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High-Intensity Intermittent Exercise: Methodological and Physiological Aspects

Article  in  International journal of sports physiology and performance · June 2013

DOI: 10.1123/ijspp.8.6.600 · Source: PubMed

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International Journal of Sports Physiology and Performance, 2013, 8, 600-610
© 2013 Human Kinetics, Inc.
www.IJSPP-Journal.com
BRIEF REVIEW

High-Intensity Intermittent Exercise:

Methodological and Physiological Aspects
Gerhard Tschakert and Peter Hofmann

High-intensity intermittent exercise (HIIE) has been applied in competitive sports for more than 100 years. In the
last decades, interval studies revealed a multitude of beneficial effects in various subjects despite a large variety
of exercise prescriptions. Therefore, one could assume that an accurate prescription of HIIE is not relevant.
However, the manipulation of HIIE variables (peak workload and peak-workload duration, mean workload,
intensity and duration of recovery, number of intervals) directly affects the acute physiological responses during
exercise leading to specific medium- and long-term training adaptations. The diversity of intermittent-exercise
regimens applied in different studies may suggest that the acute physiological mechanisms during HIIE forced
by particular exercise prescriptions are not clear in detail or not taken into consideration. A standardized and
consistent approach to the prescription and classification of HIIE is still missing. An optimal and individual
setting of the HIIE variables requires the consideration of the physiological responses elicited by the HIIE regi-
men. In this regard, particularly the intensities and durations of the peak-workload phases are highly relevant
since these variables are primarily responsible for the metabolic processes during HIIE in the working muscle
(eg, lactate metabolism). In addition, the way of prescribing exercise intensity also markedly influences acute
metabolic and cardiorespiratory responses. Turn-point or threshold models are suggested to be more appropriate
and accurate to prescribe HIIE intensity than using percentages of maximal heart rate or maximal oxygen uptake.

Keywords: interval exercise, HIIE prescription, acute responses, lactate steady state, turn-point concept

Interval exercise is a discontinuous mode of endurance
exercise that is characterized by relatively short bouts of
high-intensity workloads interspersed by periods of rest
or low-intensity activity. The rationale behind interval-
training programs is that the total accumulated time of
vigorous exercise is higher than could be achieved during
a single bout of continuous exercise at the same intensity
until exhaustion.1 Therefore, high-intensity interval training
is supposed to yield greater training effects on endurance
performance, particularly in highly trained athletes,2 but
nowadays it is also successfully applied in the rehabilita-
tion of different kinds of chronic diseases.3 A multitude
of investigations have revealed a wide range of beneficial
adaptations after high-intensity intermittent exercise (HIIE)
in various study populations. However, the interpretation of
these training effects is difficult if the acute physiological
responses during exercise are unknown or not indicated
as is the case in many published HIIE studies. Achieved
training adaptations are the consequence of a disturbance
of homeostasis during exercise (acute responses). The
extent of these acute physiological responses is strongly
influenced by the specific prescription of the single exer-
cise components such as intensity and duration of peak
workload and recovery phases.4 To date there is still a lack
The authors are with the Inst of Sports Science, University of
Graz, Graz, Austria.
of knowledge regarding the detailed acute physiological
responses induced by various interval-exercise regimens,
and a consistent systematic approach to the prescription of
intermittent exercise is still missing. It appears to be highly
important to understand, clarify, and standardize the meth-
odology of interval exercise to optimize training effects and
concurrently minimize health risks, particularly in patients
suffering from different kinds of diseases.3,5 Therefore, this
review focuses on the methodological aspects of interval
training and on the acute physiological mechanisms caused
by specific intermittent-exercise prescriptions.
Historical Review
As reviewed by Billat,6 interval training has been applied
in competitive sports since the beginning of the 20th
century. Middle- and long-distance runners such as the
Finnish athletes Hannes Kolehmainen (3-fold Olympic
champion in Stockholm 1912) and Pavoo Nurmi (9-fold
Olympic champion between 1920 and 1928) used inter-
val training to train at velocities close to their specific
competition velocity. In addition, cross-country running
and skiing at different intensities (uphill, downhill, and
in the flat), called “fartlek,” was included in the training
process of various endurance sports. The most famous
athlete to popularize interval training was Emil Zato-
pek, the Czechoslovakian runner and triple Olympic

600

gold medalist in 1952, who used short interval training
including up to 100 × 400-m runs interspersed by 200-m
recovery runs per day.6 At that time, the trainers used
specific competition velocities from 800 to 5000 m for the
prescription of interval intensity, not taking into account
any physiological parameters.6
The first description of interval training in a scientific
journal was made by Reindell and Roskamm in 1959.7 In
1960, the Swedish research group of Irma and Per Olaf
Astrand8 and Erik Hohwü Christensen9 published studies
on interval training, focusing on the acute responses of
lactate (La), oxygen uptake (VO2), and heart rate (HR)
during interval exercise of different work durations and
during continuous exercise. In their review in 1976, Saltin
et al10 pointed out the low blood La levels and the small
oscillations of VO2 between peak-workload and recovery
phases during short intervals (intervals with short work
duration), whereas long intervals (intervals with long work
durations) yielded high La levels and marked differences
between the VO2 values of work and recovery phases.
The aforementioned studies on interval training
focused on exercise performance improvements in
endurance athletes and used peak intensities between the
velocity at maximal La steady state (max LaSS) and the
minimal velocity eliciting maximal VO2max (vVO2max) or
slightly above.
However, during the last 20 years, interval training
has increasingly been applied also in recreationally active
individuals,3,11 as well as in team- and racket-sport play-
ers.12–14 As a consequence, higher peak workloads up to
maximal efforts were used in HIIE training and testing. The
so-called sprint interval training or repeated-sprint training
including short bouts of maximal intensity came into the
focus of exercise physiology research, and it was shown
that repeated brief maximal sprints induced similar effects
on the aerobic system in recreationally active individuals as
traditional endurance training, but in a very time-efficient
way (low-volume high-intensity interval training).3,15
In the last 10 years, interval exercise attained addi-
tional importance with respect to endurance training since
aerobic high-intensity interval training was applied not
only in healthy people but also in the rehabilitation of
different kinds of chronic diseases.16,17
Components
and Prescriptions of HIIE
In contrast to continuous exercise that only comprises
the workload intensity and the total duration, intermittent
exercise consists of 5 main components: peak workload
intensity (Ppeak), peak workload duration (tpeak), recovery
load (Prec), recovery duration (trec), and the mean load
(Pmean), of which the result of the latter 4 can be calculated
accordingly or set as a separate determinant.10 The number
of intervals which means the total exercise duration is a
further variable of HIIE prescription. In their recent review,
Buchheit and Laursen14 also mentioned the number of
series, the duration and intensities in recovery phases
Intermittent-Exercise Methodology   601
between the series and the exercise modality (eg, running
vs cycling) as further determinants of interval exercise.
However, they did not consider Pmean as a relevant variable.
Ppeak is usually set between the power output at the
anaerobic threshold2 and “all-out” exercise, and tpeak
ranges from a few seconds up to several minutes. The Ppeak
phases are separated by periods of low- (or moderate-)
intensity exercise or passive recovery with a trec that can
be shorter than, equal to, or longer than tpeak. Notably,
very sparse information is available concerning settings
of the Pmean. Given the different potential combinations
of Ppeak, tpeak, Prec, and trec, it is not surprising that there
is a plurality of diverse prescriptions for intermittent
exercise used in scientific studies and exercise training.
For example, Trapp et al18 applied sprint exercise for 8
seconds during work phases and slow pedaling for 12
seconds during recovery phases, whereas Helgerud et
al16 used (among others) 4-minute work phases at 90% to
95% HRmax and 3-minute recovery phases at 70% HRmax.
Despite this diversity of applied HIIE regimens,
beneficial effects could be achieved in different HIIE
studies and in various subjects (highly trained, as well as
healthy sedentary and diseased, individuals). Therefore,
one could assume that an accurate prescription of HIIE is
not relevant. However, the isolated manipulation of each
single variable presumably has a direct impact on acute
metabolic and cardiopulmonary (and neuromuscular)
responses during exercise.4 If 2 or more components are
manipulated simultaneously, the impacts on the physio-
logical responses are more complex and also more dif-
ficult to predict.14 These acute reactions lead to specific
medium- and long-term training adaptations on the one
hand, and on the other hand they might represent certain
health risks, particularly in diseased persons. Therefore,
the understanding of the acute physiological mechanisms
provoked by the manipulation of (interval) exercise set-
tings is of high relevance in exercise physiology research.
The variety of intermittent exercise regimens applied
in different studies may suggest that the acute physio-
logical responses during HIIE forced by particular exer-
cise prescriptions are not clear in detail or not taken into
consideration; a standardized and consistent approach to
the prescription of HIIE is still missing.
Shortcomings in Denominations
and Classifications of Intermittent
Exercise and in the Prescription
of Exercise Intensities
Denominations and Classifications
Besides the enormous variety in interval-exercise prescrip-
tions, there is, not less important, also an uncontrolled
growth of types and denominations of intermittent exer-
cise in the literature: intermittent exercise, interval-type
exercise, interval training, high-intensity interval training,
aerobic high-intensity interval training, repeated-sprint
exercise, sprint intervals, and low-volume high-intensity
602  Tschakert and Hofmann
interval training. A further problem is that the same terms
are diversely used by different authors: Burgomaster et al15
used the term low-volume high-intensity interval training
for sprint (all-out) intervals of 30 seconds, whereas Currie
et al19 used the same term for intermittent exercise at 89%
peak power output for 1 minute.
More important, the actual acute physiological
responses yielded by different interval regimens are not
considered for the denomination and classification of
intermittent exercise, except for the term aerobic HIIE.
However, there is only rare information about how aero-
bic is defined. Billat6 defined aerobic interval training as
training that elicits aerobic metabolism at a higher ratio
than anaerobic metabolism. With respect to the La shuttle
theory,20 we suggest to define the term aerobic as a bal-
anced condition between La production in the working
muscle and La elimination in the working muscle itself
and in the system (through other organs such as brain,
heart, liver, and resting skeletal muscles) resulting in a
blood La steady state.
In German textbooks of training science,21 intermit-
tent exercise is classified into 2 methods. One model is
Figure 1 — Suggested model for the classification of intermittent exercise. Abbreviations: PLTP2, second lactate turn point determined
in an incremental exercise test; Ppeak, peak workload during intermittent exercise; LaSS, blood lactate steady state.
characterized by rest periods that are terminated prema-
turely, permitting just partial but not full recovery; this
model is usually applied in HIIE studies (in German
called Intervallmethode). The other model includes
considerably long rest periods allowing full recovery
between the high-intensity exercise bouts (Wiederhol-
ungsmethode). Both methods are divided into the inten-
sity categories “extensive” and “intensive,” and these
intensity categories are divided again into subcategories
indicating the duration of peak workloads. Finally, a
certain range of recovery durations is assigned to each
subcategory.
However, physiological markers are also not suf-
ficiently taken into consideration for this model of
categorization of intermittent exercise. In addition, the
allocation of the actual acute physiological responses
to particular subcategories is partly incorrect due to the
relatively wide ranges of both the intensity categories
and the workload-duration categories.
Therefore, we recommend the application of the
model shown in Figure 1 for the classification of inter-
mittent exercise.

Prescription of Exercise Intensity
The intensity of intermittent exercise referred to in
German textbooks or applied in the first half of the 20th
century is prescribed by means of percentages of race
velocity. This mode of exercise-intensity setting is primar-
ily suitable for endurance athletes. However, team- and
racket-sport players, recreational athletes, and patients
need different approaches to exercise-intensity settings.
In a multitude of methodological investigations
and training-intervention studies, intermittent-exercise
intensity is set by means of percentages of maximum HR
(HRmax), HR reserve (HRR), maximum VO2 (VO2max),
and VO2 reserve. However, prescribing exercise inten-
sity via %HRmax (or HRR) and power outputs at fixed
%HRmax (or HRR) results in considerable interindividual
differences in relative Pmean, Ppeak, and Prec. As a conse-
quence, the cardiopulmonary and metabolic strain, as
well as exercise stimuli, is substantially different across
subjects, as well. This diversity is caused by different
types of HR-performance curve. This fact was recently
pointed out by Hofmann and Tschakert22 and previ-
ously shown by Hofmann et al23 and Wonisch et al24
Also, the setting of intermittent-exercise intensity by
means of %VO2max (or VO2 reserve) leads to substantial
differences in physiological demands across subjects.25
Particularly in intervals with long peak-load durations,
prescriptions of exercise intensities via %HRmax or
%VO2max are not appropriate since the heterogeneity of
acute physiological responses increases with the duration
of peak-workload phases.
Figure 2 — Three-phase model of lactate (La) metabolism during an incremental exercise test.22 Abbreviations: LTP1, first lactate
turn point determined in an incremental exercise test (IET); LTP2, second lactate turn point determined in IET; Pmax, maximal power
output from IET; M, working muscle; S, system; P, lactate production; E, lactate elimination.
Intermittent-Exercise Methodology   603
In addition, if exercise intensity is prescribed via
%HRmax, it is unclear how long it takes until each par-
ticipant reaches his or her individual target HR, and
no information is available about the power output
and the metabolic situation until target HR is reached.
Therefore, an accurate prescription of exercise intensity
by means of %HRmax—also for intermittent exercise
with short peak-load durations up to 30 seconds—is
not possible.
Another shortcoming of actual intermittent-
exercise prescriptions is that P mean is only rarely
considered despite the fact that it controls the acute
cardiorespiratory responses. However, already Astrand
et al8 mentioned the relevance of Pmean as they indicated
that HR and VO2 values oscillate around the average
power output.
Suggestions
Since the aforementioned classifications of intermittent
exercise do not consider the physiological reactions
elicited by the particular interval regimen, we want to
emphasize that exercise itself should be described in
terms of the metabolic response it elicits.26
It has been proven reasonable to prescribe exercise
intensities for continuous exercise with respect to the
first and second turn points for lactate (LTP1, LTP2)
or ventilation (VT1, VT2) determined in a preliminary
incremental exercise test (Figure 2).22,27 Therefore, we
suggest that also for the prescription of intermittent
exercise it is favorable to use submaximal thresholds or
604  Tschakert and Hofmann
turn points,14 as well as the maximal power output (Pmax)
from an incremental exercise test representing the indi-
vidual aerobic-exercise performance. The 2 thresholds
and 3 phases of metabolism, respectively, can also be
detected during a series of continuous (Figure 3) and
intermittent exercise.
Between rest and LTP1 (phase 1), all La produced
in the working muscles is aerobically eliminated in
the working muscles; therefore, there is a balance of
La production and elimination (La steady state) in the
working muscle; blood La values remain at resting
level. Between LTP1 and LTP2 (phase 2) La cannot be
oxidized in the skeletal muscle entirely and has to be
partly shifted into the blood, but it can be metabolized
by other organs. Therefore, in this phase there are
metabolically balanced (steady-state) conditions again,
but now on a systemic level. Above LTP2 (phase 3),
more La is produced in the working muscles than can
be muscularly and systemically eliminated, resulting
in a blood La accumulation (metabolically unbalanced
conditions, no La steady state).22
Concerning the mode of exercise-intensity prescrip-
tion, we suggest using %PLTP2 as Pmean, %Pmax as Ppeak,
and %PLTP1 as Prec and applying the equation Pmean = (Ppeak
× tpeak + Prec × trec)/(tpeak + trec) for intermittent exercise.
In addition, we emphasize that Pmean should not just be
calculated as the result of Ppeak, tpeak, Prec, and trec but
consciously set to consider cardiorespiratory strain during
intermittent exercise.
This new methodological approach enables the
correlation of physiological responses and adaptations
induced by interval-type exercise training to exercise
intensities related to the 3 individual phases of energy
supply. It is based on the turn-point concept,22 which is
strongly supported by the La shuttle theory.20
Figure 3 — Blood lactate (La) during continuous exercise at intensities corresponding to phase I, phase II, and phase III. Phase
I, range from rest to the first lactate turn point (LTP1)—blood La values show a steady state at resting level due to a metabolic
balance in the working muscle; phase II, range from LTP1 to second lactate turn point (LTP2)—blood La values are elevated but
show a steady state on a systemic level; phase III, range from LTP2 to maximal power output from incremental exercise test—no
La steady state is reached.
Acute Physiological Responses
to Manipulations of HIIE Variables
Creatine Phosphate, Oxymyoglobin
One of the most interesting questions in the context of
intermittent exercise is the energy yield for ATP resyn-
thesis obtained by anaerobic and/or aerobic metabolism.
Important and fundamental findings concerning the acute
metabolic (and cardiopulmonary) effects of intermittent
exercise were already revealed more than 50 years ago by
Irma and Per-Olaf Astrand, Bengt Saltin, Erik H. Chris-
tensen, and colleagues. They focused particularly on the
physiological impact of the combination of tpeak and Ppeak.
In the initial phase of work and, therefore, also
during the bulk of peak-workload phases of short inter-
vals, respiration and oxygen transport by the blood
to the working muscles does not reach the values that
correspond to the actual oxygen demand due to delayed
VO2 kinetics. Therefore, the energy for ATP resynthesis
must be obtained by means of intracellular stored oxygen
and/or anaerobically. In this regard, the importance of
oxymyoglobin as an intracellular oxygen store and of
creatine phosphate (CrP), an energy-rich phosphagen,
was emphasized by several authors since even high
energy demands are met by these pathways in the first few
seconds of work.1,8,10,14 The stores of oxymyoglobin and
CrP can be rapidly and fully restored during the recovery
periods, unless Ppeak is too high or the recovery phases
are too short or too intense.14
Lactate Metabolism
The fundamental studies of Astrand et al8 revealed that
long intervals of 2 or 3 minutes at intensities near the

power output at VO2max were extremely demanding,
yielding high blood La levels of 16.6 mmol/L. In contrast,
short intervals of 30 seconds or 1 minute at the same
peak and mean workload induced low blood La levels
of 2 mmol/L and were well tolerated for 1 hour. These
data were surprising given the high peak workloads,
but the results were supported by subsequent studies of
Christensen et al9 and Carlson and Pernow.28
It should be kept in mind that the La concentration in
the working muscle and in the blood reflects the concen-
tration of hydrogen (H+) ions at the particular site. The
H+ concentration is expressed by means of the pH value
and strongly influences the acid-base status. La and H+
ions are the result of the dissociation of lactic acid, which
is produced through anaerobic glycolysis.29
With respect to anaerobic metabolism during inter-
mittent exercise, it is assumed that metabolic acidosis
mainly takes place during the peak-workload phases.10
The rate of La production depends on Ppeak, the amount
of La production primarily depends on the product of
Ppeak × tpeak, and the blood La concentration results from
the balance between La production and elimination.20
Severe blood La accumulations can be evoked by exer-
cise durations of several minutes at workloads between
the power output at max LaSS (Pmax LaSS) and Pmax from
an incremental exercise test,8 but also by shorter exer-
cise phases of 30 seconds or more at all-out intensity
(eg, Wingate test).3 If such peak-workload periods are
applied in intermittent exercise, it is supposed that LaSS
cannot be reached. In contrast, intervals with short peak-
load durations of about 20 or 30 seconds (or less) have
been shown to be performed in LaSS conditions even if
Ppeak is markedly above the power output at max LaSS
(but below all-out exercise), although trec is not longer
than tpeak.8–10 In this case, La is produced in such small
amounts that the short recovery durations are sufficient
to reach a balance between La production and elimina-
tion.10 This means that the setting of the peak-workload
phases is a much more critical factor, whether blood La is
accumulating or not, than the duration of recovery phases.
This finding was already emphasized by Saltin et al.10 A
multitude of combinations of tpeak and Ppeak may lead to
LaSS, but one should be aware that La and, of course,
H+ concentrations (in muscle and blood) increase with
tpeak if Ppeak is set above the max LaSS.27,30,31 The higher
Ppeak is, the shorter tpeak has to be!
The advantage of a LaSS exercise is that it can be
sustained for a longer total time, resulting in a longer
accumulated training duration at high intensities than
with non-steady-state exercise.
In addition, however, HIIE that evokes high levels
of lactic acid production in the working muscle failing
to reach LaSS during total exercise duration hormonally
triggers specific responses32 and may elicit certain ben-
efits, particularly for athletes, such as the improvement
of La tolerance. In this regard, high intracellular lactic
acid levels and high blood La levels are thought to lead
Intermittent-Exercise Methodology   605
to a restriction of glycolysis during subsequent work
bouts due to a limitation of the enzyme phosphofructoki-
nase,33,34 forcing the organism to a greater contribution of
aerobic metabolism to ATP resynthesis despite workloads
above max LaSS. This mechanism may be a reason for
considerable improvements in VO2max after HIIE training
with long peak-load durations, such as the frequently
applied 4 × 4-minute HIIE protocol.16,17
However, given the marked acute physiological
responses during long intervals, the question arises as
to whether this interval regimen is suitable for diseased
individuals, as the health risks were shown to be higher.5
Our working group compared long and short inter-
vals matched by mean load and total exercise duration
in healthy individuals and subjects undergoing cardiac
rehabilitation. In both investigations, data showed signifi-
cantly higher La values during long HIIE than with short
HIIE. During long HIIE, the increase of net blood La, as
well as the respiratory-exchange ratio, became smaller
with each interval, suggesting a considerable lactic acid
production during the first peak-workload phase that led
to an inhibition of glycolysis in the following intervals
(unpublished results). These data support the results of
Von Duvillard et al35 obtained in elite alpine skiers.
VO2
VO2 is a metabolic parameter but is limited by the car-
diopulmonary system that transports O2 to the place of
oxygen consumption. Since the HIIE-induced responses
of cardiorespiratory parameters (eg, HR) are adapted to
Pmean, acute VO2 during intermittent exercise is also based
on Pmean. In this context, Astrand et al8 indicated that the
shorter the peak-workload duration is, the smaller is the
oscillation of acute VO2 values around the demand for
Pmean. These findings were supported by our own results
(Figure 4[a]).36 It was shown that in short intervals of 30
seconds or 1 minute only 63% VO2max was reached.8 In
contrast, Christensen et al9 found out that during interval
exercise with short high-intensity periods of 15 seconds at
the minimum vVO2max and with passive recovery phases
of 15 seconds, VO2max values were reached at the end
of exercise despite low blood La levels. During HIIE
with long peak-workload durations of 2 to 3 minutes at
the same peak workload, the VO2 oscillation increased,
reaching maximal VO2 values at the end of the peak-
workload periods. These findings were supported by
Seiler and Sjursen.37
In addition to %VO2max values, the time spent near or
at VO2max (t@VO2max) was reported to be a relevant crite-
rion concerning peripheral muscular and cardiovascular
effects of intermittent exercise.14 Therefore, the authors
emphasized that an optimal HIIE stimulus is one where
athletes maintain long periods of time above 90% of
their VO2max and that long peak-load durations of 2 to 3
minutes enabled a longer accumulated t@VO2max than
short HIIE. However, they primarily focused on the
606  Tschakert and Hofmann

(a) (b)

Figure 4 — (a) %VO2max and (b) %HRmax during short HIIE and CE matched by Pmean and total duration in young and healthy
sport students. Values did not show significant differences between tests despite substantially different peak workloads.36 CE: target
workload = 63% of Pmax, total duration = 28 min. Short HIIE: Pmean = 63% of Pmax, Ppeak = Pmax, tpeak = 20 s, Prec = slightly below
PLTP1, trec = calculated by means of the equation Pmean = (Ppeak × tpeak + Prec × trec)/(tpeak + trec). Abbreviations: VO2max, maximal oxygen
uptake assessed in an incremental exercise test (IET); HRmax, maximal heart rate assessed in an IET; HIIE, high-intensity intermittent
exercise; CE, continuous exercise; Pmean, mean workload during HIIE; Pmax, maximal power output assessed in an IET; Ppeak, peak
workload in HIIE; tpeak, duration of peak-workload phases; Prec, recovery load; trec, duration of recovery phases.

training goals of endurance athletes and to a lesser extent
on other athletes such as racket- and team-sport players
or on patients. Already more than half a century ago,
Astrand et al8 reported high training effects on circulation
and respiration induced by long intervals, but they also
pointed out the submaximal loading of the circulatory and
respiratory organs during short intervals, which is of high
practical and physiological interest in work physiology
and rehabilitation. We additionally want to emphasize that
intermittent exercise with a long tpeak may enable higher
%VO2max and t@VO2max values, but at the same time long
intervals may also lead to high La and low pH values.
Midgley and McNaughton38 suggested using short
peak-load durations of 15 to 30 seconds and workload
intensities between 90% and 105% vVO2max to increase t@
VO2max; however, they thereby suggest a Prec between 50%
vVO2max and the La-threshold velocity and a preliminary
5- to 10-minute warm-up period performed 1 to 2 km/h
below the La-threshold velocity to reach VO2max values as
quickly as possible during the subsequent work phases.
In the last decade, more investigations have revealed
that even sprint-interval training with a short tpeak of 30
seconds11,15,39 or even less than 10 seconds18 yielded
significant improvements in endurance performance and
VO2max. Exercise intensity was reported to be the most
important factor concerning training adaptations.38 Evi-
dence suggests that improvements of peripheral muscular
oxidative capacity and consequently of VO2max and aero-
bic performance are related to exercise intensity.40 Bartlett
et al41 and Gibala et al3 pointed out that exercise intensity
is thought to be the key factor of activation of peroxisome
proliferator-activated receptor γ coactivator-1α (PGC-
1α), the master regulator of mitochondrial biogenesis in
muscle, and of expression of PGC-1α mRNA.40
Therefore, the question arises as to whether either the
high percentages of VO2 or the high peak power outputs
cause the considerable aerobic effects after HIIE.
In this regard, the improvements in VO2max revealed
in sprint-interval studies were mainly due to adaptations
of the muscular oxidative potential, such as increases in
mitochondrial content and mitochondrial enzyme activity.
Effects on cardiac function would need peak-load dura-
tions of at least 2 or 3 minutes.14 However, Helgerud et
al16 revealed no significant differences in the increase of
VO2max and stroke volume (SV) between short HIIE with
a tpeak of 15 seconds and the 4 × 4-minute HIIE matched
for total work.
The assumption that short intervals more likely can
be sustained for a longer overall time than long HIIE is
supported by respiratory-exchange-ratio values that were
found to be higher during long HIIE than during short
HIIE.9 This indicates a higher contribution of fat oxida-
tion to energy yield during short HIIE than with long
HIIE, but no explicit data could be found on this subject.
However, Christmass et al42 compared the rates of sub-
strate oxidation during 2 different HIIE regimens with a
work-to-rest ratio of either 6:9 or 24:36 seconds (whereby
even HIIE with a tpeak of 24 s is usually not characterized
as a long interval). They showed a significantly higher fat
and lower carbohydrate oxidation with concurrent lower
La and pyruvate levels, as well as, surprisingly, higher
VO2 values during the shorter intervals.
Cardiac Output
HR.  Astrand et al 8 emphasized that in HIIE with
long tpeak of 3 minutes, the oscillations of HR values
between the peak-workload phases (188 beats/min)

and recovery periods (118 beats/min) were shown to be
great, reaching high peak values. In contrast, mean- and
peak-load-matched short intervals (tpeak = 30 s) led to
much smaller HR oscillations (150–137 beats/min) and
accordingly to HR values that were similar to mean-load-
matched constant-load-exercise HR. This is remarkable
given the fact that peak workload was twice as high
in short intervals as in continuous exercise. However,
the oscillation peak and minimum HR values around
HRmean were small during short HIIE because of the
short tpeak, and HRmean (similarly to VO2mean as mentioned
before) follows Pmean. These results were supported by
investigations of our own working group as shown in
Figure 4(b).36
In this regard, it is important to point out that the
acute HR during intermittent exercise does not neces-
sarily give information concerning the peripheral-muscle
metabolic strain. Relatively low HR values can be accom-
panied by extremely high lactate levels, nearly reaching
maximal values. Therefore, lactate measures in interval
exercise studies are highly relevant.
SV.  Common opinion often prevails that during
recovery phases of intermittent exercise, improvements
in cardiac function are achieved through an increase of
left-ventricular (LV) volume (a decreased peripheral
resistance leads to an enhanced end-diastolic volume
[EDV] and SV).14,43 However, investigations of Pokan et
al44 revealed that in sport students, the LVEDV decreased
during recovery from incremental exercise. Since the SV
remained unchanged, there was an increase in LV ejection
fraction (the percentage of SV at LVEDV) immediately
after exercise. It was pointed out by the authors that
this enhancement of LV ejection fraction was not the
result of an improved cardiac output but was caused by
a reduction of the left ventricle along with an unchanged
SV after the end of exercise. These findings are supported
by Dawson et al.45
Intensity and Duration
of Recovery Phases
Although both time and intensity of peak workloads are
suggested to be primarily responsible for the extent of
acute physiological responses to intermittent exercise,
the applied intensity and duration of recovery phases are
also relevant variables. On the one hand, the setting of
recovery phases affects the VO2 values during recovery,
influencing the time that is necessary to reach VO2max
values during the following peak-workload phases. On
the other hand, Prec and trec affect the muscle metabolic
recovery that is crucial to maximize the work capacity
during the subsequent intervals.14 The muscle metabolic
recovery was reported to be manipulated by several
variables.
The decrease of blood H+ and La concentrations
during recovery became greater with recovery duration.46
The optimal recovery intensity to reduce blood La is con-
troversially discussed, but it is supposed to be between
Intermittent-Exercise Methodology   607
rest (passive recovery) and PLTP1 since at this range of
intensities no “new” lactate is shifted from the muscle
into the blood. However, Hermansen and Stensvold47
showed that blood La removal was faster when recovery
intensity was higher (up to 65% VO2max), concluding that
an active recovery facilitates La oxidation in the working
muscles. Repeated-sprint performance, CrP resynthesis,
and muscle oxygenation were reported to be lower when
using active recovery compared with passive recovery.14
The resynthesis of CrP,14 as well as the restoration of
the oxymyoglobin store in the working muscle,8 was
shown to be impaired only if trec was too short. Seiler and
Hetlelid48 found out that moderately trained runners who
were asked to self-select their recovery modality during
HIT preferred a walking (low-intensity) recovery mode.
An additional aspect is that if the aforementioned
equation, Pmean = (Ppeak × tpeak + Prec × trec)/(tpeak + t rec), is
applied for the prescription of HIIE, and if Pmean, Ppeak,
and tpeak are matched, a passive recovery mode entails a
much shorter recovery duration than an active recovery
mode, so the acute physiological responses (even the
cardiorespiratory responses) might be markedly higher
during HIIE with passive recovery.
Practical Applications
To prescribe HIIE intensity by means of %Pmax, PLTP2
(or PVT2), and PLTP1 (or PVT1) assessed in a preliminary
incremental exercise test allows for an individual and
very accurate setting of each single interval parameter.
This is of high relevance in scientific studies, as well as
in the training process of athletes and patients. However,
the implementation of HIIE training in the field, particu-
larly in groups, might be difficult since Ppeak and Prec are
thought not to be controlled by HR but by power output
(velocity or Watts). This problem can be solved if the
velocities of work and rest phases are set by means of
time per distance or controlled by a pacer.
In addition, this HIIE prescription mode based on
the equation Pmean = (Ppeak × tpeak + Prec × trec)/(tpeak + t rec)
has another interesting aspect. Through the manipulation
of trec, different mean workloads (Pmean) can be gained.
Given a short tpeak (which is associated with a low La
production), Pmean and cardiorespiratory strain can be sub-
stantially reduced by an extension of trec, and therefore we
suggest that this type of HIIE can be applied within high-
volume training in the first preparatory period despite
high peak workloads. This is particularly important for
endurance athletes, who are reported to spend 70% to
80% of their total training volume in zone 1 (below 60%
VO2max or 70% HRmax).49 In contrast, if trec is shortened
(or tpeak is lengthened), Pmean (and cardiorespiratory strain)
increases, and this interval type can be used directly
before the competition period, depending on the structure
of the specific sport.
By this means, the application of high intensities
between PLTP2 and all-out exercise are of high relevance
not only for endurance athletes50 but also more for
608  Tschakert and Hofmann
racket- or team-sport players, since repeated-sprint abil-
ity is thought to be main aspect of competition in this
kind of sport.12
Conclusions
There is a large variety in HIIE regimens applied in exer-
cise training and scientific studies, and a standardized
and consistent model for the prescription and classifica-
tion of HIIE is still missing. In this regard, we suggest
that turn-point or threshold models are the appropriate
solution to achieve homogeneous exercise stimuli across
subjects in contrast to the use of percent HRmax and
VO2max. In addition, the HIIE prescription mode based
on the equation Pmean = (Ppeak × tpeak + Prec × trec)/(tpeak
+ t rec) represents a systematic and consistent approach
to standardize HIIE methodology. The prescription of
intermittent exercise substantially affects the level of
acute physiological responses and, later, the attainment
of specific training adaptations. The physiological
reactions induced by intermittent exercise, such as La
production and elimination or %VO2max, should be taken
into account for the setting of the HIIE variables Ppeak,
tpeak, Prec, trec, and Pmean and for the classification and
denomination of intermittent exercise.
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