol removal is known as
ischaemic heart disease by 54 % at the age of 40 years, ‘reverse cholesterol transport’. This process removes
reducing to 19 % at 80 years [12]. A reduction in total cholesterol from circulation for disposal as a result of
cholesterol is therefore still considered the gold standard in increases in LCAT and reductions in cholesterol ester
preventative cardiovascular medicine [13]. This highlights transfer protein (CETP)—the enzyme responsible for
the importance of interventions aimed at reducing serum transfer of HDL cholesterol to other lipoproteins—fol-
cholesterol levels. Furthermore, the advantage of early lowing acute and chronic exercise [23]. This increased
intervention has been demonstrated; long-term exposure to enzymatic activity increases the ability of muscle fibres to
1 mmol/L lower LDL cholesterol has been associated with oxidize fatty acids originating from plasma, VLDL cho-
a 55 % reduction in CHD risk, while treatment with statins lesterol or triglycerides [24]. This process is conceptual-
starting in later life required a threefold reduction in LDL ized in Fig. 1.
cholesterol to achieve the same magnitude of risk reduction Kesaniemi et al. [26] reviewed 51 papers describing
[14]. physical activity interventions, and reported a mean
Pedersen and Saltin [15], citing 13 meta-analyses, increase in HDL cholesterol of 4.6 %. The effects on LDL
reported improvements in the lipid profile following cholesterol and triglycerides were reported as being
exercise. They described this as Category A evidence that inconsistent. The authors concluded that the most likely
exercise can have a positive effect on the pathogenesis, physical activity-induced improvement in the lipid profile
symptomatology and physical fitness of individuals with is an increase in HDL cholesterol.
dyslipidaemia. In addition, Aadahl et al. [16] reported a
physical activity intervention based on lifestyle consul-
tations in 1,693 sedentary men and women aged 2 Physical Activity and Types of Exercise
33–64 years. Participants taking lipid-lowering medica-
tion were excluded from the analysis. At 3-year follow- The terms ‘physical activity’ and ‘exercise’ are often used
up, a significant positive association was observed interchangeably in the literature. However, it is suggested
between self-reported 24-h physical activity and HDL that the two terms denote two different concepts [27].
cholesterol levels (p = 0.0001), while a significant neg- ‘Physical activity’ refers to any bodily movement produced
ative association was reported between physical activity by skeletal muscles that results in an expenditure of energy
and triglyceride levels (p = 0.0001). Overall, the data (expressed in kilocalories), and which includes a broad
suggested a dose–response relationship between increases range of occupational, leisure and daily activities. ‘Exer-
in physical activity and improvements in triglycerides cise’ instead refers to planned or structured physical
and HDL cholesterol in previously sedentary populations. activity, performed for a reason, which can be aerobic
Five-year follow-up of a subsequent study by Aadahl exercise, resistance training or combined aerobic and
et al. [17] reported significant associations between resistance training.
Exercise Modalities and the Lipid Profile 213

current practice and, we hope, a platform for future

research and recommendations.

3 Literature Search Methodology

3.1 Selection Criteria

A PubMed search using the terms ‘aerobic exercise’,

resistance training’, ‘combined aerobic and resistance
training’, ‘intervention’ and ‘cholesterol’ was conducted
for articles published between 1975 and December 2012.
The reference lists of identified articles were also searched,
and relevant papers were identified. Articles were selected
if they assessed the impact of at least one mode of exercise
Fig. 1 The reverse cholesterol transport pathway delivers free
cholesterol from macrophages or other cells to the liver or intestine on cholesterol levels. Articles were selected only if they
for excretion. The process is regulated by enzymes such as lecithin- contained data regarding the mode, intensity, frequency
cholesterol acyltrans (LCAT) and cholesterol ester transfer protein and duration of exercise (Fig. 2). Articles were excluded if
(CETP). ApoA-1 apolipoprotein A-1, CE cholesterol esters, HDL the participants were receiving medication designed to
high-density lipoprotein, HL hepatic lipase, LDLR low-density
lipoprotein receptor, ndHDL nascent discoidal high-density lipopro- lower or control cholesterol levels (e.g. statins). An
tein, PLPT phospholipid transfer protein. From Ohashi et al. [25] by example of an excluded article is one by Hansen et al. [31],
permission of Oxford University Press which compared interventions involving aerobic exercise
alone or combined with resistance training. However, the
The Physical Activity Guidelines Advisory Commit- participants were receiving various medications for coro-
tee Report [28] highlighted the need to design a pro- nary artery disease, including statins and beta-blockers;
gramme that will provide appropriate exercise in order therefore, the observed effects could not be unambiguously
to attain maximal benefit at the lowest level of risk. attributed to the exercise intervention alone. Subsequently,
However, despite a large number of related publications, and following an early review of this article, secondary
a comprehensive overview of optimal modes, intensities database searches were extended to the Web of Knowl-
and frequencies of physical activity in the context of the edge, Science Direct and Google Scholar. These additional
lipid profile is yet to be published by any of the searches revealed no additional articles meeting the
agencies involved. A recent review by the European selection criteria for inclusion in this review.
Society of Cardiology (ESC) [29] briefly summarized
the short- and long-term effects of aerobic exercise and
resistance training in normolipidaemic subjects and hy- 4 Findings
perlipidaemic patients. The ESC concluded that it has
not yet been established how much exercise is required The findings of all studies meeting the inclusion criteria are
in order to improve the lipid profile and reduce car- presented in Sects. 4.1 (aerobic exercise), 4.2 (resistance
diovascular risk. In fact, the authors of a recent meta- training) and 4.3 (combined aerobic and resistance train-
analysis [30] highlighted the lack of evidence for ing). In total, 13 original research articles and two review
training programmes that optimally improve cardiovas- articles were included in this review. Care was taken to
cular risk, drawing particular attention to the effects of ensure that information was not ‘counted’ twice—that is, as
aerobic exercise, resistance training or both on cardio- an original research investigation and as part of a review.
vascular risk factors. The characteristics and findings of all included studies are
The present review aims to synthesize the current pub- also presented in Table 1.
lished evidence regarding the impacts on cholesterol levels
of aerobic exercise, resistance training or both. Following 4.1 Aerobic Exercise
the review, evidence-based recommendations for best
practice are presented. It is recognised by the authors that Aerobic exercise involves cardiorespiratory endurance
these guidelines should be considered tentative, given the exercises such as jogging, running and cycling [27]. Leon
range of research methods, interventions and populations and Sanchez [32] conducted a meta-analysis of 51 inter-
that are described (in short, the relative lack of program- ventions involving 12 weeks or more of aerobic exercise
matic research). However, these will provide a basis for (n = 4,700). It was reported that, on average, HDL
214 S. Mann et al.

Fig. 2 Article selection criteria

and literature search
methodology. ORA original
research article, RCT
randomized controlled trial

cholesterol increased by 4.6 % while triglyceride levels fell interval running protocol (40 min/week) [n = 36]. No
by 3.7 % and LDL cholesterol fell by 5 %. Total choles- improvements in the lipid profile were reported following
terol remained unchanged, although the HDL:LDL cho- the intense interval programme. Those authors conse-
lesterol ratio improved considerably, suggesting that the quently suggested that the training volume, as opposed to
increased intensity and structure normally associated with the training intensity, is the key to improving the lipid
aerobic exercise has a more consistent impact upon tri- profile, and that there may be a relationship between body
glycerides and LDL cholesterol than moderate levels of fat (which decreased only in the prolonged exercise group)
physical activity. Studies subsequent to or not included in and cholesterol levels, whereby a volume sufficient to elicit
that meta-analysis are reported below. changes in fat mass is required to favourably alter the lipid
It was suggested in the introduction that HDL choles- profile.
terol is the component of the lipid profile that is most likely When the intensity of aerobic exercise is increased
to improve as the result of physical activity. This is sup- during continuous effort, the effects upon HDL cholesterol
ported by evidence relating to aerobic exercise presented appear to become more consistent. Dunn et al. [35]
by Banz et al. [33], who reported a 13% increase in HDL investigated the effects of a 6-month aerobic exercise
cholesterol (from 29.8 to 33.7 mg/dL, p \ 0.05) following training programme, which progressed from 50 to 85 % of
a relatively short 10-week protocol of training three times maximum aerobic power for 20–60 min three times
weekly at 85 % of the maximal heart rate (HRmax) [from weekly, and reported significant decreases in total choles-
the second week onwards] for 40 min on ski-style exercise terol (-0.3 mmol/L, p \ 0.001) and in the total:HDL
equipment. The authors reported that HDL cholesterol was cholesterol ratio (-0.3, p \ 0.001). In this case, the inter-
the only component of the lipid profile that improved. vention period was relatively long and the intensity was
Nybo et al. [34] reported that the total:HDL cholesterol relatively high. In a 16-week study, LeMura et al. [36]
ratio was the only component of the lipid profile that reported significant reductions in plasma triglycerides
improved significantly (decreasing from 3.41 to 2.92, (from 1.4 to 1.2 mmol/L, p \ 0.05) and increases in HDL
p \ 0.05) by 150 min of exercise weekly at 65 % of the cholesterol (from 1.4 to 1.8 mmol/L, p \ 0.05) after
maximal aerobic capacity (VO2max) in previously untrained training three times weekly at 70–75 % HRmax for 30 min
participants. That investigation compared a prolonged for the first 8 weeks, progressing to four times weekly at
(150 min/week) aerobic exercise protocol with an intense 85 % HRmax for 45 min thereafter. The data suggested that
Exercise Modalities and the Lipid Profile 215

Table 1 Main characteristics and findings of studies included in this review

Reference n Design Intervention Measure Effecta p value

Banz et al. [28] 26 Quasi-experimental Aerobic exercise Total cholesterol : 4.1 mg/dL NR
10 weeks HDL cholesterol : 3.9 mg/dL \0.05b
3 sessions/week LDL cholesterol : 3.4 mg/dL NR
85 % HRmax
40 min
Nybo et al. [29] 36 RCT Aerobic exercise (prolonged) Total cholesterol ; 0.3 mmol/L NR
12 weeks HDL cholesterol : 0.1 mmol/L NR
150 min/week LDL cholesterol ; 0.1 mmol/L NR
65 % VO2max Total:HDL cholesterol ratio ; 0.49 \0.005b
Aerobic exercise (intense Total cholesterol ; 0.1 mmol/L NR
interval) HDL cholesterol NC NR
12 weeks LDL cholesterol ; 0.1 mmol/L NR
40 min/week Total:HDL cholesterol ratio ; 0.08 NR
HR [95 % during sprints
Dunn et al. [30] 235 Quasi-experimental Aerobic exercise Total cholesterol ; 0.3 mmol/L \0.001b
24 weeks HDL cholesterol NC 0.54
3 sessions/week LDL cholesterol ; 0.2 mmol/L \0.001b
50–85 % max aerobic power Total:HDL cholesterol ratio ; 0.3 mmol/L \0.001b
20–60 min
LeMura et al. [31] 48 RCT Aerobic exercise Total cholesterol ; 0.3 mmol/L NR
16 weeks HDL cholesterol : 0.4 mmol/L \0.005b
3 sessions/week LDL cholesterol ; 0.2 mmol/L NR
70–75 % HRmax Triglycerides ; 0.2 mmol/L \0.005b
(weeks 1–8), 85 % HRmax Total:HDL cholesterol ratio ;1 NR
(weeks 8–16)
30 min (weeks 1–8), 45 min
(weeks 8–16)
Kraus et al. [32] 111 RCT Aerobic exercise (jogging) Total cholesterol : 0.4 mg/dL NR
24 weeks LDL cholesterol ; 1.9 mg/dL \0.005b
65–80 % VO2peak HDL cholesterol : 4.3 mg/dL \0.005b
Jogging Triglycerides ; 28.4 mg/dL \0.005b
Calorific equivalent of
20 miles/week
O’Donovan et al. [33] 64 RCT Aerobic exercise (moderate- Total cholesterol : 0.3 mmol/L NR
intensity) LDL cholesterol : 0.17 mmol/L NR
24 weeks HDL cholesterol : 0.08 mmol/L NR
3 sessions/week Non-HDL cholesterol : 0.23 mmol/L NR
60 % VO2max Triglycerides : 0.12 mmol/L NR
400 kcal/session
Aerobic exercise (high- Total cholesterol ; 0.54 mmol/L \0.005b
intensity) LDL cholesterol ; 0.52 mmol/L \0.005b
24 weeks HDL cholesterol ; 0.01 mmol/L NR
3 sessions/week Non-HDL cholesterol ; 0.54 mmol/L \0.005b
80 % VO2max Triglycerides ; 0.05 mmol/L NR
400 kcal/session
Prabhakaran et al. [35] 24 RCT Resistance training Total cholesterol ; 0.42 mmol/L \0.005b
14 weeks LDL cholesterol ; 0.42 mmol/L \0.005b
3 sessions/week HDL cholesterol : 0.07 mmol/L NR
85 % 1 RM Triglycerides ; 0.16 mmol/L NR
LDL:HDL cholesterol ratio ; 0.42 mmol/L 0.057
Total:HDL cholesterol ratio ; 0.54 mmol/L \0.005b
216 S. Mann et al.

Table 1 continued
Reference n Design Intervention Measure Effecta p value

Vatani et al. [38] 30 RCT Resistance training HDL cholesterol : 2.3 mg/dL NR
(moderate-intensity) LDL cholesterol ; 13.5 mg/dL \0.005b
6 weeks Triglycerides ; 11.4 mg/dL NR
3 sessions/week Total cholesterol ; 12.4 mg/dL \0.005b
45–55 % 1 RM Total:HDL cholesterol ratio ; 0.38 mg/dL \0.005b
Resistance training (high- HDL cholesterol : 5.5 mg/dL \0.005b
intensity) LDL cholesterol ; 12.1 mg/dL \0.005b
6 weeks Triglycerides : 0.1 mg/dL NR
3 sessions/week Total cholesterol ; 11.3 mg/dL \0.005b
80–90 % 1 RM Total:HDL cholesterol ratio ; 0.47 mg/dL \0.005b
Fett et al. [39] 50 Quasi-experimental Resistance training, circuit Total cholesterol ; 17 mg/dL \0.01b
training LDL cholesterol ; 11 mg/dL NR
8 weeks HDL cholesterol ; 6 mg/dL NR
3 sessions/week (weeks 1–4), Total:HDL cholesterol ratio ; 0.2 mg/dL NR
4 sessions/week
(weeks 4–8) Triglycerides ; 31 mg/dL \0.05b

60 min
Shaw et al. [41] 28 RCT Aerobic and resistance LDL cholesterol ; 2.16 mmol/L \0.05b
training
16 weeks
3 sessions/week
Aerobic: 60 % HRmax,
resistance: 60 % 1 RM
45 min
Yang et al. [42] 40 Pre–post Aerobic and resistance Total cholesterol ; 1 mmol/L 0.655
training LDL cholesterol ; 0.6 mmol/L 0.172
12 weeks Triglycerides ; 0.5 mmol/L \0.01b
5 sessions/week
Aerobic: 300 kcal, resistance:
100 kcal
Ha and So [43] 16 RCT Aerobic and resistance Triglycerides ; 46.71 mg/dL \0.05b
training HDL cholesterol ; 3.71 mg/dL NR
12 weeks Total cholesterol ; 19.29 mg/dL \0.05b
3 sessions/week LDL cholesterol ; 8.57 mg/dL \0.05b
Aerobic: 60–80 % HRreserve,
resistance: 12–15 RM
Aerobic: 30 min, resistance:
30 min

HDL high-density lipoprotein, HR heart rate, HRmax maximal heart rate, HRreserve heart rate reserve, LDL low-density lipoprotein, max maximum, NC no
change, NR not reported, RCT randomized controlled trial, RM repetition maximum, VLDL very-low-density lipoprotein, VO2max maximal aerobic
capacity, VO2peak peak aerobic capacity, : increase, ; decrease
a
All comparisons are with the baseline values
b
Represents a significant (p \ 0.05) interaction or pre–post change in cholesterol levels

shorter-term interventions will be effective also if the generated an additional metabolic response—a parameter
training volume is high enough. Increasing the frequency not reported by Banz et al.
of training to four times weekly may have elicited the Kraus et al. [37] investigated the impact of increasing
additional benefits seen by LeMura et al. in comparison the volume and intensity of aerobic exercise upon the lipid
with those observed by Banz et al. (with three training profiles of 111 sedentary overweight participants, all with
sessions weekly). Further, LeMura et al. observed a 13 % mild to moderate dyslipidaemia. Participants were allo-
reduction in the body fat percentage (from 26.4 to 22.9 %, cated to either 6 months in a control group or 8 months in
p \ 0.05), suggesting that the additional volume of training one of three aerobic exercise groups. The three aerobic
Exercise Modalities and the Lipid Profile 217

exercise groups were high-intensity/high-volume aerobic maximal repetition (85 % 1 RM), where one maximal
exercise (jogging for the calorific equivalent of 20 miles/ repetition is the maximal load that can be lifted once for a
week at an intensity of 65–80 % of the peak aerobic given exercise [41]. Participants were randomized to either
capacity (VO2peak), high-intensity/low-volume aerobic resistance training or to a non-exercising control. Super-
exercise (jogging for the calorific equivalent of 12 miles/ vised exercise sessions lasted 40–50 min and were com-
week at an intensity of 65–80 % VO2peak) and moderate- pleted three times weekly. Significant (p \ 0.05) decreases
intensity/low-volume exercise (walking for the calorific in total cholesterol (from 4.6 to 4.26 mmol/L) and LDL
equivalent of 12 miles/week at an intensity of 40–55 % cholesterol (from 2.99 to 2.57 mmol/L) were observed,
VO2peak). It was reported that the high-intensity/high- along with lowered body fat (from 27.9 to 26.5 %). Acute
volume training combination resulted in the greatest changes in the lipid profile following different intensities of
improvements in 10 of 11 lipid variables (LDL cholesterol resistance training were examined by Lira et al. [23].
decreased from 130.1 to 128.2 mg/dL, p \ 0.05; HDL Untrained males (n = 30) were randomized to intensity
cholesterol increased from 44.3 to 48.6 mg/dL, p \ 0.05; groups at baseline. Measures of cholesterol were collected
triglycerides decreased from 166.9 to 138.5 mg/dL, at time points of 1, 24, 48 and 72 h following resistance
p \ 0.05). These data suggest that in relation to aerobic training at intensities of 50, 75, 90 and 110 % (in the later
exercise, both total energy expenditure and intensity are scenario in the eccentric phase only, performance was
factors in lipid reduction. assisted during the concentric phase). The total training
O’Donovan et al. [38] controlled the training volume to volume was equalized between the groups to ensure that
directly assess the impact of the training intensity. Sixty- the resistance training intensity was the factor being
four previously sedentary men were randomly allocated to assessed. Triglyceride clearance at 72 h was significantly
either a control group, a moderate-intensity exercise group (p \ 0.05) greater following 50 % 1 RM (-14.6 mg/dL)
(at 60 % VO2max) or a high-intensity exercise group (at and 75 % 1 RM (-10.7 mg/dL) than following 90 %
80 % VO2max). Both exercising groups completed three 1 RM (?9.5 mg/dL) and 110 % 1 RM (?12.1 mg/dL).
400 kcal sessions weekly for 24 weeks. By setting the Further, increases in HDL cholesterol were significantly
session volume in calories, the overall training volume was greater following 50 % 1 RM and 75 % 1 RM than fol-
controlled. Participants were instructed to maintain their lowing 110 % 1 RM (p = 0.004 and 0.03, respectively).
dietary habits. It was reported that significant lipid profile The authors concluded that low- to moderate-intensity
improvements occurred only in the high-intensity group, resistance training results in greater benefit to the lipid
with significant decreases (p \ 0.05) in total cholesterol profile than high-intensity resistance training, although the
(from 6.02 to 5.48 mmol/L), LDL cholesterol (from 4.04 to mechanisms underlying this difference are unclear. It is
3.52 mmol/L) and non-HDL cholesterol (from 4.58 to speculated that the reduction in total cholesterol is a result
4.04 mmol/L). of the exchange of cholesterol ester between tissues and
The evidence suggests that a moderate-intensity exercise lipoproteins to HDL cholesterol (Fig. 1); however, the way
programme will be effective in increasing HDL choles- this differs between 50, 75, 90 and 110 % 1 RM warrants
terol. This will have a positive impact upon atherosclerosis further investigation.
(hardening of artery walls through plaque and fat accu- Vatani et al. [42] examined the effects of various
mulation [13]) via HDL cholesterol-facilitated removal of intensities of resistance training on the lipid profile over
LDL cholesterol. To directly reduce LDL cholesterol and 6 weeks. Healthy male participants (n = 30) were ran-
triglyceride levels, however, the intensity of aerobic exer- domized to either a moderate-intensity resistance training
cise must be increased—something that may not be pos- programme (45–55 % 1 RM) or a high-intensity resistance
sible in individuals with a limited exercise capacity or training programme (80–90 % 1 RM). Both groups were
other risk factors. supervised during training sessions and attended three
sessions weekly. Significant (p \ 0.05) reductions in LDL
4.2 Resistance Training cholesterol (moderate-intensity -13.5 mg/dL vs high-
intensity -12.1 mg/dL), total cholesterol (moderate-
Theoretically, resistance training (strength-developing intensity -12.2 mg/dL vs high-intensity -11.3 mg/dL)
exercise utilizing external resistance or one’s own body and the total:HDL cholesterol ratio (moderate-intensity
weight [27]) may be a more accessible form of exercise for -0.38 vs high-intensity -0.47) were found in both groups,
less mobile groups, as well as providing an alternative to with no significant differences between the two groups.
aerobic training for more mobile individuals [39]. Pra- Significant increases in HDL cholesterol, however, were
bhakaran et al. [40] investigated the effect of 14 weeks of observed only in the high-intensity group (?5.5 mg/dL).
resistance training in premenopausal women (n = 24). This is perhaps surprising, considering that previous
Resistance training was at an intensity of 85 % of one research indicated that increased HDL cholesterol is likely
218 S. Mann et al.

to be the first lipid profile response to exercise, even at low significantly different from that achieved by 45 min of
intensities of activity [26]. This study once again demon- aerobic exercise alone (from 3.64 to 2.87 mmol/L,
strated the limited additional benefit of increasing the p \ 0.05). It can therefore be concluded that no additional
resistance training intensity when equalizing the training LDL cholesterol reduction resulted from combining the
load by reducing the numbers of sets and repetitions being two modes of exercise. However, this investigation did
completed to compensate for the increased weight being demonstrate that resistance training might successfully
lifted. In addition, the authors reported no significant compensate for reductions in aerobic exercise. Further, the
changes in lipoprotein lipase activity following the exercise authors suggested that additional physiological systems
training intervention—which was surprising, considering benefited from resistance training, making it potentially
the lipid profile changes that were elicited. This would, more effective.
however, be dependent upon the time interval between the Yang et al. [45] reported a study investigating rela-
final exercise session and the blood sample collection tionships between exercise, cholesterol and arterial stiff-
(normally longer than 24 h), because of the acute response ness in obese middle-aged women (n = 40, body mass
of lipoprotein lipase (increases have previously been shown index [25 kg/m2, age 30–60 years). The experimental
to only be maintained for 48 h following a 1,500 kcal protocol consisted of 45 min of aerobic exercise at an
exercise session and not following a B1,300 kcal session intensity of 60–75 % HRmax at 300 kcal per session and
[22]—levels unlikely to be attained by this exercise inter- 20 min of resistance training at 100 kcal per session five
vention). Thus, although the levels were unchanged at post- times weekly over a 12-week period. Reductions were
intervention testing, lipoprotein lipase should not be ruled observed in total cholesterol (from 5.2 to 4.2 mmol/L,
out as a mechanism. p = 0.655), LDL cholesterol (from 3.2 to 2.6 mmol/L,
Fett et al. [43] incorporated resistance training into cir- p = 0.172), triglycerides (from 3.0 to 2.5 mmol/L,
cuit training sessions in which no specific weight was p \ 0.001) and arterial stiffness measured via the brachial–
specified but a specific time duration was allocated to each ankle pulse wave velocity (from 1,286 to 1,195 cm/s,
exercise. Sessions lasted 60 min and were completed three p \ 0.001). While no controls were included in this study,
times weekly for 1 month and four times weekly for the these data suggested the potential clinical significance of
second month. Significant reductions were reported in total reductions in cholesterol—that is, a reduction in arterial
cholesterol (from 203 to 186 mg/dL, p \ 0.01) and tri- stiffness, which is all too often associated with heart
glycerides (from 122 to 91 mg/dL, p \ 0.05), further attacks and strokes.
adding to the speculation that the volume of movement Ha and So [46] combined 30 min of aerobic exercise at
may be just as important as—or even more important 60–80 % of the maximal heart rate reserve (maximal heart
than—the amount of weight lifted. rate - heart rate at rest) [HRreserve] with 30 min of resis-
tance training at 12–15 repetitions maximum in 16 par-
4.3 Combined Modalities ticipants aged 20–26 years for 12 weeks. The intervention
significantly reduced the participants’ waist circumference,
The evidence presented above demonstrates the effective- body fat percentage and blood pressure values, compared
ness of both aerobic exercise and resistance training in with those of non-exercising controls. The lipid profile
controlling and improving cholesterol levels through vari- improved in the exercising condition, with reductions in
ous modes, frequencies, intensities and durations of exer- total cholesterol from 180.29 to 161 mg/dL, LDL choles-
cise, in different populations. There is limited literature that terol from 112.14 to 103.57 mg/dL and triglycerides from
has examined the two modalities combined, although a 97.14 to 50.43 mg/dL, although the changes did not reach
recent review by Tambalis et al. [44] suggested that statistical significance when compared with values in the
although some combination protocols have been effective controls. The authors suggested that the participants was
in lowering LDL cholesterol and increasing HDL choles- too young to elicit the clinical and significant effects shown
terol, others have not. by previous research in predominantly elderly or middle-
Shaw et al. [24] examined the effect of a 16-week aged participants.
moderate-intensity combined aerobic and resistance train-
ing protocol in previously untrained but otherwise healthy
young men (n = 28). The protocol lasted 45 min and 5 Exercise Recommendations
combined aerobic exercise at 60 % HRmax with resistance
training (two sets of 15 repetitions) at 60 % 1 RM. It was On the basis of the above data relating to the effects
reported that LDL cholesterol was significantly reduced of exercise on cholesterol levels, exercise recommenda-
following aerobic and resistance training (from 4.39 to tions have been formulated (Table 2). Interventions
3.23 mmol/L, p \ 0.05), although the reduction was not that have demonstrated particular effectiveness—that is,
Exercise Modalities and the Lipid Profile 219

Table 2 Evidence-based exercise recommendations for maintaining/improving cholesterol levels in different patient groups
Patient group Cholesterol targets Exercise recommendations

Healthy Maintain low LDL cholesterol Increase physical activity to [30 min/day 5 times weekly [16,
and triglycerides; increase HDL 17]; prolonged moderate-intensity aerobic exercise at
cholesterol 70–80 % HRreserve [43], combined with low-intensity
resistance training at 50 % 1 RM [23]
Elevated cholesterol (dyslipidaemia) Reduce LDL cholesterol and Increase physical activity to [30 min/day 5 times weekly [16,
triglycerides; increase HDL 17]; prolonged moderate-intensity aerobic exercise at
cholesterol 70–80 % HRreserve [43], progressing to 85 % HRmax [35, 36],
combined with moderate- to high-intensity resistance training
at 75–85 % 1 RM [23, 40]
Elevated cholesterol (dyslipidaemia) and Reduce LDL cholesterol and Increase physical activity as much as is feasible [16, 17];
limited mobility (disabled, elderly triglycerides; increase HDL resistance training progressing from 50 to 75 % in major
populations, etc.) cholesterol muscle groups [23], can be incorporated into circuit sessions
and maintained at moderate intensity [43]
HDL high-density lipoprotein, HRmax maximal heart rate, HRreserve heart rate reserve, LDL low-density lipoprotein, RM repetition maximum

higher-intensity aerobic exercise [38] and moderate-inten- Prolonged moderate-intensity aerobic exercise should be
sity resistance training [23]—have been incorporated. recommended as a starting point for those who have pre-
Previous evidence has highlighted a dose–response rela- viously been sedentary or are new to exercise. Resistance
tionship between activity levels and increases in HDL training presents a viable alternative to aerobic exercise or
cholesterol [16]; therefore, the exercise recommendations is an effective intervention independently. High-intensity
are to be considered a minimum. These evidence-based exercise ([85 % 1 RM) has been shown to be no more
recommendations should aid in the prescription and deliv- effective than moderate-intensity exercise (50–85 %
ery of interventions designed to reduce cholesterol levels. 1 RM). The addition of resistance training to aerobic
exercise will supplement—and possibly enhance—the
effects on the lipid profile, although there is limited liter-
6 Conclusion ature comparing the three modes of exercise, rendering
definitive statements problematic. There will, however, be
The above data provide some support for the proposal that no reduction in the effect, and the additional physiological
physical activity and exercise can be utilized to improve and psychological systems that are impacted may manifest
cholesterol levels. Regular physical activity has been additional benefits when aerobic exercise and resistance
shown to increase HDL cholesterol while maintaining, and training are combined.
theoretically offsetting increases in, LDL cholesterol and The data included in this review confirm the beneficial
triglycerides. There appears to be a linear dose–response effects of regular physical activity on cholesterol levels.
relationship between activity levels and HDL cholesterol Such knowledge should aid in the prevention and man-
levels. More intense activity, however, is required to elicit agement of dyslipidaemia while reducing the risks of
reductions in LDL cholesterol and triglyceride levels. heart attacks, strokes and coronary artery disease. Having
Aerobic exercise at high intensities appears to be effective considered the baseline condition of their patients, clini-
in improving the lipid profile, and the effects surpass those cians should encourage as much physical activity as
of physical activity by initiating clearance of plasma LDL possible while, where feasible, highlighting the additional
cholesterol and triglycerides. The dose–response relation- impact or appropriateness of aerobic exercise, resistance
ship between the lipid profile and energy expenditure training or both to obtain optimal benefits in their
seems to transcend the mode of exercise. Increases in patients.
calorific expenditure associated with aerobic exercise (via
increased intensity and/or duration) have been shown to Acknowledgments The authors wish to thank Drs Judith Allgrove,
Silvano Zanuso and Steffano Balducci for assistance in the early
positively influence lipoprotein lipase activity, HDL cho- editing and proof reading of this review article.
lesterol levels [22] and the lipid profile [37]. During No sources of funding were used in the preparation of this review.
resistance training, it has been shown consistently that the The authors report no conflict of interest.
increased volume of movement via increased numbers of
Open Access This article is distributed under the terms of the
sets and/or repetitions has a greater impact upon the lipid Creative Commons Attribution Noncommercial License which per-
profile than increased intensity (e.g. via high-weight low- mits any noncommercial use, distribution, and reproduction in any
repetition training) [23, 43]. medium, provided the original author(s) and the source are credited.
220 S. Mann et al.

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