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The Scientific Basis for High-Intensity
Interval Training
Optimising Training Programmes and Maximising
Performance in Highly Trained Endurance Athletes
Paul B. Laursen and David G. Jenkins
School of Human Movement Studies, University of Queensland, Brisbane, Australia ((Author:
please confirm that both authors share this affiliation.)),
Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Endurance Training in the Untrained and Recreationally Active . . . . . . . . . . . . . . . . . . .
1.1 Submaximal Endurance Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2 High-Intensity Interval Training (HIT) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2. Endurance Training in Highly Trained Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1 Submaximal Continuous Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2 HIT
2.2.1 Quantifying the Demands of HIT in Highly Trained Athletes . . . . . . . . . . . . . . . . .
2.2.2 The Influence of HIT on Performance and Related Variables . . . . . . . . . . . . . . . .
2.2.2 Potential Mechanisms to Improved Performance . . . . . . . . . . . . . . . . . . . . . .
2.2.3 Enhanced Physiological Efficiency: An Issue of Practical Versus Statistical
Significance? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3. HIT Programme Optimisation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1 Significance of the Time to Exhaustion at the Velocity at Which V
.
O
2max
is
Achieved (V
max
) [T
max
] in Highly Trained Runners . . . . . . . . . . . . . . . . . . . . . . . .
3.1.1 Use of T
max
to Prescribe HIT Sessions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2 Cycling Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.1 T
max
During Cycle Ergometry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3 Rate of Performance Enhancement Following HIT . . . . . . . . . . . . . . . . . . . . . . . . .
3.4 Recovery Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Abstract
While the physiological adaptations that occur following endurance training
in previously sedentary and recreationally active individuals are relatively well
understood, the adaptations to training in already highly trained endurance ath-
letes remain unclear. While significant improvements in endurance performance
and corresponding physiological markers are evident following submaximal en-
durance training in sedentary and recreationally active groups, an additional in-
crease in submaximal training (i.e. volume) in highly trained individuals does not
appear to further enhance either endurance performance or associated physiolog-
ical variables [e.g. peak oxygen uptake (
V
.
O
2peak
), oxidative enzyme activity]. It
seems that, for athletes who are already trained, improvements in endurance
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performance can be achieved only through high-intensity interval training (HIT).
The limited research which has examined changes in muscle enzyme activity in
highly trained athletes, following HIT, has revealed no change in oxidative or
glycolytic enzyme activity, despite significant improvements in endurance per-
formance (p < 0.05). Instead, an increase in skeletal muscle buffering capacity
may be one mechanism responsible for an improvement in endurance perfor-
mance. Changes in plasma volume, stroke volume, as well as muscle cation
pumps, myoglobin, capillary density and fibre type characteristics have yet to be
investigated in response to HIT with the highly trained athlete. Information re-
lating to HIT programme optimisation in endurance athletes is also very sparse.
Preliminary work using the velocity at which
V
.
O
2max
is achieved (V
max
) as the
interval intensity, and fractions (5075%((Author: 50 to 75%?))) of the time to
exhaustion at V
max
(T
max
) as the interval duration has been successful in eliciting
improvements in performance in long-distance runners. However, V
max
and T
max
have not been used with cyclists. Instead, HIT programme optimisation research
in cyclists has revealed that repeated supramaximal sprinting may be equally
effective as more traditional HIT programmes for eliciting improvements in en-
durance performance. Further examination of the biochemical and physiological
adaptations which accompany different HIT programmes, as well as investigation
into the optimal HIT programme for eliciting performance enhancements in
highly trained athletes is required.
Compared with the volume of research that de-
scribes the physiological adaptations to endurance-
exercise training in sedentary and recreationally
trained individuals, relatively little work has exam-
ined the physiological and performance responses
of already highly trained athletes to a modified
training programme. In part, this may be because
of the difficulty of persuading highly trained ath-
letes to alter their training programmes to
accommodate the interests of exercise scientists.
[1]
Consequently, recommendations made by exercise
scientists to coaches and athletes are largely based
on training studies completed with sedentary and
recreationally trained individuals coupled with an-
ecdotal hearsay of some successful coaches.
[1,2]
Highly trained athletes already have a high aerobic
capacity, lactate threshold (T
lac
), and economy of
motion.
[3,4]
Therefore, the physiological adapta-
tions that generally account for improved perfor-
mance in sedentary or recreationally trained indi-
viduals
[5,6]
may not necessarily apply to the highly
trained athlete.
[7]
Indeed, in the highly trained ath-
lete, an additional increase in submaximal exercise
training (i.e. volume) does not appear to further
enhance either endurance performance or associ-
ated variables such as maximal oxygen uptake
(V
.
O
2max
), anaerobic threshold, economy of motion
and oxidative muscle enzymes.
[8-10]
In these individuals, it appears that further im-
provements in performance can only be achieved
through high-intensity interval training (HIT).
[8]
The only research to date that has examined the
physiological responses of already highly trained
athletes to HIT
[7]
indicates no up-regulation of ox-
idative or glycolytic enzyme activity, despite sig-
nificant improvements in 40km cycling time-trial
performance and peak power output (P
peak
) ob-
tained during a progressive exercise test (p < 0.05).
Skeletal muscle buffering capacity significantly in-
creased (p < 0.05), but the increase was not related
to improvements in P
peak
and 40km time-trial per-
formance. Thus, the mechanisms responsible for
improvements in performance following HIT in the
already highly trained athlete remain unclear. This
article will: (i) briefly review the adaptations to
endurance training known to occur in sedentary
and recreationally active individuals; (ii) outline
some physiological mechanisms that may further
Author proof
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enhance performance following HIT in the already
highly-trained athlete; and (iii) consider the issue
of HIT programme optimisation in the highly-
trained athlete.
1. Endurance Training in the Untrained
and Recreationally Active
1.1 Submaximal Endurance Training
It is generally accepted that many of the bio-
chemical and physiological adaptations that ac-
company endurance training occur in response to
an increase in muscle cell energy demands.
[11,12]
Indeed, manipulation of the intensity and duration
of work and rest intervals changes the relative de-
mands on particular metabolic pathways within
muscle cells, as well as oxygen delivery to muscle.
The subsequent adaptations that occur, both at the
cellular and systemic level, are specific to the par-
ticular characteristics of the training programme
employed.
Several short- and long-term training studies
performed with sedentary individuals have chal-
lenged the aerobic energy system through daily
submaximal training (i.e. 2 h/d, 65 to 75%
V
.
O
2max
).
[13-15]
In these studies, the improvements
in physical work capacity (i.e. P
peak
[13]
), were at-
tributed to an increased delivery of oxygen to the
exercising muscles (central adaptations),
[6,16]
cou-
pled with increased utilisation of oxygen by the
working muscles (peripheral adaptations).
[17-20]
Central adaptations to endurance training result in
a lower heart rate at pre-training workrates
[6]
cou-
pled with an increase in blood and plasma volume
(hypervolaemia).
[6,13]
These changes are accompa-
nied by a greater cardiac output (stroke vol-
ume),
[6,21]
and increases in muscle and cutaneous
blood flow during exercise at the same pre-training
workrate.
[22,23]
Although these central adaptations
may allow relatively rapid (i.e. 3 days) improve-
ments in physical work capacity (p < 0.05),
[13]
a
longer period of training (three to five times per
week, 12 to 38 days) may be needed for increases
in V
.
O
2max
to occur (p < 0.05).
[16,24,25]
Indeed, sev-
eral weeks of training may be needed before
changes in muscle capillary density and mitochon-
drial volume are observed (p < 0.05).
[26-29]
Other
adaptations to endurance training include a reduc-
tion in glucose
[30-32]
and muscle glycogen utilisa-
tion,
[33]
as well as lower blood lactate levels at the
same absolute workload (p < 0.05).
[6,17,20,34-37]
Thus, with previously untrained individuals,
exercise-induced cellular hypoxia increases blood
flow, oxygen delivery, oxygen extraction and fat
metabolism in working muscles during submaxi-
mal exercise after training. As a result, muscle con-
traction becomes more efficient and physical work
capacity increases. However, when submaximal
endurance training becomes habitual, such as for
the endurance athlete, further improvements in ex-
ercise performance with an increase in training
volume do not normally occur.
[8,9,25,38]
Indeed, the
muscle of trained athletes has three to four times
higher oxidative enzyme activity, up to three times
more capillaries per muscle fibre, and a greater per-
centage of slow twitch fibres when compared with
untrained muscle.
[39]
In these individuals, addi-
tional improvements in endurance performance
and associated physiological markers appear to re-
quire a different training stimulus than simply an
increase in volume.
[8,25,40,41]
1.2 High-Intensity Interval Training (HIT)
It is generally believed that in sedentary
(V
.
O
2max
< 45 ml/kg/min) and recreationally active
individuals (V
.
O
2max
≈ 45 to 55 ml/kg/min), several
years are required to increase V
.
O
2max
to that of the
highly trained athlete (V
.
O
2max
> 60
ml/kg/min).
[21,42]
However, Hickson et al.
[43]
showed, in eight sedentary and recreationally ac-
tive individuals, that V
.
O
2max
could be markedly
increased (+44%; p < 0.05) after 10 weeks of high-
intensity exercise training (alternating 40 minutes
cycling intervals at V
.
O
2max
1 day, with 40 minutes
high-intensity running the next, 6 d/wk). Interest-
ingly, in four of these individuals, V
.
O
2max
ap-
proached or exceeded 60 ml/kg/min. This clearly
shows how an increase in high-intensity exercise
training can elicit a rapid improvement in ‘aerobic
fitness’.
[43]
Author proof
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In contrast to submaximal exercise training,
which is characterised by prolonged, continuous
activity, HIT is normally achieved through the use
of intervals. HIT can be broadly defined as re-
peated bouts of short to moderate duration exercise
(i.e. 10 seconds to 5 minutes) completed at an in-
tensity that is greater than the anaerobic threshold.
Exercise bouts are separated by brief periods of
low-intensity work or inactivity that allow a partial
but often not a full recovery. The purpose of HIT
is to repeatedly stress the physiological systems
that will be used during a specific endurance-type
exercise
[44]
to a greater extent than that which is
actually required during the activity. Despite the
fact that coaches have long used HIT to improve
the performance of endurance athletes,
[1]
studies
describing the influence of HIT on muscle respira-
tion have largely been limited to previously seden-
tary or recreationally active individuals (table
I).
[45]
Several studies have indicated that intermittent
HIT may increase fat oxidation when compared
with continuous training. Essen and associates
[61]
compared 1 hour of continuous exercise at 50%
V
.
O
2max
with 1 hour of intermittent exercise (15
seconds work at P
peak
, 15 seconds rest) of the same
mean workload (157W). In these previously un-
trained individuals, more lipids and less glycogen
were used when exercise was performed intermit-
tently, as opposed to continuously. In another study
with untrained individuals,
[45]
HIT (5 × 4 minutes
at 100% V
.
O
2max
, 2 minutes rest; n = 13) was found
to enhance the oxidative capacity (succinate dehy-
drogenase and cytochrome oxidase) of type II fi-
bres (p < 0.05), when compared with a continuous
exercise training group (n = 8) which performed
exercise of a similar duration at the same average
intensity (79% V
.
O
2max
). A recent study in rats has
provided support for this earlier finding; mitochon-
drial fatty acid oxidation rates have been shown to
increase to a greater extent following HIT than fol-
lowing continuous submaximal endurance training
(p < 0.05).
[62]
Somewhat in contrast, however, Gorostiaga and
colleagues
[63]
reported an increase in citrate syn-
thase (CS) activity in response to continuous but
not HIT. The opposite trend was seen in the activity
of adenylate kinase, which increased by 25% fol-
lowing HIT, but not continuous training. The au-
thors compared the physiological effects of contin-
uous training (50% V
.
O
2max
; n = 6) versus HIT
(repeated 30 seconds at 100% V
.
O
2max
, 30 seconds
rest; n = 6). Their participants cycled 30 min/d, 3
d/wk, for 8 weeks, with both groups exercising at
the same mean intensity. Following training,
V
.
O
2max
, exercising work rates and P
peak
obtained
during the incremental test were all higher (p <
0.05) in the HIT group (+9 to 16%) compared with
the continuous training group (+5 to 7%). How-
ever, the exercise intensity in the continuous train-
ing group was adjusted so that individuals trained
at the same heart rate throughout the 8 weeks of
training. It is generally accepted that continuous
submaximal training will reduce the heart rate cor-
responding to a pre-training workrate.
[6]
Thus, the
continuous training group likely received an in-
crease in their continuous training intensity
throughout their 8 weeks of training, which may
help explain why CS activity was improved more
than in the HIT group in this study.
In a more recent study by Franch et al.,
[64]
the
effects of continuous and HIT were compared in
recreational runners (n = 36; V
.
O
2max
= 54.8 ± 3.0
ml/kg/min). Individuals were equally matched into
three groups; either short HIT (30 to 40 × 15 sec-
onds at 20.4 km/h, 15 seconds inactive rest), long
HIT (4 to 6 × 4 minutes at 16.6 km/h, 2 minutes
inactive rest), or continuous running (15 km/h, ~26
minutes). All groups trained three times per week
(2.2 h/wk) at a mean exercise intensity of ~65%
maximum heart rate for 6 weeks. Both the contin-
uous running and the long HIT groups improved
their V
.
O
2max
significantly more than the short HIT
group (6vs 3%; p < 0.05). Furthermore, time to
exhaustion at 85% V
.
O
2max
increased significantly
more in the continuous running group (+93%; p <
0.05) compared with the long (+67%) and short
(+65%) HIT groups. It is important to note, how-
ever, that the individuals in this study had low lev-
els of initial fitness, so the finding of a greater im-
Author proof
4 Laursen & Jenkins
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Table I. Findings from high-intensity interval-training studies in sedentary and recreationally active individuals
a
Reference n Mode Frequency
(d/wk)
Weeks Reps Intensity Work
duration
Rest duration Results
Hickson et
al.
[43]
8 M R and
C
6 10 6 100%
V
.
O
2max
5 min 2 min ↑V
.
O
2max
, ↑T
lim
Green et
al.
[46]
10 M C 1 1 16 90% V
.
O
2max
6 min 54 min ↑PCr, ↑Gly, ↓Lac
-
Green and
Fraser
[47]
6 M C 3 1 12-24 120%
V
.
O
2max
1 min 4 min ↑UA
Keith et
al.
[48]
7 M C 2-4 8 2 T
lac
+ 30% 7.5 min 30 min ↑V
.
O
2max
, ↑P
peak
, ↑CS, ↑3-HcoA, ↑T
lac
Keith et
al.
[48]
8 M C 2-4 8 1 T
lac
30 min 0 ↑V
.
O
2max
, ↑P
peak
, ↑CS, ↑3-HCoA, ↑T
lac
Burke et
al.
[49]
21 F C 4 7 NR 85-98%
V
.
O
2max
30-120 sec 30-120 sec ↑V
.
O
2max
, ↑T
lac
, ↑T
vent
Simoneau
et al.
[50]
24M,
F((Auth
or: n
=?))
C 4-5 15 4-15 60-90%
P
peak
15-90 sec HR =
120-130 bpm
↑type I, ↓type IIb, ↔ type IIa
Rodas et
al.
[51]
5 M C 7 2 4-7 All-out 15-30 sec 45s-12 min ↑PCr, ↑Gly, ↑CK, ↑PFK, ↑LDH,
↑3-HcoA, ↑CS, ↑V
.
O
2max
, ↑P
peak
, ↔ WIN
Parra et
al.
[52]
5 M C 2 6 4-7 All-out 15-30 sec 45s-12 min ↑PFK, ↑ALD, ↑CS, ↑3-HCoA, ↑P
peak
,
↑WIN
MacDougall
et al.
[53]
12 M C 3 7 4-10 All-out 30 sec 2.5-4 min ↑HK, ↑PFK, ↑CS, ↑SD, ↑MD, ↑P
peak
,
↑WIN, ↑V
.
O
2max
Linossier et
al.
[54]
10 M,
F((Auth
or: n
=?))
C 4 7 8-13 All-out 5 sec 55 sec ↑WIN, ↑Lac
-
, ↑PFK, ↑LDH, ↑Type I,
↓Type IIb, ↔ Type IIa
Simoneau
et al.
[55]
19M,
F((Auth
or: n
=?))
C 2-3 15 10-15 60-90%
P
peak
15-30 sec HR =
120-130 bpm
↑HK((Author: hexokinase activity?)),
↑PFK, ↑LDH, ↑MD, ↑3-HcoA, ↑OGDH
Henritze et
al.
[56]
23 F C 5 12 1 T
lac
–T
lac
+
69W
NR NA ↑T
lac
, ↔ V
.
O
2max
Nevill et
al.
[57]
8 M,
F((Auth
or: n
=?))
R 3-4 8 2-10 All-out 6-30 sec 1-10 min ↑WIN, ↑Lac
-
, ↑NE, ↔ β
m
, ↑H
+
Tabata et
al.
[58]
7 M C 5 6 7-8 170%
V
.
O
2max
20 sec 10 sec ↑V
.
O
2max
, ↑AN
cap
Ray
[59]
6 M C 4 6 5 90-100%
V
.
O
2max
5 min 3 min ↑V
.
O
2max
, ↓HR
rest
, ↓MAP, ↓MSNA
Harmer et
al.
[60]
7 M C 3 7 4-10 All-out 30 sec 3-4 min Before maximum work-rate: ↑T
lim
, ↓Lac
-
m, pl
, ↓H
+
, ↓
an
ATP
prod
, ↓IMP, ↓Gly,
↓ATP
deg
, ↓K
+
, ↓NE. After maximum
work-rate: ↔Lac
-
m
, ↑Lac
-
pl
, ↓H
+
m
, ↑H
+
pl
, ↑NE, ↓ATP
deg
, ↓
an
ATP
prod
, ↓IMP
a Changes indicated based on statistical significance at the p< 0.05 level.
ALD = aldosterone;
an
ATP
prod
= anaerobic ATP production; AN
cap
= anaerobic capacity; ATP
deg
= ATP degradation; b = blood; ((Author:
“b” does not seem to be used in this table. Delete from abbrev list?)) C = cycle training; CK = creatine kinase activity; CS = citrate
synthase activity; F = female; Gly = glycogen content; H
+
= hydrogen ions; HR = heart rate; HR
rest
= resting HR; IMP = inosine
monophosphate; K
+
= potassium ions; Lac
–
= lactate; LDH = lactate dehydrogenase activity; M = male; m = muscle; MAP = mean arterial
pressure; MD = malate dehydrogenase activity; MSNA = muscle sympathetic nerve activity; n = number of participants; NA = not applicable;
NE = plasma norepinephrine (noradrenaline); NR = not reported; OGDH = oxoglutarate dehydrogenase activity; PCr = phosphocreatine; PFK
= phosphofructokinase activity; pl = plasma; P
peak
= peak power output, R = run training; Reps = repetitions; SD = succinate dehydrogenase
activity; T
lac
= lactate threshold; T
lim
= time to exhaustion; T
vent
= ventilatory threshold; type I, IIa, IIb = type I, IIa, and IIb muscle fibres;
UA = ((Author: please define)); V
.
O
2max
= maximal oxygen uptake; WIN = Wingate anaerobic test performance; 3-HCoA = 3-hydroxyacyl
coenzyme A dehydrogenase activity; β = buffering capacity; ↓ = ((Author: decrease?)); ↑ = ((Author: increase?)); ↔ = ((Author: no
change?)).
Author proof
Interval Training and Endurance Performance 5
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
provement in V
.
O
2max
and time to exhaustion fol-
lowing the continuous training is not surprising.
Had highly trained athletes been exposed to the
same training stimulus, it is unlikely that the same
magnitude of changes would have been observed,
as highly trained athletes train regularly at these
continuous submaximal intensities
[65,66]
at least
once per week (generally called tempo training).
[1]
The effects of repeated supramaximal HIT in
previously untrained individuals have also been
examined by Harmer et al.,
[60]
MacDougall et
al.,
[53]
Parra et al.
[52]
and Rodas et al.
[51]
MacDougall and co-workers
[53]
examined the in-
fluence of supramaximal HIT on muscle enzyme
activity and exercise performance in 12 previously
active students (V
.
O
2max
= 3.73 ± 0.13 L/min). For
7 weeks, individuals performed 4 weekly HIT ses-
sions that became progressively more challenging,
in terms of a progressive increase in the number of
interval bouts (4 to 10 × 30 seconds all-out cycle
sprints) and a progressive reduction in the duration
of recovery between interval bouts (4 to 2.5 min-
utes). Individuals significantly enhanced their peak
anaerobic power output and total work done over
30 seconds, as well as their V
.
O
2max
. The maximal
enzyme activities of CS, hexokinase (HK), phos-
phofructokinase (PFK), succinate dehydrogenase
and malate dehydrogenase also significantly in-
creased following training (p < 0.05). Thus, in con-
trast to submaximal endurance training, that has
little or no effect on glycolytic enzyme activ-
ity,
[67,68]
relatively brief but intense supramaximal
HIT training can elicit concurrent up-regulation of
both glycolytic and oxidative enzyme activity,
maximum short-term power output, and V
.
O
2max
in
untrained individuals. The findings of the concur-
rent up-regulation of aerobic and anaerobic meta-
bolism may have been due to the progressive re-
duction in recovery periods between HIT bouts,
which likely would have created for a greater reli-
ance on aerobic metabolism.
[69]
A more recent
study has produced similar findings.
[51]
The au-
thors had their five moderately active individuals
sprint train on a cycle ergometer (8 to12 × 15 sec-
onds all out, 45 seconds rest) each day for 2 weeks.
Significant increases were found in the muscle ac-
tivities of creatine kinase (CK) [+44%], PFK
(+106%), lactate dehydrogenase (LDH) [+45%],
3-hydroxyacyl coenzyme A (CoA) dehydrogenase
(+60%) and CS (+38%) [all p < 0.05]. While par-
ticipants did not show improvements in the 30-sec-
ond sprint after only 1 day of rest (compared with
their pre-training cycle sprint performance), a re-
assessment 5 days later revealed significant in-
creases in V
.
O
2max
(+11.3%) and P
peak
(+10.0%) ob-
tained during the progressive exercise test (p <
0.05). Finally, Harmer et al.
[60]
have reported that
sprint training (4 to 10 all-out cycle sprints, 3 to 4
minutes rest, 3 d/wk, 7 weeks) improves time to
fatigue (+21%; p < 0.001) at 130% of the pre-train-
ing V
.
O
2max
workload. This increase in exercise ca-
pacity was attributed to reduced anaerobic ATP
generation, and an increased contribution of aero-
bic metabolism to the energy yield.
There is some evidence to suggest that as the
recovery time between repeated sprints declines, so
does the contribution of glycolysis to the energy
yield during subsequent sprints.
[69]
Consequently,
aerobic metabolism increases to meet the energy
deficit.
[53,60]
Linossier et al.
[54]
have suggested that
aerobic metabolism during recovery from high-in-
tensity exercise is important for the resynthesis of
phosphocreatine and for the oxidation (i.e. re-
moval) of lactic acid. It would appear, therefore,
that intermittent high-intensity sprint training, that
involves a significant contribution of energy de-
rived from aerobic sources, improves the capacity
for aerobic metabolism.
[53,60]
From these studies in previously untrained indi-
viduals,
[51,53,60]
one significant advantage of HIT is
the simultaneous up-regulation of both oxidative
and glycolytic energy systems, producing an im-
proved energy state in the working muscle through
the preservation of high-energy phosphates.
[11]
As
a final example to illustrate this point, Tabata et
al.
[58]
compared the effects of HIT (8 × 20 seconds
at 170% P
peak
, 10 seconds rest, 5 d/wk for 6 weeks),
and submaximal training (70% V
.
O
2max
, 60 min/d,
5 d/wk) with two groups of active, but relatively
untrained individuals (n = 7 per group; V
.
O
2max
,
Author proof
6 Laursen & Jenkins
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
~50 ml/kg/min). While the submaximal exercise
training group significantly increased their V
.
O
2max
(+9.4%; p < 0.05), there was no effect on their an-
aerobic capacity measured through maximal accu-
mulated oxygen deficit.
[70]
However, those in the
HIT group significantly improved both their
V
.
O
2max
(+15%) and their anaerobic capacity
(+28%) [p < 0.05].
In summary, HIT in sedentary and recreation-
ally active individuals improves endurance perfor-
mance to a greater extent than does continuous sub-
maximal training alone. This improvement appears
due, in part, to an up-regulated contribution of both
aerobic and anaerobic metabolism to the energy
demand,
[51,53,55]
which enhances the availability of
ATP and improves the energy status in working
muscle. An improved capacity for aerobic metabo-
lism, as evidenced by an increased expression of
type I fibres,
[54]
capillarisation and oxidative en-
zyme activity
[53,61,62,71]
is the most common re-
sponse to HIT in untrained or moderately active
individuals.
2. Endurance Training in Highly Trained
Athletes
Many exercise scientists base their advice to
athletes on training principles developed from
studies completed with previously untrained or
recreationally active individuals. As shown in the
previous section, this is problematic; research has
consistently shown that endurance training in pre-
viously untrained individuals will increase
V
.
O
2max
, capillary density, oxidative enzyme activ-
ity and plasma volume. However, changes in these
variables do not occur when already highly trained
athletes increase the volume of their submaximal
training.
[9,39]
Indeed, endurance trained athletes
and untrained individuals do not show the same
response to submaximal (continuous) training.
[8]
2.1 Submaximal Continuous Training
It appears that once an individual has reached a
V
.
O
2max
> 60 ml/kg/min, endurance performance is
not improved by a further increase in submaximal
training volume.
[8]
Indeed, Costill and associates
[9]
showed that when swim-training distance was
more than doubled from 4 266 to 8 979 m/d over a
10-day period (while average training intensity
was maintained), there was no change in swim-
ming performance, aerobic capacity or CS activity
in the deltoid muscle. While it might be argued that
well trained athletes need more time for adapta-
tions to occur than the time frame used in the for-
mer study, it should be noted that adaptations to a
submaximal training stimulus are generally ob-
served within this time period in untrained individ-
uals.
[6,16,20,72,73]
In all likelihood, athletes in the
trained state will have reached a plateau in the me-
tabolic adaptations that result from submaximal
endurance training. Evidence for this comes from
a meta-analysis completed by Londeree.
[8]
This
group compared training status (trained vs un-
trained) with the influence of continuous training
at an exercise intensity corresponding to either the
ventilatory threshold (T
vent
) or T
lac
. Although stud-
ies using previously untrained individuals have
consistently shown a marked influence of training
in terms of performance and associated physiolog-
ical variables, analysis by Londeree et al.
[8]
showed that continuous training failed to elicit fur-
ther improvements in already highly trained ath-
letes. The authors did note, however, that trained
individuals tended to respond better to higher in-
tensity training.
2.2 HIT
Generally, training programmes undertaken by
highly trained endurance athletes consist of an
early ‘aerobic base’ component, complemented by
HIT sessions nearer to the competitive season. De-
spite the fact that coaches have long used HIT to
improve the performance of their elite endurance
athletes,
[1]
exercise scientists have only recently
sought to understand the physiological mecha-
nisms behind the practice.
[7,74-84]
Despite this in-
creased attention, the mechanisms responsible for
these improvements in endurance performance fol-
lowing HIT remain unclear.
[7,80]
Author proof
Interval Training and Endurance Performance 7
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
2.2.1 Quantifying the Demands of HIT in Highly
Trained Athletes
Recent work has examined the short-term
[85]
and long-term
[82]
influences of HIT in highly
trained cyclists. Stepto and colleagues
[85]
investi-
gated the metabolic demands of a single session of
HIT [8 × 5 minutes at 86% peak oxygen uptake
(V
.
O
2peak
), 60 seconds recovery] in seven highly
trained cyclists (V
.
O
2peak
= 5.14 L/min). These cy-
clists showed high rates of carbohydrate oxidation
(340 µmol/kg/min), coupled with a progressive in-
crease in fat oxidation (16 to 25 µmol/kg/min)
measured throughout the HIT session. Laursen and
colleagues
[82]
recently reported changes in cardio-
respiratory and performance variables following
four HIT sessions (20 × 60 seconds at P
peak
, 2 min-
utes recovery) over 2 weeks in seven highly trained
cyclists (V
.
O
2peak
= 68.7 ± 1.3 ml/kg
/
min). These
individuals were able to perform a greater number
of HIT bouts and complete more total work follow-
ing training. The improved HIT performance was
accompanied by reductions in both the respiratory
exchange ratio and 1-minute recovery heart rates
from the first to the fourth HIT session (p < 0.05);
T
vent
and P
peak
obtained during the progressive ex-
ercise test also improved as a result of the four HIT
sessions (p < 0.05).
2.2.2 The Influence of HIT on Performance and
Related Variables
HIT has been shown to improve 3km
(+3%),
[86,87]
and 10km (+3%)
[74]
running perfor-
mance in middle- and long-distance runners, as
well as 40km time-trial performance in endurance-
trained cyclists (+2.1 to 4.5%) [p < 0.05].
[7,80,81,83]
Well established laboratory-based markers of en-
durance performance have also changed following
HIT. These include T
vent
,
[74,82]
and the P
peak
ob-
tained during a progressive exercise test (p <
0.05).
[7,80-83]
However, improvements in economy
of motion
[10,75,88]
and V
.
O
2max
have not been ob-
served.
[74,75,82]
It should be mentioned however
that most of these studies did not involve control
individuals.
[7,74,75,80,81,83,88]
Indeed, improvements
in performance-related variables may, at least in
part, be attributed to ‘psychological factors’ that
are naturally inherent with training studies (i.e. ‘the
last test’). Some studies have shown improvements
in P
peak
, time to exhaustion and time-trial perfor-
mance, merely as a result of it being the last of a
series of tests (p < 0.05).
[89,90]
The following section will examine studies that
have investigated potential mechanisms responsi-
ble for an improved endurance performance fol-
lowing HIT in the already highly trained athlete.
Potential Mechanisms to Improved Performance
Insight into the potential ways in which HIT
may benefit endurance performance is possible
through examining the particular physiological pa-
rameters that have been identified as being impor-
tant in endurance events. V
.
O
2max
, the sustainable
fractional utilisation of V
.
O
2max
, and economy of
motion all contribute to endurance performance.
[4]
Included in the following section is a review of the
processes that regulate these variables and deter-
mine the delivery of oxygen to working muscles
and facilitate the utilisation of oxygen by working
muscles.
[11]
Central Adaptations
Central adaptations to endurance training facil-
itate improved delivery of oxygen to working mus-
cles. Given that maximal heart rate remains un-
changed in response to endurance training,
[91]
improvements in oxygen delivery to exercising
muscles during high-intensity exercise can be at-
tributed to an increase in stroke volume.
[21]
Stroke
volume can increase through a higher left-ventric-
ular contractile force and/or through an increase in
cardiac filling pressure, which raises end-diastolic
volume and resultant stroke volume.
[21]
Surpris-
ingly, potential changes in stroke volume and
plasma volume in response to HIT in the already
highly trained athlete have, to our knowledge, not
been examined. However, if stroke volume does
increase following HIT in the highly trained ath-
lete, it may be difficult to detect, as V
.
O
2max
, which
is strongly related to maximal cardiac output,
[16]
has rarely been shown to change following HIT in
the highly trained athlete.
[86]
The increase in plasma volume, caused by either
training or heat acclimation, has been regarded as
Author proof
8 Laursen & Jenkins
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
the single most important event in promoting car-
diovascular stability and improving thermoregula-
tion during prolonged exercise.
[92]
Hypervolaemia
serves to minimise cardiovascular stress by pre-
venting significant reductions in mean arterial
pressure, central venous pressure, and cardiac fill-
ing,
[93]
thereby maintaining or improving stroke
volume.
[94]
Plasma volume expansion through ei-
ther training or heat acclimation has been attrib-
uted to elevated plasma renin levels, vasopressin
and plasma albumin content, which facilitates wa-
ter and sodium retention in the blood.
[95]
Artificial
plasma volume expansion (i.e. 200 to 300ml above
normal) has been reported to increase both V
.
O
2max
and exercise time to fatigue by 4 and 11% (p <
0.05), respectively, in untrained individuals de-
spite a 4% reduction in haemoglobin concentra-
tion.
[94]
However, artificial plasma volume expan-
sion does not appear to significantly enhance
stroke volume in highly trained individuals, who
already have a relatively high plasma volume.
[96]
One other potential mechanism that might be
partially responsible for enhanced endurance per-
formance following HIT in the highly trained ath-
lete is an improvement in heat tolerance via an aug-
mented cutaneous blood flow and/or sweating
rate.
[97]
Although experimental HIT sessions are
normally completed under controlled thermoneut-
ral environments, high-intensity exercise produces
high core temperatures (~40°C),
[98]
and endurance
training itself has been shown to independently ex-
pand plasma volume, creating partial heat
acclimatisation.
[99]
Because a strong association
has been established between volitional fatigue
and elevated core temperatures,
[100,101]
it is possi-
ble that highly trained athletes may adapt some-
what to successive HIT sessions by means of im-
proved temperature regulation.
[102]
Indeed, HIT
can elicit improved work-heat tolerance in physi-
cally active individuals,
[103]
but this has yet to be
investigated in highly trained athletes. The fact that
endurance trained athletes have an enhanced ca-
pacity for sweating and cutaneous blood flow sup-
ports this as a possible adaptive response to HIT.
[22]
Peripheral Adaptations
Peripheral adaptations to exercise training refer
to an improved ability of working muscle to pro-
duce and utilise ATP. The integration of the meta-
bolic pathways, which serve to resynthesise ATP
and the excitation-contraction processes utilising
ATP, determine this efficiency.
[11]
Due to the ab-
sence of data relating to peripheral changes follow-
ing training in already highly trained athletes, un-
derstanding of this area has been limited to studies
which have used untrained and recreationally ac-
tive individuals.
Some authors
[45,104]
have assumed that further
adaptations in the already highly trained athlete in
response to continued training originate from the
same well-established adaptations known to occur
with untrained and recreationally active individu-
als. In particular, endurance training promotes an
improved energy state in the working muscle as
indicated by better protection of the high-energy
phosphate potential.
[11]
Increases in both oxidative
and glycolytic enzyme activity coupled with an im-
proved exercise capacity have been shown to occur
in untrained and recreationally active individuals
following HIT.
[51-54]
To our knowledge, however,
only one published study to date
[7]
has examined
the underlying metabolic adaptations responsible
for improved endurance performance following
HIT in already highly trained athletes. Weston and
associates
[7]
found that the activities of HK, PFK,
CS and 3-hydroxyacyl-CoA dehydrogenase did
not change with HIT. Nevertheless, there was a sig-
nificant improvement in 40km time-trial perfor-
mance, P
peak
, and time to fatigue at 150% P
peak
in
these six highly trained cyclists following six HIT
sessions over 3 weeks (p < 0.05; table II). There-
fore, factors other than the activities of the en-
zymes measured by the authors must have contrib-
uted to the observed improvements in
performance. Despite the findings of Weston and
associates,
[7]
Billat
[104]
contends that HIT may pro-
mote a greater use of fatty acids, even in the highly
trained athlete. In support of this possibility,
Shepley and co-workers
[105]
while examining the
effects of tapering (i.e. reduction in volume before
an endurance contest) on endurance performance
Author proof
Interval Training and Endurance Performance 9
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
and CS activity in highly trained middle distance
runners, showed that a high-intensity taper (3 to 5
× 500m at 120% V
.
O
2peak
, 800m jog recovery, five
times per week) improved run time to exhaustion
at ~115% V
.
O
2peak
(+22%) and CS activity (+18%),
compared with low-intensity taper and no taper
scenarios (p < 0.05). Interestingly, the high-inten-
sity taper programme consisted of training intensi-
ties that were greater than those typically com-
pleted by the athletes during their normal training
programme .
[105]
This suggests that an increase in
training intensity may enhance oxidative enzyme
activity, even in highly trained athletes. Moreover,
some authors have reported lower respiratory ex-
change ratio values at submaximal workloads fol-
lowing HIT.
[80,82]
Thus, further examination of po-
tential changes in oxidative enzyme activity as a
result of HIT in the already highly trained athlete
is needed.
Increased glycogenolytic capacity is another av-
enue through which endurance performance could
be improved. However, while the simultaneous in-
crease in both aerobic and anaerobic capacity has
been documented in untrained individuals follow-
ing HIT,
[58,106]
Weston et al.
[7]
showed that with
already highly trained athletes, the activities of HK
and PFK remained unchanged following HIT. Con-
sidering that highly-trained athletes already have
high muscle glycolytic enzyme activities,
[107]
it is
possible that the intervals used by Weston et al.
[7]
were performed at too low an intensity (85% of
P
peak
) for adaptations to the glycolytic pathway to
occur. In addition to potential changes to key gly-
colytic enzyme activity, there are other peripheral
mechanisms that could contribute to an improved
performance in the highly trained athlete following
HIT. These include the capacity of skeletal muscle
to buffer H
+
ions, and an up- or down-regulation of
muscle cation pumps.
The capacity of working muscle to buffer H
+
ions is related to sprint performance in un-
trained
[108]
and highly trained individuals.
[7]
More-
over, sprint training has been shown to improve
skeletal muscle buffering capacity in untrained in-
dividuals
[109]
and in already highly trained ath-
letes.
[7]
Weston et al.
[7]
reported a significant in-
crease in skeletal muscle buffering capacity
following only 3 weeks of HIT (p < 0.05). They
Table II. Summary of findings in high-intensity interval-training (HIT) studies in highly trained cyclists
a
Reference n HIT
sessions
Reps Intensity
(% P
peak
)
Work
duration
Rest
duration
HIT duration
(wk)
Results
Lindsay et al.
[83]
8 6 6-8 80 5 min 60 sec 4 ↑P
peak
, ↑TF
150
, ↑TT
40
Weston et al.
[7]
6 6 6-8 80 5 min 60 sec 4 ↑P
peak
, ↑TF
150
, ↑TT
40
, ↑β,
↔HK, ↔PFK, ↔CS,
↔3-HCoA
Westgarth-Taylor et al.
[80]
8 12 6-9 80 5 min 60 sec 6 ↑P
peak
, ↑TT
40
, ↓CHO
OX
((Author: please define))
Stepto et al.
[81]
4 6 4 80 8 min 1 min 3 No change ((Author: ↔ ?))
Stepto et al.
[81]
4 6 8 85 4 min 1.5 min 3 ↑P
peak
, ↑TT
40
Stepto et al.
[81]
4 6 12 90 2 min 3 min 3 No change ((Author: ↔ ?))
Laursen et al.
[82]
7 4 20 100 1 min 2 min 2 ↑P
peak
, ↑T
vent
((Author:
ventilatory threshold?)),
↑TF
100
,,
Stepto et al.
[81]
3 6 12 100 1 min 4 min 3 No change ((Author: ↔ ?))
Stepto et al.
[81]
4 6 12 175 30 sec 4.5 min 3 ↑P
peak
, ↑TT
40
a Changes indicated based on statistical significance at the p < 0.05 level.
CS = citrate synthase activity; HK = hexokinase activity; n = number of participants; PFK = phosphofructokinase activity; P
peak
= peak
aerobic power output; Reps = repetitions; TF
100
= time to fatigue at 100%; TF
150
= time to fatigue at 150% of P
peak
; TT
40
= 40km time-trial
performance; 3-HCoA = 3-hydroxyacyl coenzyme A dehydrogenase activity; β = buffering capacity; ↓ = ((Author: decrease??)); ↑ = ((Author:
increase?)); ↔ = ((Author: no change?)).
Author proof
10 Laursen & Jenkins
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
also found a significant relationship between 40km
time-trial performance and skeletal muscle buffer-
ing capacity in their six highly trained cyclists (r =
0.82; p < 0.05). The findings of these workers
[7]
suggest that improvements in endurance perfor-
mance following HIT may be related to an in-
creased ability to buffer H
+
ions. The findings of
enhanced 30km time-trial performance in moder-
ately trained cyclists (V
.
O
2max
= 54.7 ± 1.7
ml/kg/min) following sodium citrate consumption
also supports this premise.
[110]
More evidence for skeletal muscle buffering ca-
pacity as a key regulatory mechanism in the highly
trained athlete arises from the findings of Stepto
and colleagues.
[81]
These workers used trend anal-
ysis to examine the effects of different HIT pro-
grammes on the rate of 40km time-trial perfor-
mance improvements in already highly trained
cyclists. They found that improvements in P
peak
and 40km time-trial performance arose from two
distinctly different HIT programmes. One of these
programmes (8 × 4 minutes at 85% P
peak
, 1 minute
recovery) has been shown to consistently produce
performance improvements in highly trained cy-
clists (table II).
[7,80,81,83]
However, similar im-
provements in performance have also resulted
from repeated ‘supramaximal’ HIT (12 × 30 sec-
onds at 175% P
peak
, 4.5 minutes recovery). Al-
though skeletal muscle buffering capacity was not
measured, the improved performance following
supramaximal HIT may well have been accompa-
nied by an increase in muscle buffering capacity,
as has been shown following repeated supramaxi-
mal sprint training in untrained individuals.
[109]
A high concentration of H
+
ions has a known
inhibitory effect on enzyme activity, including
PFK.
[111]
Thus, improved skeletal muscle buffer-
ing capacity could indirectly contribute to an im-
proved glycolytic ATP yield and higher exercise
intensity by improving the activity of PFK. Al-
though, further examination of this mechanism is
required, endogenous skeletal muscle buffering ca-
pacity remains a prospective mechanism to the im-
provement in performance found in highly trained
athletes following HIT.
Another possible mechanism that may contrib-
ute to improved endurance performance following
HIT in already highly trained individuals is altered
expression of Na
+
-K
+
-ATPase and sarcoplasmic
reticulum Ca
2+
-ATPase. These enzymes are re-
sponsible for regulating the activity of pumps in-
volved in cation transport, which in turn maintain
muscle membrane potential.
[112]
Resistance train-
ing,
[113]
endurance training
[114]
and altitude
acclimatisation
[115,116]
have all been shown to alter
the levels of these enzymes. Improved submaximal
cycling efficiency was recently shown to be related
to a down-regulation in Na
+
-K
+
-ATPase pump
density in well trained mountain climbers follow-
ing prolonged exercise at high altitude.
[115,117,118]
A similar response could be associated with HIT in
the already highly trained athlete. Given that
highly trained athletes can become hypoxaemic
during exercise at high intensities,
[85,119]
and since
hypoxaemia appears to be a stimulus for alteration
in Na
+
-K
+
-ATPase pump density,
[114,115]
further re-
search needs to examine the possibility that HIT
training evokes an altered expression of cation
pumps in already highly trained athletes.
Other factors that may contribute to the en-
hanced endurance performance of the highly
trained athlete following HIT include biomechani-
cal changes, adaptation of the central nervous and
endocrine systems, as well as other peripheral
changes such as increases in myoglobin, capillary
density and fibre type characteristics. Biomechani-
cal changes could improve exercise efficiency fol-
lowing HIT. However, Lake and Cavanagh
[10]
in-
vestigated the effects of 6 weeks HIT on various
biomechanical variables in a group of moderately
trained runners (V
.
O
2max
= 57.7 ± 6.2 ml/kg/min),
and found no relationship between changes in per-
formance, V
.
O
2max,
running economy and
biomechanical variables. The authors concluded
that improvements in performance following HIT
were more likely to be caused by physiological
rather than biomechanical factors.
[10]
The effect of HIT on the central nervous and
endocrine systems has not yet been examined in
highly trained athletes. In untrained individuals,
Author proof
Interval Training and Endurance Performance 11
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
muscle sympathetic nerve activity following exer-
cise training appears attenuated during exercise,
[59]
suggesting a reduced sympathetic outflow at a
given submaximal workload. However, the capac-
ity for noradrenaline (norepinephrine) release dur-
ing a progressive exercise test appears superior fol-
lowing HIT.
[57]
Myoglobin stores, which represent ~10% of the
accumulated oxygen deficit,
[120]
have been re-
ported to increase,
[121,122]
decrease
[123]
and remain
unchanged
[124]
following endurance training in un-
trained individuals. Myoglobin stores, which are
yet to be examined following HIT in already highly
trained athletes, may be related to the enhanced
oxygen uptake (V
.
O
2
) witnessed during
HIT;
[104,125]
the reloading of myoglobin stores dur-
ing recovery phases could increase oxygen avail-
ability during subsequent interval bouts.
[126]
This
mechanism could, in part, explain our observation
that highly trained athletes can complete a greater
number of high-intensity intervals following suc-
cessive HIT sessions.
[82]
Myoglobin levels have
been shown to increase in response to a hypoxic
stress.
[11,127]
Considering that athletes become
hypoxaemic during high-intensity exercise,
[85,119]
an examination of muscle myoglobin levels before
and after HIT in the highly trained athlete warrants
consideration.
An increased expression of type I fibres has
been reported following multiple sprint training in
untrained individuals.
[54]
Type I fibres may play an
important role during the recovery phase of HIT for
the resynthesis of phosphocreatine and for the re-
moval (oxidation) of lactic acid. It is questionable,
however, whether the expression of type I fibres
would be altered following HIT in the highly
trained athlete, as highly trained athletes already
have a high proportion of type I fibres.
[107]
A large number of capillaries and a high capil-
lary to fibre area ratio are characteristic of highly
trained skeletal muscle.
[107,128,129]
It is therefore
unlikely that further enhancement of capillary den-
sity could occur following HIT in already highly
trained athletes. Interestingly, in a group of highly
trained female cyclists, Bishop and co-work-
ers
[130]
recently reported a negative correlation (r =
–0.77, p < 0.01) between the diameter of the type
II fibres and 1-hour cycling performance. The au-
thors suggested that a reduction in type II fibre size
might allow for an increase in capillary density and
improve lactate removal.
2.2.3 Enhanced Physiological Efficiency: An Issue
of Practical Versus Statistical Significance?
The highly trained athlete already has a high
aerobic capacity,
[4]
and a high degree of adaptation
in a number of physiological variables associated
with oxygen delivery and utilisation.
[9,107,128]
Moreover, improvements in endurance perfor-
mance following HIT, although statistically signif-
icant, have been relatively small (2 to
4%).
[7,74,80,81,83]
One issue is that while these im-
provements in performance are extremely impor-
tant to an elite athlete, they may be too small to
statistically detect and explain.
In summary, HIT, but not continuous submaxi-
mal training, elicits significant enhancements in
endurance performance. These performance im-
provements have been shown to parallel the en-
hancements in T
vent
and P
peak
, but generally not
V
.
O
2max
or economy of motion. Very little research
has examined the adaptation of central and periph-
eral factors following HIT in highly trained ath-
letes. However, in the only study to analyse muscle
tissue following HIT, there was no evidence of an
up-regulation in the glycolytic and oxidative en-
zyme activity. Instead, this study revealed that an
improved skeletal muscle buffering capacity may
play an important role in the enhancement of en-
durance performance following HIT. Other mech-
anisms warranting future examination following
HIT in the highly trained athlete include the expres-
sion of muscle cation pumps, neuromuscular and
endocrinological adaptations, as well as the adjust-
ment of myoglobin levels, capillary density, and
fibre type expression.
3. HIT Programme Optimisation
Very little information is available concerning
HIT programme optimisation in highly trained en-
durance athletes. Optimisation in the current con-
Author proof
12 Laursen & Jenkins
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
text refers to the optimal exercise intensity, exer-
cise duration and number of interval bouts, in ad-
dition to the type (activevs passive) and duration
of the recovery between exercise bouts. These vari-
ables require manipulation according to the peri-
odisation phase of annual training programmes,
[1]
training status and the individual response that an
athlete has to a training stimulus. The last major
section of this review will focus on how best to use
HIT in the preparation of trained athletes for com-
petition.
Research has generated a wide range of vari-
ables for use in prescribing exercise intensities to
individuals undertaking endurance training. Some
of these include V
.
O
2max
,
[78,131,132]
anaerobic
threshold,
[133,134]
T
lac
,
[56,135,136]
T
vent
,
[4,137,138]
on-
set of blood lactate accumulation (OBLA)
[139-141]
and critical power.
[142-149]
However, the physiolog-
ical significance, feasibility and rationale for using
such measures to establish suitable and effective
exercise intensities have been questioned.
[150]
A
variable that has been used with reasonable success
in runners is the velocity at which V
.
O
2max
is
achieved (V
max
),
[66,78,125,132,150-157]
defined as the
running speed during an incremental test at which
V
.
O
2max
is attained.
[155]
3.1 Significance of the Time to Exhaustion
at the Velocity at Which V
.
O
2max
is
achieved (V
max
) [T
max
] in Highly Trained
Runners
V
max
has been shown to predict performance in
middle- and long-distance running
events,
[79,131,158,159]
and appears useful for pre-
scribing HIT programmes.
[78,86,125,160]
The ratio-
nale for using V
max
in HIT programme prescription
is based on the assumption that further improve-
ments V
.
O
2max
in the highly trained athlete will
only result from exercise training at or above
V
.
O
2max
. Moreover, V
max
may be the lowest veloc-
ity at which V
.
O
2max
is elicited.
[104,106,125,155]
The
basis for this premise is that the onset of muscular
fatigue during high-intensity exercise performed
near V
.
O
2max
is dependent on oxygen delivery to
the sarcolemma.
[161]
Although most studies em-
ploying HIT have not sampled V
.
O
2
during the
training intervention, Billat et al.
[125]
recently
showed that repeated bouts of intermittent running
(30 seconds at 100% V
max
, 30 seconds 50% V
max
)
enabled runners to maintain V
.
O
2max
from the 5
th
to
the 18
th
repetition (~10 minutes). This is nearly
three times longer than V
.
O
2max
can be sustained
during a single timed-to-exhaustion bout at V
max
(p < 0.05).
[66,125]
If one accepts that V
max
is an appropriate exer-
cise intensity to use in HIT programming, then
what remains is to decide on the optimal exercise
duration for each bout of exercise. Because the
time that an athlete can run at his or her V
max
[the
time to exhaustion at V
max
(T
max
)] is highly subjec-
tive, even amongst runners with the same
V
max
,
[66,152,153]
the fractional utilisation of T
max
emerges as an appropriate marker for establishing
interval duration.
3.1.1 Use of T
max
to Prescribe HIT Sessions
Despite wide variation in times between indi-
viduals with similar V
.
O
2max
values (coefficient of
variation = 25%), Billat et al.
[153]
have demon-
strated the reproducibility of T
max
in sub-elite run-
ners (404 ± 101 seconds vs 402 ± 113 seconds; r =
0.86; p < 0.05). T
max
has been shown to correlate
negatively with V
.
O
2max
[154,162]
and V
max
,
[66,154]
and positively with the anaerobic threshold.
[132,152-
154]
Hill and Rowell
[150]
found that the minimal time
it took for V
.
O
2max
to be reached was 60% of T
max
in a group of highly trained female middle-distance
runners. Consequently, 60% of T
max
has been ac-
cepted as an optimal interval duration for use in
studies examining the effects of HIT at V
max
(table
III). In a recent study, Smith and colleagues
[86]
trained five middle-distance runners twice a week
for 4 weeks (8 × 60 to 75% of T
max
, 2
:
1 work to
rest ratio) and found that mean V
max
, T
max
, and
3000m-run performance increased (p < 0.05). In
further work, the same group
[87]
used a larger co-
hort of well-trained runners (n = 26) that were ran-
domly assigned into either a control group, or one
of two HIT groups (V
max
intervals at 60 or 70% of
T
max
; 1
:
2 work to rest ratio). Both T
vent
and
Author proof
Interval Training and Endurance Performance 13
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
3000m-running performance improved signifi-
cantly more in the 60% T
max
group than in either
the 70% T
max
or control group (p < 0.05). However,
despite randomisation, runners performing 60%
T
max
intervals had slower overall 3000m-run times
to begin with, and this disparity may have biased
the results. Thus, it cannot be unequivocally stated
that intervals performed at 60% T
max
are the opti-
mal HIT programme duration for improving endur-
ance performance. Indeed, Billat et al.
[78]
examined
the effects of 4 weeks of HIT in highly trained run-
ners (V
.
O
2max
= 71.6 ± 4.8 ml/kg/min), using only
one session per week at 50% of T
max
, and found
that V
max
(+5%) and running economy (–6.1%) sig-
nificantly improved, despite there being no change
in T
max
or V
.
O
2max
. Although further work is re-
quired in terms of HIT optimisation, preliminary
data suggest that HIT performed somewhere be-
tween 50 to 60% of T
max
may be optimal for im-
proving endurance performance.
Another variable that some researchers have
suggested to be an important component for en-
hancing endurance performance is the distance run
at V
max
during a given HIT session.
[104,163]
Accord-
ingly, Billat et al.
[160]
reported that 16 highly
trained male runners (V
.
O
2max
= 69.1 ± 4.3
ml/kg/min) were able to run 2.5 times their T
max
distance during a HIT workout using a 1
:
1 work
:
rest ratio at 50% T
max
, with recovery between
bouts approximating 60% V
max
.
[104]
Longer HIT performed at an intensity between
T
lac
and V
max-
(also known as critical velocity
[164]
)
has the potential to increase V
.
O
2
to the level of
V
.
O
2max
as a result of the V
.
O
2
slow component phe-
nomenon.
[165,166]
Poole and Gaesser
[136]
have stated
that the critical velocity may be the threshold in-
tensity for eliciting V
.
O
2max
. However, Billat et
al.
[167]
reported that 14 highly trained runners
(V
.
O
2max
= 74.9 ± 3.0 ml/kg/min) reached steady-
state V
.
O
2
at 93% of V
.
O
2max
during a time to ex-
haustion test (~17 minutes) at 90% of V
max-
. In-
deed, endurance training has also been shown to
reduce the magnitude of the V
.
O
2
slow compo-
nent.
[168,169]
Thus, although critical velocity/criti-
cal power may be an appropriate exercise intensity
for use with moderately trained individuals,
[170-172]
a more demanding exercise intensity is needed for
use with elite athletes.
[104]
3.2 Cycling Studies
Research with cyclists has taken a more conven-
tional approach to HIT programme optimisation,
but as is the case with runners, scientific data are
sparse (table II). In a heterogeneous group of pre-
viously trained, but not highly trained cyclists
(V
.
O
2max
= 56.8 ± 6.6 ml/kg/min), Norris and
Table III. Summary of findings of high-intensity interval-training (HIT) studies in highly-trained runners (V
.
O
2max
> 60 ml/kg/min)
a
Reference n HIT
sessions
Reps Intensity Work
duration
Rest
duration
HIT Duration
(wk)
Results
Acevedo and
Goldfarb
[74]
7 24 NR 90-95%
HR
max
NR NR 8 ↓10km time, ↑T
vent
, ↔V
.
O
2max
Zavorsky et
al.
[88]
12 3 10 96% V
max
NR 60-180
sec
2 ↑RE, ↓RER
Smith et al.
[86]
58 5 V
max
60-75% T
max
1
:
2 4 ↑V
.
O
2max
, ↑V
max
, ↑T
max
, ↓3000m time
Billat et al.
[78]
84 5 V
max
50% T
max
1
:
1 4 ↑
v
V
.
O
2max
, ↑RE, ↔V
.
O
2max
, ↔T
max
Smith et al.
[87]
98 8 V
max
60% T
max
1
:
2 4 ↑T
max
, ↓ 3000m time, ↔V
.
O
2max,
↔
v
V
.
O
2max
Smith et al.
[87]
98 8 V
max
70% T
max
1
:
2 4 ↔T
max
, ↔ 3000m time, ↔V
.
O
2max,
↔V
max
a Changes indicated based on statistical significance at the p < 0.05 level.
HR
max
= maximum heart rate; n = number of participants; NR = not reported; RE = running economy; Reps = repetitions; RER = respiratory
exchange ratio; T
max
= time to exhaustion while running at V
max
; T
vent
= ventilatory threshold; V
max
= running speed at V
.
O
2max
; V
.
O
2max
=
maximal oxygen consumption; v V
.
O
2max
= ((Author: please define. Do you mean V
max
?)); ↓ = ((Author: decrease?)); ↑ = ((Author:
increase?)); ↔ = ((Author: no change?)).
Author proof
14 Laursen & Jenkins
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
Petersen
[173]
reported increases in V
.
O
2max
(+7%),
T
vent
(+16%), and 40km time-trial performance
(+8%) after 8 weeks of HIT at T
vent
heart rate (p <
0.05). Thus, improvements in aerobic capacity and
T
vent
can occur following HIT in previously or
moderately trained athletes. Only one study to
date, however, has attempted to examine HIT pro-
gramme optimisation in highly trained cyclists. In
this study, Stepto and colleagues
[81]
investigated
the effects of five different HIT programmes, per-
formed twice per week for 3 consecutive weeks, on
the rate of performance improvements in twenty
endurance-trained cyclists. The authors found that
performance (40km time trial and P
peak
) improve-
ments resulted from two markedly different HIT
programmes. One of these was a commonly used
HIT programme of ‘aerobic’ type intervals (8 × 4
minutes at 85% P
peak
, 90 seconds recovery) that has
previously been shown to improve endurance per-
formance.
[7,80,81,83]
However, a comparable im-
provement in performance resulted from intermit-
tent supramaximal training (12 × 30 seconds at
175% P
peak
, 4.5 minutes recovery). The other HIT
programmes (table II) failed to significantly im-
prove endurance performance. That intermittent
supramaximal training improved 40km time-trial
performance is intriguing, as training of this nature
has not previously been associated with improve-
ments in endurance performance. Thus, because
the mechanisms remain unknown, repeated sprint
training may be more important to the endurance
athlete than was previously thought. Further re-
search into HIT programme optimisation is re-
quired with cyclists, including the use of those con-
cepts that have shown success in highly trained
runners; namely the prescription of a HIT pro-
gramme using T
max
.
3.2.1 T
max
During Cycle Ergometry
As reviewed earlier((Author: please specify in
which section)), although T
max
has been devel-
oped as a practical method for determining the ap-
propriate length of the interval bout at V
max
in
highly trained runners,
[86]
HIT programme pre-
scription using this method has yet to be applied to
cycling. Use of the fractional utilisation of T
max
for
HIT prescription in cyclists is possible; Billat et
al.
[174]
determined T
max
in nine elite cyclists to be
222 ± 91 seconds, which was not significantly dif-
ferent to that of elite runners (321 ± 84 seconds).
Future research could utilise multisport athletes
(triathletes and duathletes) to determine whether or
not true statistical differences in T
max
exist between
exercise modes.
In brief, HIT prescription with highly trained
runners has been reasonably successful when V
max
is used to establish the intensity, and 50 to 60% of
T
max
is used for the exercise duration. Despite the
feasibility of using T
max
for prescribing HIT pro-
grammes in cyclists, longitudinal studies in cy-
clists have used more conventional programmes,
revealing that supramaximal sprinting may be a
more effective means of endurance performance
enhancement than previously thought.
3.3 Rate of Performance Enhancement
Following HIT
Very little information is available concerning
the rate at which endurance performance improves
following a given HIT stimulus. This is probably
due, at least in part, to the challenging nature of
carrying out research of a longitudinal repeated-
measure design. Lindsay et al.
[83]
showed, with
eight endurance-trained cyclists, that HIT elicited
no change in P
peak
or 40km time-trial performance
after 2 weeks, but there was an increase in both
P
peak
(+4.3%; p = 0.01) and 40km time-trial perfor-
mance (+3.5%; p < 0.001) after 4 weeks. Interest-
ingly, a similar time course of change in these vari-
ables has been shown in another study using the
same HIT programme repeated over 6 weeks,
[80]
suggesting that regular assessments of training sta-
tus and subsequent adjustments to HIT pro-
grammes are required to maximise improvements
in endurance performance. Indeed, Laursen and
co-workers
[82]
have recently shown that the in-
creases in T-
vent
(+22%) and P
peak
(+4.3%) in
highly trained cyclists are possible following just
four HIT sessions (20 × 60 seconds at P
peak
, 120
seconds recovery) over 2 weeks during the off-sea-
son (p < 0.05).
Author proof
Interval Training and Endurance Performance 15
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
In well trained runners, a single HIT session has
failed to elicit changes in V
.
O
2max
and T-
max
,
[162]
or
running economy in elite long-distance run-
ners.
[159]
In contrast, a recent study in untrained
individuals has shown that skeletal muscle adapta-
tions begin to occur after just one 16-hour training
session involving cycling for 6 minutes each hour
at ~90% V
.
O
2max
.
[46]
In this study, muscle was
biopsied from the vastus lateralis during a two-
stage (2 × 20 minutes) standardised submaximal
cycle protocol before and 36 to 48 hours after the
HIT session. Analysis revealed an attenuated de-
cline in phosphocreatine and glycogen use, as well
as a smaller rise in muscle lactate after the training.
There was no effect, however, on the maximal ac-
tivities of CS and malate dehydrogenase, suggest-
ing that adjustments in high-energy phosphates are
an early adaptive event that occur before increases
in oxidative potential following endurance exer-
cise training, at least in untrained individuals. Fu-
ture research is required to describe the time course
of adaptations resulting from HIT with highly
trained athletes.
3.4 Recovery Considerations
The importance of recovery following a HIT
session has been demonstrated in untrained indi-
viduals. Balsom et al.
[175]
showed that the distance
of repeated sprints (15, 30, 40m; 30 seconds recov-
ery) was positively related to a reduction in sprint
performance and an associated decline in the aden-
ine nucleotide pool. Furthermore, Rodas et al.
[51]
found significant increases in both oxidative and
glycolytic enzyme activities after 2 weeks of supra-
maximal cycle sprint training (table I), but after
only one rest day there was no change in 30 seconds
all-out performance. Nevertheless, marked in-
creases were found in V
.
O
2max
(+11.3%) and P
peak
(+10%) measured 5 days later (p < 0.05), suggest-
ing that fatigue or overtraining may have played a
role in preventing a significant improvement in the
30 seconds all-out test. In another study by the
same authors,
[52]
the aforementioned training
group was compared with a matched group of in-
dividuals completing the same training pro-
gramme, except that a 2-day rest period separated
each HIT session in the latter group. This length-
ened the entire training programme to 6 weeks.
While muscle enzyme activities were not signifi-
cantly increased in this study, performance in the
30 seconds all-out test was significantly improved
(p < 0.05). A comparison of these studies suggests
that muscle fibres experience fatigue or injury fol-
lowing HIT, indicating that sufficient recovery fol-
lowing the final training session is necessary for
the benefits of training to be detected.
Unfortunately, very little information is avail-
able concerning the optimal recovery duration be-
tween HIT bouts. Generally, coaches and re-
searchers have used fixed work-recovery ratios
(i.e. 2
:
1, 1
:
1, 1
:
2),
[78,85,86]
or recovery du-
rations based on heart rate returning to a fixed per-
centage of its maximum.
[55,74]
A recent study
[106]
compared the contribution of aerobic and anaero-
bic metabolism of different HIT programmes in ac-
tive (V
.
O
2max
= 57 ± 6 ml/kg/min) but not highly
trained individuals, using maximal accumulated
oxygen deficit as a measure of anaerobic capac-
ity.
[70]
A short recovery HIT protocol (6 to 7 × 20
seconds at 170% V
.
O
2max
, 10 seconds recovery) re-
sulted in a higher accumulated oxygen deficit and
V
.
O
2
than a long recovery HIT protocol (4 to 5 × 30
seconds at ~200% V
.
O
2max
, 2 minutes recovery),
suggesting that supramaximal HIT with short re-
covery periods may maximally tax aerobic and an-
aerobic capacities. One apparent limitation to a
shortened recovery in untrained individuals, is that
a reduced number of intervals might be completed
and thus less work achieved.
[175]
However, evi-
dence for this was not found in a recent study by
Zavorsky et al.
[88]
In this study, 12 highly trained
runners (V
.
O
2max
= 72.5 ± 4.3 ml/kg/min) were as-
signed to different HIT recovery groups (duration
= 1, 2 or 3 minutes) following three HIT sessions
(10 × 400m running) run at 4% below V
max-
over 2
weeks. While there was an overall increase in run-
ning economy when the group was considered as a
whole, no differences were found between the
groups. Thus, the optimal recovery duration be-
tween HIT bouts is yet to be determined.
Author proof
16 Laursen & Jenkins
Adis International Limited. All rights reserved. Sports Med 2001; 32 (1)
The importance of active versus passive recov-
ery bouts following HIT work bouts has recently
been addressed.
[104]
Because high lactate levels de-
velop during interval training performed at an in-
tensity greater than T
lac
, active recovery facilitates
lactate removal
[176,177]
and allows athletes to toler-
ate heavy work rates for longer periods.
[104,125]
The
use of active recovery in the prescription of HIT
programmes therefore appears justified. Interest-
ingly, training status seems to be unrelated to the
decline in plasma lactate during passive recovery
from exercise at equivalent relative maximal work
intensities.
[178]
In athletes, the importance of a taper following
a phase of increased training volume and intensity
appears essential.
[105,179]
Most recently, Mujika et
al.
[180]
examined the physiological and perfor-
mance responses to different 6-day tapers in eight
well-trained male middle-distance runners. In this
study, runners completed 15 weeks of their regular
training programme, and were then assigned to ei-
ther a moderate (50% reduction in training volume
and intensity) or a low volume taper (75% reduc-
tion in training volume and intensity). The type of
taper showed no effect on either 800m-run perfor-
mance or changes in haematological status, sug-
gesting that middle-distance runners can progres-
sively reduce their usual training volume by at least
75% during a 6-day taper.
4. Conclusion
Considerable information is available relating
to the physiological responses that result from sub-
maximal training and HIT in untrained individuals.
In contrast, very little is known of how already
highly trained athletes respond to a modified train-
ing programme. However, it does not appear that
additional submaximal endurance training volume
improves endurance performance or related phys-
iological variables in this particular population.
[9]
In contrast, HIT, in many forms, can elicit signifi-
cant improvements in endurance performance in
already highly trained athletes.
[81,82,86]
To date,
however, researchers have been unsuccessful in
explaining the reasons for this improve-
ment.
[7,74,80]
Further investigation into the re-
sponse of central and peripheral factors to HIT in
the highly trained athlete is therefore warranted.
Finally, coaches and athletes are in need of more
knowledge concerning HIT programme optimisa-
tion; the optimal HIT programme intensity, dura-
tion and recovery that elicit the greatest rate of im-
provement in endurance performance are yet to be
reported.
Acknowledgements
‘Author: please provide information, for publication
in the acknowledgements section of the manuscript, on
any sources of funding that were used to assist in the
preparation of this manuscript; and on any potential
conflicts of interest that the authors may have that are
directly relevant to the contents of this manuscript’.
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Correspondence and offprints: Paul B. Laursen, School of
Human Movement Studies, University of Queensland,
Brisbane, 4072, Australia. ((Author: Please confirm that
this is your correct postal address))
E-mail: plaursen@hms.uq.edu.au ((Author: would you
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