Curr Cardiol Rep (2016) 18:117

DOI 10.1007/s11886-016-0797-7

DIABETES AND CARDIOVASCULAR DISEASE (S MALIK, SECTION EDITOR)

The Effect of Vigorous- Versus Moderate-Intensity Aerobic

Exercise on Insulin Action
Robert W. McGarrah 1,2 & Cris A. Slentz 1 & William E. Kraus 1,2

# Springer Science+Business Media New York 2016

Abstract Due to the beneficial effects on a wide range of

modern medical conditions, most professional societies recommend regular aerobic exercise as part of a healthy lifestyle.
Many of the exercise-related health benefits exhibit a doseresponse relationship: Up to a point, more exercise is more
beneficial. However, recent studies have suggested that different exercise intensities may provide distinct health benefits,
independent of energy expenditure (i.e., exercise dose). One
of these benefits, primarily mediated by the skeletal muscle, is
exercise-related changes in insulin action and glucose homeostasis. Glucose uptake in the exercising muscle occurs through
insulin-independent mechanisms whose downstream signaling events ultimately converge with insulin-signaling pathways, a fact that may explain why exercise and insulin have
additive effect on skeletal muscle glucose uptake. Although
the existing evidence is somewhat conflicting, well-controlled
randomized studies suggest that, when controlled for total
energy expenditure, moderate-intensity aerobic exercise improves insulin sensitivity more than vigorous-intensity aerobic

This article is part of the Topical Collection on Diabetes and Cardiovascular

Disease
* Robert W. McGarrah
robert.mcgarrah@duke.edu
Cris A. Slentz
cris.slentz@duke.edu
William E. Kraus
william.kraus@duke.edu
1

Duke Molecular Physiology Institute, Duke University Medical

Center, 300 North Duke Street, Durham, NC 27701, USA

Division of Cardiology, Department of Medicine, Duke University

Medical Center, Durham NC, USA

exercise. The mechanisms underlying this difference are

largely unknown. One possible explanation involves enhanced metabolism of fatty acid stores in the skeletal muscle
by moderate-intensity exercise, which may directly improve
insulin sensitivity. Overall, new technologic and physiologic
investigative tools are beginning to shed light on the biology.
Further understanding of these mechanisms will lead to better
understanding of the clinical implications of a healthy lifestyle
and may ultimately offer new therapeutic targets for common
medical conditions such as insulin resistance and diabetes.

Keywords Exercise intensity . Aerobic training . Insulin

sensitivity . Insulin action

Introduction
Modern life begets a sedentary lifestyle. As people become
less and less active, not only do they expend less energy
through physical activity, leading to the development of obesity and consequent obesity-related chronic health conditions,
but also their overall physiology and metabolism changes [1].
To this point, sedentary behavior, independent of comorbid
risk factors, is associated with increased risk for cardiovascular disease (CVD), metabolic syndrome, diabetes, cancer, and
all-cause mortality [25]. Because of these well-recognized
risks of prolonged physical inactivity, most professional societies have issued formal activity guidelines in an attempt to
reduce the incidence of these increasingly more common
conditions. In this review, we will focus on the role of physical activity in glucose homeostasis. In particular, we will
address the effects of different aerobic exercise intensities
on insulin action.

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General Effects of Exercise on Glucose Homeostasis

While multiple organ systems are involved in the bodys response to exercise, skeletal muscle is one of the most important determinants of exercise-related changes in glucose homeostasis. Exercising muscle first consumes glucose within
the tissue, followed by muscle glycogen stores. As muscle
glycogen stores are depleted, skeletal muscle relies more for
an energy source on circulating glucose from hepatic glycogenolysis and gluconeogenesis. Glucose uptake in contracting
muscle undergoes complex regulation depending on several
factors: glucose delivery, glucose transport, and tissue-level
glucose metabolism [6]. During exercise, there is an up to
20-fold increase in blood flow enhancing glucose delivery to
exercising muscle [7]. Additionally, capillary recruitment to
exercising muscle increases the vascular surface area for glucose delivery.
Glucose transport into the exercising muscle primarily relies on the glucose transporter, GLUT4. The majority of
GLUT4 is stored in intracellular vesicles in resting muscle.
In other tissues, GLUT4 translocation to the cell surface occurs in response to insulin. However, due to the high demand
for substrate transport to exercising muscle, insulin secretion
is suppressed, preventing uptake of glucose by non-muscle
tissues. Therefore, skeletal muscle GLUT4 translocation in
exercising muscle occurs through insulin-independent mechanisms. Muscle contraction during exercise leads to translocation of GLUT4 to the sarcolemma and enhanced glucose uptake [6].
Though evidence is conflicting, there may be two intracellular pools of GLUT4 in skeletal muscle: one recruited by
insulin and the other by muscle contraction [8]. These two
pathways have distinct proximal signals but converge downstream, which may explain why exercise and insulin have an
additive effect on skeletal muscle glucose transport [911].
Trained muscle utilizes fuels more efficiently than the untrained muscle. Regular exercise enhances overall insulin- and
contraction-stimulated skeletal muscle glucose uptake. This
adaptation occurs, in large part, due to increased GLUT4 expression and cellular GLUT4 protein content. The subsequent
increase in GLUT4 tissue concentration leads to improved
insulin action, glucose disposal, and glycogen storage [6].
Additionally, training leads to expansion of muscle capillary
networks, increased size and number of mitochondria, and an
increased ability to utilize fatty acids, thus sparing glycogen
stores. Many of these metabolic changes correlate with the
switching of muscle fibers from the fast glycolytic (FG) type
(type IIX) to the fast oxidative glycolytic (FOG) type (type
IIA), which are more efficient at fat oxidization.
Physical inactivity leads to insulin resistance; conversely,
increased physical activity improves insulin sensitivity.
Indeed, this is a well-accepted phenomenon [12]. One difficulty in interpreting the effect of exercise per se on insulin

Curr Cardiol Rep (2016) 18:117

sensitivity is the other lifestyle interventions used in clinical

studies: diet, weight loss, and induced adiposity changes.
These interventions may have independent effects on insulin
action. Thus, although exercise enhances insulin action
through molecular changes in skeletal muscle, global changes
in insulin sensitivity may also be modified by non-skeletal
muscle mechanisms.

Exercise Intensity Effects on Insulin Action

What is the optimal exercise prescription to improve insulin
sensitivity? Professional society exercise guideline recommendations generally agree. The World Health Organization
and the 2008 Physical Activity Guidelines for Americans recommend at least 150 min of moderate intensity aerobic activity or 75 min of vigorous intensity activity weekly for all
adults [13]. Guidelines from the American Heart Association
and the American College of Sports Medicine are similar,
recommending either moderate-intensity exercise for 30 min
for a minimum of 5 days a week, or vigorous exercise for
20 min 3 days a week [14]. Underlying these guidelines is a
consistent message: the health benefits derived from exercise
are due to the total amount of energy expended, without respect to the type of exercise performed. However, are there
different effects with different exercise intensities?
The answer to this question is complicated and the evidence is conflicting. When reviewing and interpreting the data, four other questions must be asked:
1. Did the study control for the amount of exercise (energy
expenditure) among intensity groups? Energy expenditure is composed of three components: exercise intensity,
frequency, and duration per session. Exercise intensity is
usually determined as a percentage of VO 2 peak.
Guidelines and most studies define moderate-intensity exercise as an effort of 50 % VO2 peak (the equivalent of
brisk walking) and vigorous-intensity exercise as an effort
of 75 % VO2 peak (the equivalent of jogging). For studies
to compare exercise intensity effects on insulin sensitivity,
it is critical to control for total exercise energy expenditure, because increased energy expenditure per se can improve insulin sensitivity [15, 16, 17].
2. When was insulin sensitivity measured in relation to the
last bout of training? As discussed in the previous section,
exercise induces acute changes in glucose homeostasis
and insulin action. Therefore, in order to avoid capturing
this transient response to the acute exercise bout, insulin
sensitivity assessments are generally performed before the
next bout of training. However, it is often difficult to separate the effects on insulin action from the most recent
training bout versus the cumulative effects from an entire
training program. To illustrate this point, we assigned

Curr Cardiol Rep (2016) 18:117

overweight/obese individuals to 8 months of either lowvolume/moderate-intensity (equivalent to brisk walking

12 miles/week, 1200 kcal/week at 4055 % VO2 peak,
200 min exercise/week), low-volume/vigorous-intensity
(jogging 12 miles/week, 1200 kcal/week at 6580 %
VO2 peak, 125 min/week), or high-volume/vigorous-intensity (jogging 20 miles/week, 2000 kcal/week at 65
80 % VO2 peak, 200 min/week). Insulin sensitivity, as
measured by an intravenous glucose tolerance test, was
measured when subjects were sedentary and at 1624 h
and 15 days after the final training bout. All exercise
groups had improved insulin sensitivity at 1624 h after
the last bout of training compared with the sedentary condition. However, only the low-volume/moderate-intensity
and high-volume/vigorous-intensity groups had persistent
improvements in insulin sensitivity at the 15-day time
point, which may be attributed to changes in body composition rather than changes in skeletal muscle [16].
3. How was insulin sensitivity measured? The most common methods used in exercise intensity studies are the
oral glucose tolerance test (OGTT), intravenous glucose
tolerance test (IVGTT), and the hyperinsulinemiceuglycemic clamp. All of these methods reliably measure
insulin sensitivity; however, they differ slightly in what
organ systems they assess. For instance, IVGTTs and
hyperinsulinemic-euglycemic clamps primarily assess peripheral (i.e., skeletal muscle) insulin sensitivity while the
OGTT provides an integrated assessment of whole body
glucose disposal by taking into account gastric emptying,
hepatic first-pass metabolism, glucose sensing by the pancreas, and then glucose delivery and insulin-stimulated
glucose uptake by the skeletal muscle. Because of these
differences, studies may reflect slightly different exerciserelated effects on insulin action depending on what measure of insulin sensitivity was employed. As an example,
an OGTT would be able to assess the effect of exercise on
gastrointestinal hormones such as incretins whereas an
IVGTT would mainly assess changes in skeletal muscle
insulin sensitivity.
4. Can the changes in insulin sensitivity be explained by
changes in other metabolic parameters? Exercise provides
additional health benefits, such as weight loss and decrease in visceral adiposity, that can indirectly improve
insulin sensitivity. If possible, studies should make efforts
to take into account changes in these other factors when
drawing conclusions about the mechanisms mediating responses in insulin sensitivity.

Vigorous-Intensity Exercise Is Better

Several studies suggest that vigorous-intensity exercise improves insulin sensitivity to a greater extent than low- or

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moderate-intensity exercise. DiPietro et al. studied 25 older

women (mean age 73 years) in a 9-month training program
with vigorous-intensity (80 % of VO2 peak achieved by jogging, rowing, or step aerobics); moderate-intensity (65 % of
VO2 peak achieved by the same activities as the vigorousintensity group), or low-intensity (50 % of VO2 peak achieved
by stretching and strengthening exercises) exercise as a control; energy expenditure of the exercise regimens was the same
(300 kcal/session). Insulin sensitivity was measured by
hyperinsulinemic-euglycemic clamp 72 h after the last bout
of training. Only the vigorous-intensity group experienced a
training-induced increase in glucose disposal (21 %, P = 0.02)
compared with control. Glucose disposal improved in the
moderate-intensity (65 % of VO2 peak) group to a similar
degree compared with control; however, this difference was
not statistically significant (16 %, P = 0.17). There were no
changes in body composition in any of the groups [18]. With
only 25 individuals divided among three exercise conditions,
the study may have been underpowered to detect differences
among the groups. Also, at 65 % of VO2 peak, the Bmoderateintensity exercise^ was a greater intensity than more contemporary studies, which typically define Bmoderate^ as 50 % of
VO2 peak.
Coker et al. also examined the effects of various degrees of
exercise intensity on insulin sensitivity in an elderly population
[19]. Twenty-one overweight (body mass index 29 1 kg/m2)
elderly individuals (age 74 1 years) were randomized to a 12week regimen, controlled for energy expenditure, of vigorousintensity exercise (75 % of VO2 peak, exact exercise regimen
not specified), moderate-intensity exercise (50 % of VO2 peak),
or sedentary controls. There were no changes in weight or body
fat composition in any of the groups. Glucose disposal, as measured by hyperinsulinemic-euglycemic clamp 72 h after the last
bout of training, improved only in the vigorous-intensity group.
Again, with only 21 individuals randomized to three groups, the
study may have been underpowered to detect differences
among the exercise regimens.
One of the largest studies to date to address the question of
exercise-intensity effect on insulin sensitivity enrolled 300
obese individuals (age 51 8 years, BMI 33 5 kg/m2) and
randomized them to a 24-week exercise regimen, controlled
for energy expenditure, of no-exercise control, low-amount/
low-intensity (50 % of VO2 peak achieved by brisk walking),
high-amount/low-intensity (50 % of VO2 peak achieved by
brisk walking), or high-amount/vigorous-intensity (75 % of
VO2 peak achieved by jogging) [20]. Insulin sensitivity was
measured by the 2-h glucose level after an oral glucose tolerance test performed 36-48 h after the last exercise bout at 16
and 24 weeks. All groups experienced a significant decrease
in waist circumference compared with the control group, but
there was no difference among the exercise groups. Only the
vigorous-intensity exercise group experienced a significant
change in 2-h glucose level compared with the control group.

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Curr Cardiol Rep (2016) 18:117

Our Studies of a Targeted Risk Reduction Intervention

through Defined Exercise (STRRIDE) study was a randomized controlled study of amount and intensity effects of exercise training on metabolic markers of cardiovascular risk.
Conducted during 19982003, we studied 260 men and women that were overweight or moderately obese (25 BMI (kg/
m2) 35) with atherogenic dyslipidemia (HDL 40 mg/dl for
men, 45 mg/l for women; 130 LDL (mg/dl) 190) [21].
Individuals were assigned to a 6-month no-exercise control
group or 8-month low-amount/moderate-intensity (1200 kcal;
800 MET-min at 4055 % VO2 peak; equivalent to brisk
walking 12 miles/week) per week, low-amount/vigorous-intensity (1200 kcal; 800 MET-min at 6075 % VO2 peak;
equivalent to jogging 12 miles/week) per week, or highamount/vigorous-intensity (2200 kcal; 1314 MET-min at
6075 % VO2 peak; equivalent to jogging 20 miles/week)
per week.
Compared with the no-exercise control group, all exercise
groups had beneficial effects on body weight and composition
[22], whole body insulin sensitivity [15], metabolic syndrome [23], and cardiorespiratory fitness variables [24].
However, moderate-intensity exercise was three times as effective at improving insulin action (Si) of an IVGTT as was
vigorous-intensity exercise (Fig. 1) [15]. Additionally,
moderate-intensity exercise improved the disposition index
(a marker of pancreatic beta-cell function) more than the calorically equivalent vigorous-intensity regimen [25]. These
findings were independent of weight loss or changes in body
composition.
It is important to note that, although the participants in
STRRIDE were all overweight or obese, they were not
selected according to glycemic traits. Sixty-four of the

260 participants had fasting glucose from 100 to 125 mg/

dl and seven participants had fasting glucose >125 mg/dl.
In STRRIDE-PD (ClinicalTrials.gov NCT00962962), we
randomized 195 sedentary 45- to 75-year-old adults with
body mass indices 25 to 35 kg/m2 and fasting plasma glucose between 95 and 125 mg/dl to 6-month exercise regimens of the following: (1) low-amount/moderate-intensity
exercise: exercise energy expenditure of 10 kcal per kg of
body weight per week (10 KKW) at 50 % VO 2 peak
(equivalent to walking 8.6 miles/week); (2) highamount/moderate-intensity exercise: 16 KKW at 50 %
VO2 peak (equivalent to walking 13.8 miles/week); (3)
high-amount/vigorous-intensity exercise: 16 KKW at 75 %
VO2 peak (equivalent to jogging 13.8 miles/week); (4)
clinical lifestyle intervention (diet + exercise): 10 KKW
at 50 % VO2 peak plus a calorically restricted diet designed to reduce body weight by 7 % over 6 months
[17]. For improvement in glucose tolerance (glucose area
under the curve of an oral glucose tolerance test measured
1624 h after the last exercise training bout), moderateintensity exercise was about four times as potent as was
vigorous-intensity exercise in these pre-diabetic subjects
(Fig. 1).
Additionally, moderate-intensity exercise in STRRIDE
improved metabolic syndrome variables compared with inactive controls while the same amount of vigorousintensity exercise had no effect on these variables [23].
The changes in the metabolic syndrome paralleled the
changes in insulin sensitivity seen with moderate- versus
vigorous-intensity exercise.
Regardless of the conflicting data presented above, one
conclusion is shared: compared to no exercise, either
moderate- or vigorous-intensity exercise improves markers
of insulin sensitivity.

Fig. 1 Effect of moderate- and vigorous-intensity aerobic exercise on

insulin sensitivity. a In STRRIDE, with the same amount of energy
expenditure (1200 kcal; 800 MET-min), moderate-intensity exercise
(4055 % VO2 peak) improved insulin sensitivity (Si) as measured by
IVGTT more than vigorous-intensity exercise (6075 % VO2 peak),
#
P < 0.05 versus low-dose vigorous-intensity exercise, *P < 0.05 versus

inactive controls [15]. Of note, too, is the dose effect of exercise: highdose (2200 kcal; 1314 MET-min) vigorous-intensity exercise improved Si
more than low-dose vigorous-intensity exercise. b In STRRIDE-PD,
moderate-intensity exercise improved insulin sensitivity as measured by
OGTT compared with calorically equivalent vigorous-intensity exercise
in pre-diabetic individuals, **P < 0.05 [17]

Moderate-Intensity Exercise Is Better

Curr Cardiol Rep (2016) 18:117

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Possible Mechanisms for Moderate Intensity?

Compliance with Ethical Standards

Based on the STRRIDE studies findingscalorically equivalent moderate-intensity exercise improves insulin action
more than vigorous-intensity exercisethe next logical step
is to find the mechanisms underlying this difference.
Understanding these mechanisms is important not only for
understanding the clinical implications of lifestylespecifically exercisefor preventing type 2 diabetes; this understanding also is important for the possible development of
pharmacologic exercise analogues and biochemical targets
for new drug therapies. Given the complexity of systemic
glucose homeostasis, which involves the interplay of multiple
organ systems, the search for mechanisms will not be easy. It
will require a comprehensive and integrative approach to simultaneously investigate whole body and skeletal metabolism
on both physiologic and molecular levels. To begin this endeavor, we used targeted metabolomics in skeletal muscle of
STRRIDE participants in an attempt to identify molecular
signatures that could differentiate exercise intensity groups
and relate to changes in insulin sensitivity [26]. Moderateintensity exercise of the same amount as vigorous-intensity
exercise resulted in significantly greater elevations of skeletal
muscle medium chain acylcarnitines and succinate; this implicates a differential metabolic response in muscle by exercise
intensity when controlling for exercise amount. Moreover,
these changes in metabolites were significantly related to
change in insulin sensitivity in response to exercise. These
findings suggest that moderate-intensity exercise may enhance the metabolism of fatty acid stores within skeletal muscle. Because lipid accumulation in skeletal muscle is associated with insulin resistance [27], moderate-intensity exercise
may, in part, improve insulin sensitivity by reducing lipid
stores in muscle.

Conflict of Interest Robert W. McGarrah, Cris A. Slentz, and William

E. Kraus declare that no relevant conflicts of interest exist.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.

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Conclusions
In an increasingly sedentary culture, the need for increased
physical activity to improve the overall health of the global
population is more urgent than ever. Of all the potential health
benefits of exercise, improved insulin sensitivity is one that
appears to respond differently to different intensities of calorically equivalent exercise regimens: the balance of evidence
points toward improved insulin sensitivity with moderateintensity exercise compared with vigorous-intensity exercise.
The mechanisms responsible for this difference are undoubtedly complex. However, modern physiologic and molecular
investigative tools are beginning to shed light on the underlying biology. With these discoveries comes the potential to
improve our understanding of how and why exercise impacts
metabolic health.

8.

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