J Physiol 590.

5 (2012) pp 1077–1084 1077

Physiological adaptations to low-volume, high-intensity

interval training in health and disease
Martin J. Gibala1 , Jonathan P. Little2 , Maureen J. MacDonald1 and John A. Hawley3
1
Department of Kinesiology, McMaster University, Hamilton, Ontario L8S 4K1, Canada
2
School of Arts and Sciences, University of British Columbia Okanagan, Kelowna, British Columbia V1V 1V7, Canada
3
Exercise Metabolism Group, RMIT University, Bundoora, Victoria 3083, Australia

Abstract Exercise training is a clinically proven, cost-effective, primary intervention that delays
and in many cases prevents the health burdens associated with many chronic diseases. However,
the precise type and dose of exercise needed to accrue health benefits is a contentious issue
with no clear consensus recommendations for the prevention of inactivity-related disorders and
chronic diseases. A growing body of evidence demonstrates that high-intensity interval training
The Journal of Physiology

(HIT) can serve as an effective alternate to traditional endurance-based training, inducing similar
or even superior physiological adaptations in healthy individuals and diseased populations, at
least when compared on a matched-work basis. While less well studied, low-volume HIT can
also stimulate physiological remodelling comparable to moderate-intensity continuous training
despite a substantially lower time commitment and reduced total exercise volume. Such findings
are important given that ‘lack of time’ remains the most commonly cited barrier to regular exercise
participation. Here we review some of the mechanisms responsible for improved skeletal muscle
metabolic control and changes in cardiovascular function in response to low-volume HIT. We
also consider the limited evidence regarding the potential application of HIT to people with, or
at risk for, cardiometabolic disorders including type 2 diabetes. Finally, we provide insight on the
utility of low-volume HIT for improving performance in athletes and highlight suggestions for
future research.

(Received 16 November 2011; accepted after revision 23 January 2012; first published online 30 January 2012)
Corresponding author M. J. Gibala: Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton,
Ontario, L8S 4K1 Canada. Email: [email protected]
Abbreviations HIT, high-intensity interval training; PGC-1α, peroxisome-proliferator activated receptor γ coactivator;
PPO, peak aerobic power output.

Introduction of vigorous activity, interspersed by periods of rest or

low-intensity exercise. HIT is infinitely variable with the
High-intensity interval training (HIT) describes physical specific physiological adaptations induced by this form of
exercise that is characterized by brief, intermittent bursts

Martin Gibala (pictured) is Professor and Chair of the Department of Kinesiology at McMaster University. He studies the
regulation of skeletal muscle energy metabolism including the impact of nutrition and training on exercise performance.
Maureen MacDonald is also a Professor of Kinesiology at McMaster, where she studies the effect of exercise on cardiovascular
regulation. Jonathan Little completed doctoral studies at McMaster and is currently a postdoctoral fellow at the University
of British Columbia. John Hawley is Professor and Head of the Exercise Metabolism Group at RMIT University, whose focus
is skeletal muscle energy metabolism related to exercise and diabetes.

This review is from the symposium Exercise metabolism at The Biomedical Basis of Elite Performance, a joint meeting of The Physiological Society
and the British Pharmacological Society, together with The Journal of Physiology, Experimental Physiology, British Journal of Pharmacology and The
Scandinavian Journal of Medicine and Science in Sports, at the Queen Elizabeth Hall, London on 20 March 2012.


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1078 M. J. Gibala and others J Physiol 590.5

Table 1. Summary of protocols in studies from our laboratory that directly compared 6 weeks of either high-intensity interval training
(HIT) or traditional endurance training

Variable HIT group Endurance group

Protocol 30 s × 4–6 repeats, 4.5 min rest (3 sessions per week) 40–60 min cycling (5 sessions per week)
Training intensity (workload) ‘All out’ maximal effort (∼500 W) 65% of V̇O2 peak (∼150 W)
Weekly training time commitment ∼10 min (∼1.5 h including rest) ∼4.5 h
Weekly training volume ∼225 kJ ∼2250 kJ

From Burgomaster et al. (2008). V̇O2 peak , peak oxygen uptake.

training determined by a myriad of factors including the exercise during a training session that lasts ∼20 min. As
precise nature of the exercise stimulus (i.e. the intensity, little as six sessions of this type of training, totalling
duration and number of intervals performed, as well ∼15 min of all out cycle exercise over 2 weeks, increased
as the duration and activity patterns during recovery). skeletal muscle oxidative capacity as reflected by the
When compared on a matched-work basis or when maximal activity and/or protein content of mitochondrial
estimated energy expenditure is equivalent, HIT can serve enzymes (Burgomaster et al. 2005; Gibala et al. 2006).
as an effective alternate to traditional endurance training, We have also directly compared 6 weeks of Wingate-based
inducing similar or even superior changes in a range of HIT with traditional endurance training that was designed
physiological, performance and health-related markers according to current public health guidelines (Table 1)
in both healthy individuals and diseased populations (Burgomaster et al. 2008; Rakobowchuk et al. 2008). We
(Wisloff et al. 2007; Tjonna et al. 2009; Hwang et al. found similar training-induced improvements in various
2011). Less is known regarding the effects of low-volume markers of skeletal muscle and cardiovascular adaptation
HIT, but growing evidence suggests this type of training despite large differences in weekly training volume
stimulates physiological remodelling comparable with (∼90% lower in the HIT group) and time commitment
moderate-intensity continuous training despite a sub- (∼67% lower in the HIT group). In addition to an
stantially lower time commitment and reduced total increased skeletal muscle oxidative capacity (Fig. 1), other
exercise volume (Gibala & McGee 2008). These findings endurance-like adaptations have been documented after
are important from a public health perspective, given several weeks of low-volume HIT including an increased
that ‘lack of time’ remains one of the most commonly resting glycogen content, a reduced rate of glycogen
cited barriers to regular exercise participation (Stutts utilization and lactate production during matched-work
2002; Trost et al. 2002; Kimm et al. 2006). Moreover, exercise, an increased capacity for whole-body and skeletal
recent evidence suggests that HIT is perceived to be more muscle lipid oxidation, enhanced peripheral vascular
enjoyable than moderate-intensity continuous exercise structure and function, improved exercise performance
(Bartlett et al. 2011). Here we review some of the as measured by time-to-exhaustion tests or time trials
mechanisms responsible for improved skeletal muscle and increased maximal oxygen uptake (Burgomaster et
metabolic control and changes in cardiovascular function al. 2005, 2008; Gibala et al. 2006; Rakobowchuk et al.
in response to low-volume HIT, as well as the potential 2008).
health-related implications for patients with chronic Wingate-based HIT is, however, extremely demanding
diseases including type 2 diabetes and cardiovascular and may not be safe, tolerable or appealing for some
disease. We also speculate on the practical application individuals. We therefore sought to design a more practical
of low-volume HIT for elite performance. Although it is model of low-volume HIT that is time efficient while
recognized that the underlying mechanisms are probably also having wider application to different populations
different compared with less-trained subjects (Iaia & including people at risk for chronic metabolic diseases. To
Bangsbo 2010), responses in elite athletes may help our accomplish this goal we decreased the absolute intensity of
understanding of why low-volume HIT is such a potent the work bouts, but increased their duration and shortened
exercise stimulus. the rest intervals. Our new practical HIT model consists
of 10 × 60 s work bouts at a constant-load intensity that
elicits ∼90% of maximal heart rate, interspersed with
Physiological remodelling after low-volume HIT 60 s of recovery. The protocol is still time efficient in
The most common model employed in low-volume HIT that only 10 min of exercise is performed over a 20 min
studies has been the Wingate test, which consists of a 30 s training session. Importantly, this practical, time-efficient
‘all out’ cycling effort against a supra-maximal workload. HIT model is still effective at inducing rapid skeletal
Subjects typically perform four to six work bouts separated muscle remodelling towards a more oxidative phenotype,
by ∼4 min of recovery, for a total of 2–3 min of intense similar to our previous Wingate-based HIT studies and


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J Physiol 590.5 Adaptations to low-volume, high-intensity interval training 1079

The molecular mechanisms underlying skeletal muscle

metabolic adaptations to low-volume HIT have recently
been investigated. Given the potency of HIT to increase
mitochondrial capacity, it is perhaps not surprising that
investigations have examined the influence of low-volume
HIT on the activation of peroxisome-proliferator activated
receptor γ coactivator (PGC)-1α, which is regarded as the
‘master regulator’ of mitochondrial biogenesis in muscle
(Wu et al. 1999). Evidence suggests that exercise intensity
is the key factor influencing PGC-1α activation in human
skeletal muscle (Egan et al. 2010). In this respect, acute
low-volume Wingate-based HIT increases PGC-1α mRNA
by several-fold when measured 3 h post-exercise (Gibala
et al. 2009; Little et al. 2011b). This is comparable with the
acute increase in PGC-1α mRNA expression observed after
a bout of continuous endurance-type exercise (Norrbom
et al. 2004; Egan et al. 2010). Similar to endurance
exercise (Wright et al. 2007; Little et al. 2010a), acute
Wingate-based HIT may activate PGC-1 by increasing its
nuclear translocation (Little et al. 2011b). The increase
in nuclear PGC-1 following low-volume HIT coincides
with increased mRNA expression of several mitochondrial
Figure 1. Peak oxygen uptake (top panel) and the maximal genes (Little et al. 2011b), suggesting that a program
activity of the mitochondrial enzyme citrate synthase of mitochondrial adaptation is engaged with these short
measured in biopsy samples (bottom panel) obtained before
bursts of intensity exercise (Fig. 2).
(PRE) and after (POST) 6 weeks of Wingate-based
high-intensity interval training (HIT) or traditional The upstream signals that activate PGC-1α and
moderate-intensity endurance training (ET) mitochondrial biogenesis in response to low-volume HIT
Total exercise volume was 90% lower in the HIT group. Redrawn have not been clearly elucidated but probably relate to
from Burgomaster et al. (2008) with permission. ∗ P  0.05 vs Pre; robust changes in intramuscular ATP:ADP/AMP ratio
main effect for time.
following exercise (Chen et al. 2000) and the concomitant
high-volume endurance training (Little et al. 2010b). Both activation of 5’-adenosine monophosphate-activated
types of low-volume HIT protocols are also effective for protein kinase (AMPK) (Gibala et al. 2009; Little et al.
improving functional performance, as shown by cycling 2011b). Activation of p38 mitogen-activated protein
time trials that resemble normal athletic competition kinase (MAPK), possibly via increased generation of
(Gibala et al. 2006; Little et al. 2010b). reactive oxygen species (ROS) (Kang et al. 2009), may

Figure 2. Potential intracellular signalling

mechanisms involved in HIT-induced
mitochondrial biogenesis
Low-volume HIT has been shown to activate
5’-AMP-activated protein kinase (AMPK) and
p38 mitogen-activated protein kinase (MAPK).
Both of these exercise-responsive signalling
kinases are implicated in direct phosphorylation
and activation of PGC-1α. Increased nuclear
abundance of PGC-1α following HIT is
hypothesized to co-activate transcription
factors (TF) to increase mitochondrial gene
transcription, ultimately resulting in
accumulation of more mitochondrial proteins
to drive mitochondrial biogenesis.


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1080 M. J. Gibala and others J Physiol 590.5

also be involved (Gibala et al. 2009; Little et al. 2011b). increased endothelial function in the trained legs to an
Elevated levels of PGC-1 protein also accompany increased extent that is comparable to changes observed after a
markers of mitochondrial content following a period much higher volume of continuous moderate-intensity
of low-volume HIT. Six weeks of Wingate-based HIT training (Rakobowchuk et al. 2008). The mechanisms
increased the protein content of PGC-1 by ∼100% in regulating cardiovascular adaptations to various forms
young, healthy individuals (Burgomaster et al. 2008) of low-volume HIT have yet to be comprehensively
and 2 weeks of 10 × 1 min HIT resulted in a ∼25% examined.
increase in nuclear PGC-1 protein (Little et al. 2010b).
Collectively, these results indicate that PGC-1α is probably
involved in regulating some of the metabolic adaptations Potential application of HIT in people with or at risk
to low-volume HIT. Given the positive effects that a modest
for cardiometabolic disorders
increase in muscle PGC-1α appears to have on oxidative
capacity, anti-oxidant defence, glucose uptake, resistance While much of the work conducted to date has involved
to age-related sarcopenia and anti-inflammatory pathways relatively high-volume protocols that are comparable in
(Sandri et al. 2006; Benton et al. 2008; Wenz et al. 2009), volume to traditional endurance training, HIT has been
the increase in PGC-1α following low-volume HIT may shown to improve cardiorespiratory fitness in a range of
highlight potential widespread health benefits for this type populations including those with coronary artery disease,
of exercise. congestive heart failure, middle age adults with metabolic
The impact of interval types of training programs syndrome and obese individuals (Warburton et al. 2005;
on cardiovascular structure and function has also been Wisloff et al. 2007; Moholdt et al. 2009; Munk et al.
investigated (Wisloff et al. 2009), but few studies have 2009). In many cases, the increase in cardiorespiratory
utilized low-volume HIT models. However, as little as fitness after HIT was superior to after continuous
2 weeks of Wingate-based HIT has been reported to moderate-intensity training (Wisloff et al. 2007; Tjonna et
increase cardiorespiratory capacity as reflected by changes al. 2008, 2009; Moholdt et al. 2009). Endothelial function,
in peak oxygen uptake (V̇O2 peak ) (Whyte et al. 2010) assessed using flow-mediated dilatation of the brachial
although this is not a universal finding (Burgomaster artery, is improved to a greater extent following HIT
et al. 2005). Another study showed that 6 weeks of compared with continuous moderate-intensity training
Wingate-based HIT increased V̇O2 peak to the same extent (Wisloff et al. 2007; Tjonna et al. 2008, 2009; Moholdt
as traditional endurance training despite a markedly et al. 2009). Other studies have documented beneficial
reduced time commitment and total training volume changes in various components of resting blood pressure
(Burgomaster et al. 2008). We have also shown in (Rognmo et al. 2004; Schjerve et al. 2008; Whyte et al. 2010)
young healthy men and women that low-volume HIT and left ventricular morphology (Wisloff et al. 2007). It
increases compliance in peripheral but not central appears that this type of cardiac remodelling requires a
arteries (Rakobowchuk et al. 2008). The protocol also longer duration of training and greater exercise volume
than the load required to alter cardiorespiratory fitness
or peripheral vascular structure and function. It could be
that the short intense bursts of activity with low-volume
HIT induce large-magnitude increases in cellular and peri-
pheral vascular stress, while effectively ‘insulating’ the
heart from those stresses due to the brief duration of
the exercise bouts. This relative central insulation permits
individuals to train at much higher intensities than they
would otherwise, but may also result in different timelines
and effective stimulus loads between the central and peri-
pheral components of the cardiovascular system.
Low-volume HIT studies in persons who might be
at risk for cardiometabolic disorders or patients with
Figure 3. The effect of varying the intensity of interval chronic disease are very limited. However, recent work has
training on changes in 40 km time-trial performance shown that as few as six sessions of either Wingate-based
Well-trained male cyclists were randomly assigned to one of five HIT and the more practical constant-load model over
different doses of high-intensity interval training (HIT): 12 × 30 s at 2 weeks improve estimated insulin sensitivity in previously
175% of peak sustained power output (PPO), 12 × 1 min s at 100%
sedentary, overweight individuals (Whyte et al. 2010;
PPO, 12 × 2 min at 90% PPO, 8 × 4 min at 85% PPO, or 4 × 8 min
at 80% PPO. Cyclists completed six HIT sessions over a 3 week Hood et al. 2011). Insulin sensitivity in these studies
period in addition to their habitual aerobic base training. Redrawn was calculated based on either single fasting glucose
from Stepto et al. (1999) with permission. and insulin measurements (Hood et al. 2011) or the


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J Physiol 590.5 Adaptations to low-volume, high-intensity interval training 1081

response to an oral glucose tolerance test (Whyte et al. V̇O2 peak ) work bouts undertaken twice a week throughout
2010) and therefore primarily reflects hepatic as opposed a 3 week intervention period (see Hawley et al. 1997
to peripheral (skeletal muscle) insulin sensitivity. Peri- for review). We systematically examined the effect
pheral insulin sensitivity following exercise training may of this interval training protocol on a variety of
be improved by increased skeletal muscle glucose trans- outcome measures including performance (Lindsay et al.
port capacity, mediated in part by the protein GLUT4. 1996; Stepto et al. 1999), skeletal muscle metabolism
Skeletal muscle GLUT4 content after short-term HIT is (Westgarth-Taylor et al. 1997; Stepto et al. 2001), cell
increased by a comparable magnitude (∼2-fold) to that signalling (Yu et al. 2003; Clark et al. 2004) and the
observed after high-volume endurance training (Hood et interaction of HIT with various diet manipulations
al. 2011). We also recently demonstrated that low-volume (Stepto et al. 2002; Yeo et al. 2008). Stepto et al. (1999)
HIT was well tolerated and rapidly improved skeletal employed a novel approach to determine the effects
muscle GLUT4 content in eight patients with type 2 of divergent interval training protocols on performance
diabetes (Little et al. 2011a). This small pilot study also lasting ∼1 h by fitting polynomial or other curves
showed that six sessions of HIT over 2 weeks reduced to the responses for each interval training dose for
average 24 h blood glucose concentration and post- individual athletes. As we originally hypothesized, training
prandial glucose excursions, measured via continuous sessions that employed work bouts that were closely
glucose monitoring under standardized diet but otherwise matched to race-pace (8 × 4 min at 85% of peak aerobic
free-living conditions (Little et al. 2011a). These beneficial power output (PPO)) significantly enhanced performance
adaptations were realized even though the weekly training (2.8%, 95% CI = 4.3–1.3%). Yet, somewhat surprisingly,
time commitment was much lower than common public short-duration, supra-maximal work bouts (12 × 30 s
health guidelines that generally call for at least 150 min at 175% of PPO) were just as effective in improving
of moderate to vigorous exercise per week to promote performance (2.4%, 95% CI = 4.0–0.7%). Consistent
health. While the preliminary evidence from these with this observation, Psilander et al. (2010) recently
small, proof-of-principle studies are intriguing, large-scale reported that a single bout of low-volume HIT (7 × 30 s
studies are clearly needed to resolve whether low-volume ‘all out’ efforts) stimulated increases in mitochondrial
HIT is a realistic, time-efficient exercise alternative to gene expression that were comparable to or greater than
reduce the risk of cardiometabolic disease or improve the changes after more prolonged (3 × 20 min bouts
health and wellbeing in patients with chronic disease. at ∼87% of V̇O2 peak ) endurance exercise in well-trained
cyclists. Given the lower volume of work and the fact
HIT and athletic performance that mitochondrial transcription factor A, the down-
stream target of PGC-1α, was only increased after the 30 s
HIT has been an integral part of training programs for the protocol, the authors concluded that brief intense inter-
enhancement of athletic performance since the beginning val training might be a time-efficient strategy for highly
of the 19th century. Yet despite being a core component trained individuals.
of competition preparation, the unique effect of specific Guellich and colleagues (2009) have recently extended
training interventions on the performances of well-trained our early findings (Stepto et al. 1999, Fig. 3) that
individuals is sparse. This, perhaps, is understandable ‘polarized training’ enhanced endurance performance.
for several practical reasons. First, exercise physiologists These workers reported that elite endurance athletes from
have found it difficult to convince elite athletes that it a range of sports including rowing, running, cycling and
could be worthwhile to experiment with their normal cross-country skiing perform only a small portion of
training programs. Second, even if athletes (and their their training at competition/race-pace intensities, with
coaches) were willing to modify their training practices, the bulk of their workload comprising low-intensity,
conventional approaches to investigate the response to high-volume workouts, and exposure to extreme HIT
different doses of a treatment (i.e. interval training) using sessions. In a recent review Laursen (2010) proposed
repeated-measures design in which each athlete receives that a polarized approach to training, in which ∼75%
all the different doses is totally impractical for studies of of total training volume be performed at low intensities,
physical training; the long-lasting effects of any given dose with 10–15% performed at supra-maximal intensities may
of training prevent athletes from receiving more than one be the optimal training intensity distribution for elite
dose of the treatment. athletes who compete in intense endurance events. We
Over a decade ago we embarked on a series of suggest that the unique genetic and/or molecular signature
investigations into the effects of interval training in resulting from polarized training is a fertile area for
competitive endurance athletes using a standardized future research. Indeed, directly linking exercise-induced
training protocol, namely, replacing a portion (∼15–20%) signalling cascades in skeletal muscle to defined metabolic
of an athletes’ aerobic base training with six to eight responses and specific changes in gene and protein
sessions of continuous (5 min) high-intensity (90% of expression that occur after diverse interval training


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1082 M. J. Gibala and others J Physiol 590.5

regimens may provide clues as to why HIT is such a Benton CR, Nickerson JG, Lally J, Han XX, Holloway GP, Glatz
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Conclusion and directions for future research Burgomaster KA, Howarth KR, Phillips SM, Rakobowchuk M,
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Considerable evidence currently exists to support a role for metabolic adaptations during exercise after low volume
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interval training to maximize cardiac benefits of exercise
training? Exerc Sport Sci Rev 37, 139–146. Work cited from the authors’ laboratories has been supported
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Holloszy JO (2007). Exercise-induced mitochondrial of Canada, the Canadian Institutes of Health Research, the
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C 2012 The Physiological Society