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 Sports Med 2006; 36 (1): 65-78
REVIEW ARTICLE 0112-1642/06/0001-0065/$39.95/0

 2006 Adis Data Information BV. All rights reserved.

Possible Stimuli for Strength and

Power Adaptation
Acute Metabolic Responses
Blair Crewther, John Cronin and Justin Keogh
Institute of Sport and Recreation Research New Zealand, Division of Sport and Recreation,
Auckland University of Technology, Auckland, New Zealand

Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
1. Metabolic Stimulus and Resistance Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
1.1 Lactate Production . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
1.2 Mechanisms for Adaptation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
1.3 Acute Lactate Response . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
1.3.1 Programme Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
1.3.2 Sex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
1.3.3 Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
1.3.4 Weight Training Status (Trained vs Untrained) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
1.3.5 Weight Training Status (Highly Trained vs Untrained) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
1.3.6 Training Status (Weight Trained vs Endurance Trained) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
1.3.7 Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
2. Implications for Strength and Power Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74
3. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Abstract The metabolic response to resistance exercise, in particular lactic acid or

lactate, has a marked influence upon the muscular environment, which may
enhance the training stimulus (e.g. motor unit activation, hormones or muscle
damage) and thereby contribute to strength and power adaptation. Hypertrophy
schemes have resulted in greater lactate responses (%) than neuronal and dynamic
power schemes, suggesting possible metabolic-mediated changes in muscle
growth. Factors such as age, sex, training experience and nutrition may also
influence the lactate responses to resistance exercise and thereafter, muscular
adaptation. Although the importance of the mechanical and hormonal stimulus to
strength and power adaptation is well recognised, the contribution of the metabol-
ic stimulus is largely unknown. Relatively few studies for example, have
examined metabolic change across neuronal and dynamic power schemes, and not
withstanding the fact that those mechanisms underpinning muscular adaptation, in
relation to the metabolic stimulus, remain highly speculative. Inconsistent find-
ings and methodological limitations within research (e.g. programme design,
sampling period, number of samples) make interpretation further difficult. We
contend that strength and power research needs to investigate those metabolic
mechanisms likely to contribute to weight-training adaptation. Further research is
66
also needed to examine the metabolic responses to different loading schemes, as
well as interactions across age, sex and training status, so our understanding of
how to optimise strength and power development is improved.
The importance of the acute mechanical and hor-
monal stimulus for strength and power adaptation is
well recognised.[1-5] Literature now suggests that the
acute metabolic stimulus may also be important for
resistance training adaptation to occur.[6,7] Compari-
son of eccentric and concentric training provides
some insight into the importance of the metabolic
stimulus. That is, concentric-only training has been
found equally effective in stimulating strength and
hypertrophy compared with eccentric-only train-
ing,[8-11] despite the mechanical benefits afforded by
eccentric actions (e.g. greater forces, greater muscle
damage).[12-14] This may be attributed to the greater
metabolic costs associated with concentric ac-
tions.[15,16] The responses to weight training com-
bined with vascular occlusion, provide further evi-
dence of the metabolic contribution to adaptation.
Occluding the muscle during resistance exercise
leads to greater accumulation of metabolic by-prod-
ucts, enhancing the metabolic stimulus and the
adaptive responses to such exercise. As a result,
similar adaptations have been found when compar-
ing light-load training with occlusion and
heavy-load training,[17] and greater adaptation with
light-load training with occlusion, than that found
without occlusion.[18,19]
The acute metabolic stimulus is itself related to
the build-up of metabolic by-products, in particular
lactic acid, within the muscular environment. A
build-up of these products may increase the secre-
tion of various anabolic hormones (e.g. growth hor-
mone [GH])[20-22] or lead to greater motor unit acti-
vation at a given load,[20,23] thereby contributing to
the weight-training stimulus. An increase in meta-
bolic waste products, combined with altered hydro-
gen ion concentrations and adenosine triphosphate
(ATP) deficiency, may also produce some muscle
damage,[24] further enhancing the training stimulus.
Over time, it may be expected that these acute
 2006 Adis Data Information BV. All rights reserved.
Crewther et al.
responses (i.e. greater hormone secretion, increased
motor unit recruitment, muscle damage) would fa-
cilitate adaptations leading to changes in the
force-generating capacity of muscle and thus,
greater strength and/or power. Traditionally, it is
believed that large ‘metabolic responses’, such as
those seen during endurance-type exercises, does
not produce any significant changes in strength and
power. However, during weight training, blood sup-
ply is occluded during movement and in the pres-
ence of other mechanical and hormonal stimuli,
produce adaptations that may vary quite considera-
bly from that seen with endurance exercise.
The measurement of lactic acid, or lactate, is
frequently used to determine the anaerobic contribu-
tion from glycolysis during exercise.[25,26] Thus, pro-
gramme design (e.g. load intensity, volume, rest
periods) plays an important role in determining the
metabolic response to such exercise and the likely
contribution of the metabolic stimulus. For example,
those programmes designed to induce the greatest
change in morphological adaptation, or muscle
growth, are characterised by relatively large in-
creases (%) in blood lactate levels,[27-33] hence,
greater contribution from the metabolic stimulus.
However, little is known regarding the metabolic
stress imposed on the system by other strength and
power schemes used within practice (e.g. neuronal
and dynamic power). Debate also surrounds those
mechanisms that may potentially underlie weight-
training induced adaptation. The aim of this review
is to therefore critique what literature there is availa-
ble in this area, so that we may develop a better
understanding as to the possible contribution of the
metabolic stimulus to strength and power develop-
ment. Such an understanding may enable resistance
exercise to be prescribed more effectively for induc-
ing these changes, thereby improving strength and
conditioning practice.
Sports Med 2006; 36 (1)
Possible Stimuli for Strength and Power Adaptation
1. Metabolic Stimulus and
Resistance Exercise
Weight training is a powerful exercise stimulus
for strength and power adaptation, which may be
partly attributed to the lactic acid response, or its
blood equivalent (lactate), during a single exercise
bout. Examining those schemes specifically de-
signed to improve strength and power will provide
understanding as to the importance of the metabolic
stimulus in the development of these qualities. In the
first instance, those energetic processors influencing
lactic acid production will be briefly reviewed, fol-
lowed by an examination of those mechanisms that
underlie weight training-induced adaptation, in rela-
tion to the metabolic stimulus. This article will then
examine the acute lactate responses to three broad
types of programmes often used within practice: (i)
hypertrophy (controlled movements, moderate
loads, short rest periods, high total work); (ii) neu-
ronal (explosive intent, heavy loads, long rest peri-
ods, lower total work); and (iii) dynamic power
(explosive and/or ballistic movements, light loads,
moderate rest periods, lower total work) schemes.
The influence of age, sex, training status and nutri-
tion, upon the acute lactate response to resistance
exercise, will also be investigated.
1.1 Lactate Production
The energy source for all muscular contractions
is ATP and due to the fact that only small amounts
of this compound are stored inside the muscle cell, it
must be continually resynthesized at its rate of use.
The resynthesis of ATP is predominantly achieved
through the three classic energy systems or path-
ways: (i) phosphagen system; (ii) anaerobic glycoly-
sis; and (iii) oxidative phosphorylation.[34,35] Briefly,
when the muscle is contracting at low intensities the
energy for muscular activity is provided primarily
through the aerobic energy system, oxidative phos-
phorylation. During high-intensity activities, how-
ever, this system is unable to supply ATP at the rate
at which it is required. Energy supply for intense
activities of short duration is met through the phos-
phagen system, which relies on stored creatine
phosphate to synthesize ATP. Given that this system
 2006 Adis Data Information BV. All rights reserved.
67
has only a limited capacity for energy restoration,
intense activities of longer duration require a greater
proportion of ATP to be resynthesized via glycoly-
sis. This process involves the breakdown of carbo-
hydrates (CHO), in the form of glucose or glycogen,
to synthesize ATP and in doing so, results in lactic
acid formation within the muscle. Once lactic acid is
formed in the muscle, it diffuses rapidly into the
blood, where it is buffered to form lactate. Thus, an
accumulation of lactic acid or blood lactate may be
observed when there is greater reliance upon glycol-
ysis, to meet the energetic demands of exercise.
Although blood lactate concentration is not a defini-
tive measure of lactic acid production, it does pro-
vide an indirect measure of lactic acid and one that is
less invasive to extract compared with muscle biop-
sies, and more widely used within research. For
these reasons, this article will focus primarily upon
blood lactate responses to resistance exercise.
1.2 Mechanisms for Adaptation
The contribution of the mechanical and hormonal
stimuli to resistance training adaptation is well
recognised. For instance, the production of high
forces and time under tension are important mechan-
ical factors thought necessary for improving maxi-
mal strength.[1,36,37] Changes in muscle morphology
are further mediated by the interaction of the anabol-
ic (e.g. testosterone, GH, insulin) and catabolic (e.g.
cortisol) hormones.[2-4] In order to adequately train
power, movements producing high power outputs
with high contractile velocities are thought impor-
tant.[38,39] The role of the metabolic stimulus in
facilitating improvement in strength and power
would appear to be more indirect. First, an accumu-
lation of lactic acid in response to resistance exer-
cise produces a shift in the acid balance of muscle,
reducing muscle pH, increasing muscle acidity and
the build-up of hydrogen ions. As a result of these
changes in the muscular environment, various other
training mechanisms may be stimulated (e.g. motor
unit activation, hormones, muscle damage), thereby
enhancing the weight-training stimulus and signal-
ling pathways for long-term adaptation to occur
Sports Med 2006; 36 (1)
68
Resistance
exercise stimulus
Strength and
power adaptation
Fig. 1. Schematic representation of those events signalling long-term adaptation.
during the recovery period. These events are out-
lined in figure 1.
The mechanisms by which the metabolic stimu-
lus contributes to adaptation are often based on
research where the metabolic environment is artifi-
cially altered (i.e. occlusion). By occluding the mus-
cle during voluntary contractions, greater lactic acid
accumulation occurs, enhancing the metabolic stim-
ulus. Takarada and Ishii[23] for example, found that
the integrated electromyography (EMG – an index
of muscle activity) of a low intensity (40% one
repetition maximum [1RM]) exercise performed
with occlusion, was almost equal to that of a high-
intensity (80% 1RM) exercise performed without
occlusion. Enhanced EMG has also been found with
an exercise performed with a light load (20% 1RM)
in an occluded state, compared with that performed
with the same load in a non-occluded state.[20] It
would seem from these findings that an increase in
lactic acid accumulation, at a given load, would
produce a concomitant increase in motor unit activa-
tion. Takarada et al.[20] also reported a 290-fold
increase in plasma GH concentrations with the low-
intensity exercise (with occlusion), whereas no such
effect was found after the same exercise without
occlusion. This finding supports suggestions that an
increase in blood lactate and hydrogen ion concen-
trations may augment the hypophyseal secretion of
GH.[20-22] Research supports such a notion with the
largest GH responses observed in those protocols
producing the greatest lactate responses.[27,29-33,40]
Although occlusion enhances metabolic activity
within the muscle, this type of methodology may not
reflect the metabolic environment occurring under
normal weight-training conditions.
 2006 Adis Data Information BV. All rights reserved.
Crewther et al.
Lactic acid Altered muscular
accumulation environment
Enhanced stimulus (e.g. motor unit
recruitment, hormones, muscle damage)
Increase force- Cumulative training
generating capacity response
There is some speculation that an accumulation
of metabolic by-products (e.g. lactate), combined
with altered hydrogen ion concentrations and ATP
deficiency, plays a role in mediating muscle tissue
damage.[24] Greater muscle damage, as indicated by
elevated creatine kinase levels, has also been ob-
served in those schemes producing the greatest lac-
tate responses,[28] thereby possibly demonstrating a
causal relationship between lactate accumulation
and muscle tissue breakdown. The importance of
muscle damage as a mediator for adaptation, lies in
the overcompensation processors associated with
muscle recovery and repair (e.g. greater protein
[PRO] synthesis). If muscle damage mediated the
remodelling of muscle tissue and subsequently,
muscle growth, then the metabolic stimulus may be
an important component for inducing changes in
muscle morphology. However, most data indicate
that the mechanisms for muscle damage are more
likely to involve mechanical (e.g. high forces,
greater active strain), rather than metabolic fac-
tors.[14,41,42] It also remains to be seen if muscle
damage is a prerequisite for muscle growth to occur,
as changes in muscle morphology are also linked to
factors such as age, nutrition, sex, genetic predispo-
sition and training status.
Fatigue is often thought an important component
for strength adaptation to occur[43] and as such,
places some emphasis on the metabolic stimulus
(i.e. increase lactate accumulation = greater fatigue).
The rationale for training in this manner lies in the
belief that additional motor units, in particular the
high-threshold motor units, are recruited when try-
ing to maintain performance when fatigued.[44] If
motor units are trained upon recruitment, then train-
ing to fatigue would stimulate a greater number of
Sports Med 2006; 36 (1)
Possible Stimuli for Strength and Power Adaptation
fibres (and greater adaptation) than non-fatigue
training. The findings of Takarada et al.[20] and
Takarada and Ishii[23] lend support to this conten-
tion. Although bodybuilders often train in this man-
ner, there is still little scientific data to support such
a practice. In fact, studies have found that training to
failure or exhaustion is not necessary for optimal
adaptation to occur,[45-48] which may be partially
explained by the complex nature of fatigue. As well
as lactate accumulation, fatigue may also result from
changes in CNS drive to the motor neurons, changes
in neuromuscular propagation, dehydration and the
availability of various metabolic substrates.[43,49,50]
Such mechanisms may also vary depending on fac-
tors such as muscle fibre type,[43] age or sex.[51]
Regardless of the mechanism, it should be
recognised that exercising in a fatigued state is like-
ly to compromise the ‘quality’ of performance (e.g.
high power output). Further research is therefore
needed to elucidate those mechanisms underpinning
the metabolic stimulus, as well as the relative impor-
tance of these effects to weight training adaptation.
1.3 Acute Lactate Response
1.3.1 Programme Design
Those resistance exercise schemes designed to
increase strength through primarily morphological
adaptation (i.e. hypertrophy) generally result in
large increases (%) in circulating blood lactate
levels from pre-exercise (see table I). In comparison,
those programmes designed to increase strength
through mainly neural adaptation (i.e. neuronal)
have generally resulted in much lower blood lactate
responses (see table II). For example, Kraemer et
al.[27] compared the lactate response to eight exer-
cises performed with a 5RM load for 3–5 sets per
exercise and 3 minutes of rest between sets or a
10RM load (three sets per exercise) with 1-minute
rest periods. The peak lactate response to the hyper-
trophy scheme (433%) was found to be much
greater than that reported following the neuronal
scheme (133%). This may be attributed to the
greater amount of work performed in the hypertro-
phy scheme (greater work = greater time under
tension) in conjunction with the much shorter rest
 2006 Adis Data Information BV. All rights reserved.
69
periods between sets and exercises. Such a result is
in agreement with other research.[28-33]
Dynamic power schemes have also been shown
to elicit significant lactate responses (see table II). A
50% increase in serum lactate was found in response
to an exercise session consisting of half-squat exer-
cises (ten sets × six repetitions), performed with 1-
and 4-minute rest periods.[67] Another study investi-
gated the effect of six sets of leg extensions with
loads of 70% (I-70) and 35% (I-35) 1RM.[54] The
response found in the I-35 condition was similar to
the I-70 condition (13- to 14-fold increase in lac-
tate), which may be due to the average number of
repetitions performed in each set, with I-35 more
than twice that performed in I-70 (13 vs 6, respec-
tively). This value is much greater than other dy-
namic power schemes and may be explained by
extraction from a muscle biopsy (lactic acid) and
with each set performed to failure. Whilst subtle
differences in programme design make it difficult to
determine the overall response to each scheme, on
average, hypertrophy schemes have produced
greater lactate responses (500%) than the neuronal
(200%) and dynamic power (70%) schemes. It is
evident, however, that much less research has pro-
filed the lactate response to neuronal and dynamic
power, than hypertrophy schemes. Additional re-
search into the metabolic nature of neuronal and
dynamic power schemes would improve our under-
standing as to the contribution of the metabolic
stimulus to adaptive changes associated with these
training methods.
1.3.2 Sex
It has been reported that males exhibit greater
lactate responses to a bout of resistance exercise
compared with females.[31,69-71] For instance, Krae-
mer et al.[31] observed greater lactate responses
among recreationally trained males to a hypertrophy
scheme consisting of eight exercises (three sets × ten
repetitions, 10RM), when compared with a similar
female population (648% vs 468%, respectively). A
similar result was found, in the same study, when
examining the lactate responses to a neuronal type
scheme in both males (230%) and females (140%).
The observed differences may be attributed to males
Sports Med 2006; 36 (1)
70 Crewther et al.

Table I. Acute lactate response to hypertrophy schemes

Study Subjects Protocols Lactate response
exercise(s), sets × reps (load) (% change)
Vanhelder et al.[52] 5 M, UT 1 ex, 7 × 10 (10RM) ↑ 650
Tesch et al.[53] 9 M, T 4 ex, 5 × 6–12 (6–12RM) ↑ 391a
Kraemer et al.[29] 9 M, T 8 ex, 3 × 10 (10RM) ↑ 592
Robergs et al.[54] 8 M, T 1 ex, 6 × 6 (70% 1RM) ↑ ~1300a
Kraemer et al. [31]
8 M, T 8 ex, 3 × 10 (10RM) ↑ 648
8 F, T 8 ex, 3 × 10 (10RM) ↑ 478
Kraemer et al.[55] 8 M, UT 4 ex, 3 × 10 (10RM) ↑ ~750
Kraemer at al.[28] 8 M, T 8 ex, 3 × 10 (10RM) ↑ ~600
Kraemer at al.[27] 9 F, T 8 ex, 3 × 10 (10RM) ↑ 433
Hakkinen and Pakarinen[30] 10 M, T 1 ex, 10 × 10 (10RM) ↑ 971
Fahey et al.[56] 10 M, T 9 ex, 5 × 8–12 (70% 1RM) SUP ↑ ~313
10 M, T 9 ex, 5 × 8–12 (70% 1RM) PLA ↑ ~290
McBride et al.[57] 8 F, UT (RJ) 9 ex, 3 × 10 (10RM) ↑ ~623
8 F, UT (CR) 9 ex, 3 × 10 (10RM) ↑ ~750
Mulligan et al.[58] 10 F, T 8 ex, 1 × 10 (10RM) ↑ ~550
8 ex, 3 × 10 (10RM) ↑ ~430
Gotshalk et al.[59] 8 M, T 8 ex, 1 × 10 (10RM) ↑ ~440
8 ex, 3 × 10 (10RM) ↑ ~690
Kraemer et al.[60] 9 M, T 4 ex, 4 × 10 (10RM) ↑ ~718
Hakkinen et al.[61] 10 M (26y), UT 2 ex, 4 × 10 (100% MVC) ↑ ~200
10 M (70y), UT 2 ex, 4 × 10 (100% MVC) ↑ ~75
Kraemer et al.[62] 8 M (30y), UT 1 ex, 4 × 10 (10RM) ↑ ~700
9 M (62y), UT 1 ex, 4 × 10 (10RM) ↑ ~420
Kraemer et al.[63] 8 M (30y), UT 1 ex, 4 x 10 (10RM) ↑ ~700
9 M (62y), UT 1 ex, 4 x 10 (10RM) ↑ ~380
Kraemer et al.[64] 7 M, T 1 ex, 1 × failure (80% 1RM) ↑ ~340
12 M, UT 1 ex, 1 × failure (80% 1RM) ↑ ~310
MacDougall et al.[65] 8 M, T 1 ex, 1 × failure (80% 1RM) ↑ 105a
1 ex, 3 × failure (80% 1RM) ↑ 176a
Linnamo et al.[66] 8 M, UT 1 ex, 5 × 10 (67% MVC) ↑ 527
Zafreiridis et al.[33] 10 M, T 4 ex, 4 × 10 (75% 1RM) ↑ ~744
Smilios et al.[32] 11 M, T 4 ex, 2 × 10 (75% 1RM) ↑ ~700
4 ex, 4 × 10 (75% 1RM) ↑ ~850
4 ex, 6 × 10 (75% 1RM) ↑ ~760
a Lactic acid.
CR = competitive runners; ex = exercises; F = females; M = males; MVC = maximal voluntary contraction; PLA = placebo; reps =
repetitions; RJ = recreational joggers; RM = repetition maximum; SUP = supplement; T = trained; UT = untrained; ↑ indicates increase.

generally possessing greater lean muscle mass and
using heavier relative loads than females. Muscle
composition may also be important, one study re-
porting differences in the relative cross-sectional
area of the three major fibres, in the vastus lateralis
muscle, in males (IIA > I > IIB) and females (I > IIA
> IIB), respectively.[72] Given that the type II or fast
twitch fibres have a greater glycolytic capacity than
the type I or slow twitch fibres,[26,73] male muscle is
likely to exhibit greater potential for lactate produc-
tion than female muscle. Still, some researchers
have reported similar lactate responses between
males and females, performing the same resistance
exercise programmes.[21,74] Disparate findings may
be explained by differences in programme design,
sampling procedures (e.g. number) post-exercise
and the relative training experience of subjects.
1.3.3 Age
Subject age would appear to be an important
factor modulating the lactate response to a single

 2006 Adis Data Information BV. All rights reserved. Sports Med 2006; 36 (1)
Possible Stimuli for Strength and Power Adaptation 71

resistance exercise session. Mero and colleagues[68]
examined the lactate response of adult and pubertal
males, to an exercise programme consisting of half-
squat lifts (ten sets × six repetitions, 1- and 4-minute
rest periods), performed with a relative load of 50%
1RM. The lactate responses were found to be lower
among the adult males compared with the younger
males, for both the 1- (94% vs 27%) and 4-minute
(35% vs 0%) rest periods. Another study[71] also
reported a greater lactate response among pubescent
boys, than men, when examining the lactate re-
sponse to a single exercise bout of knee extensions
(five sets × ten repetitions, 40% 1RM), followed by
two additional sets to exhaustion. The larger re-
sponses in the younger males may be partially attrib-
uted to differences in maturation, trainability and the
ability to tolerate stressful exercise. To our knowl-
edge no research has examined the same age-related
effects among female populations. Given the limited
data in this area, it is suggested that further research
be conducted in order to differentiate the lactate
responses across these groups (pubescent and adult),
in both males and females.
A reduction in the lactate response to resistance
exercise, with increasing age after adulthood, has
been reported previously. A group of adult males
(30 years) for example, reported a 700% increase in
blood lactate, whereas a group of older males (60
years) reported a 420% increase, performing an
identical exercise session.[62] Other researchers have
also reported greater lactate responses among young
adult males, when compared with elderly
males.[61,63,70] The greater lactate responses for
younger adults may be explained by the use of
heavier absolute loads (i.e. greater 1RM strength)
and their ability to exercise at a greater relative
intensity. The differential lactate responses may be
further attributed to a reduction in the size of the

Table II. Acute lactate response to neuronal and dynamic power schemes
Subjects Subjects Protocols Lactate response
exercise(s), sets × reps (load) (% change)
Neuronal schemes
Kraemer et al.[29] 9 M, T 8 ex, 3/5 × 5 (5RM) ↑ 180
Kraemer et al.[31] 8 M, T 8 ex, 3/5 × 5 (5RM) ↑ 230
Kraemer et al.[31] 8 F, T 8 ex, 3/5 × 5 (5RM) ↑ 140
Kraemer at al.[27] 9 F, T 8 ex, 3/5 × 5 (5RM) ↑ 133
Hakkinen and Pakarinen[30] 10 M, T 1 ex, 20 × 1 (100% 1RM) ↑ 84
Kraemer at al.[28] 8 M, T 8 ex, 3/5 × 5 (5RM) ↑ ~223
Zafeiridis et al.[33] 10 M, T 4 ex, 4 × 5 (88% 1RM) ↑ ~319
Smilios et al.[32] 11 M, T 4 ex, 2 × 5 (88% 1RM) ↑ ~350
4 ex, 4 × 5 (88% 1RM) ↑ ~400
4 ex, 6 × 5 (88% 1RM) ↑ ~350

Dynamic power schemes

Robergs et al.[54] 8 M, T 1 ex, 6 × 13 (35% 1RM) ↑ ~1400a
Mero et al.[67] 9 M, T 1 ex, 10 × 6 (50% 1RM)b ↑ ~50
1 ex, 10 × 6 (50% 1RM)c ↑ ~50
Mero et al.[68] 6 M (24y) 1 ex, 10 × 6 (50% 1RM)b Nil
1 ex, 10 × 6 (50% 1RM)c ↑ 27
6 M (15y) 1 ex, 10 × 6 (50% 1RM)b ↑ 35
1 ex, 10 × 6 (50% 1RM)c ↑ 94
Linnamo et al.[66] 8 M, UT 1 ex, 5 × 10 (40% MVC) ↑ 209
a Lactic acid.
b 4-minute rest.
c 1-minute rest.
ex = exercises; F = females; M = males; MVC = maximal voluntary contraction; reps = repetitions; RM = repetition maximum; T = trained;
UT = untrained; ↑ indicates increase.

 2006 Adis Data Information BV. All rights reserved. Sports Med 2006; 36 (1)
72
type II muscle fibres, with the aging process[75,76]
and hence, a reduction in the glycolytic capabilities
of muscle. Whilst increasing age would appear to
lower lactate responses among males, age-related
differences among females are less clear. Copeland
et al.[77] found no differences in the lactate response
to a single resistance exercise bout, performed
across five different age groups (mean age 25, 34.5,
43.8, 52.4 and 62.3 years). The findings of Hakkinen
et al.,[70] however, support those found among
males, with greater lactate responses among middle-
aged (39 years) women, than elderly (67 years)
women, to a single exercise bout. Differences in
programme design and in the age groups assessed
again make comparisons difficult. More research is
needed to determine if elderly females show an
inhibited lactate response to resistance exercise.
1.3.4 Weight Training Status (Trained vs Untrained)
A group of previously untrained males reported a
reduced blood lactate response (700% vs 500%), to
an acute exercise bout (4 sets of 10RM squats), after
10 weeks of periodised weight training.[63] A similar
finding was reported by Pierce et al.[78] after 8 weeks
of weight training. It would seem from these find-
ings that short periods of resistance training elicits
those adaptations more commonly observed with
aerobic training (e.g. lowered lactate response to
exercise) among previously untrained individuals.
Such training effects may, however, diminish with
increasing age.[63] It is accepted that these effects are
the result of adaptations in muscle fibre capillarisa-
tion, oxygen extraction, fibre conversion, enzyme
activity and substrate levels.[7,79,80] For instance,
studies examining the effect of different strength
programmes, among those previously untrained,
have reported an increase in the percentage of type
IIA and decrease in the percentage of type IIB
fibres.[81-84] Combined with proportional increases
in capillary density,[84,85] such changes may enhance
the oxidative potential of muscle and reduce lactate
accumulation. However, the above findings are not
necessarily typical, with another study reporting no
changes in acute lactate responses with training.[21]
A major factor to consider is the type of training
programme employed, with endurance-based
 2006 Adis Data Information BV. All rights reserved.
Crewther et al.
programmes likely to lead to adaptations that would
improve oxidative capacity, more so than maximal
strength or power-based programmes. The health
status of subjects may be another point to consider,
with untrained sedentary adults less likely to experi-
ence training specific adaptations than those who are
untrained but active.
1.3.5 Weight Training Status (Highly Trained
vs Untrained)
Given that weight training is often performed in
such a manner as to activate the glycolytic system,
one may also expect highly trained individuals to
exhibit training adaptations, leading to increased
production of lactate (e.g. increase glycolytic en-
zymes, increase fast twitch fibre size). Brown et
al.,[86] for instance, reported a greater lactate re-
sponse among weight-trained males (570%), than
untrained males (330%), performing three sets of
leg press movements to failure. Such a finding sup-
ports the earlier work by Stone et al.[87] who also
reported a greater lactate response in well trained
individuals. The differential responses were attribut-
ed to the greater 1RM strength of those with weight-
training experience and the greater muscle mass of
these subjects. Weight-trained individuals also ex-
hibit greater levels of lactate dehydrogenase, an
important mediator in pyruvate conversion to lac-
tate, in both fast and slow twitch muscle,[88] provid-
ing ‘trained muscle’ with a greater glycolytic capac-
ity than untrained muscle. It may be further specu-
lated that weight-trained individuals have a
psychological makeup for intense anaerobic exer-
cise, which would allow them to exhaust their mus-
cle to a greater extent (increase lactate production),
than untrained individuals.
In contrast to the above findings, Ahtiainen et
al.[89] reported no differences in the lactate response
to two different squat sessions (four sets × 12RM
and four sets × 8RM plus four forced repetitions),
performed by strength trained and untrained ath-
letes. Other research are in agreement with this
finding,[64,90,91] thereby suggesting no differences in
acute lactate responses, as a function of training
status. Differences in programme design again make
comparisons problematic. For instance, weight-
Sports Med 2006; 36 (1)
Possible Stimuli for Strength and Power Adaptation
trained individuals may only exhibit greater lactate
responses when lifting maximal or near maximal
loads.[86] McMillan et al.[90] did, however, report
lower lactate concentrations at 90 minutes post-
exercise in the trained group, which suggests greater
lactate clearance in those who are well trained.
When comparing data, one must also account for the
nature of the weight-training experience. Olympic/
power lifting is typically characterised by heavier
loads, lower volume and longer rest periods than
bodybuilding-type programmes. The different train-
ing strategies may explain the greater percentage of
slow twitch fibres and greater mitochondrial density
seen among bodybuilders, than Olympic/power lift-
ers,[88,92] and consequently, different lactate re-
sponses to resistance exercise. Still, Kraemer et
al.[93] found no differences in the lactate response to
a heavy resistance exercise session performed by
competitive bodybuilders and power lifters, al-
though the bodybuilders appeared to better tolerate
exercise based upon enhanced performance and re-
duced sympatomatology.
One of the difficulties with research interpreta-
tion lies in the different sampling procedures em-
ployed (e.g. sampling duration and intervals), when
determining the metabolic response to resistance
exercise. For example, a single sample collected
after exercise may not adequately characterise the
metabolic environment afforded by such exercise,
particularly given the time-course delay in lactate
accumulation, due to lactic acid diffusion into the
blood. Employing longer sampling periods, and col-
lecting a greater number of samples post-exercise,
would no doubt prove beneficial in determining the
lactate responses afforded by different exercise
programmes, as well as differentiating the effects of
age, sex, training status, etc. The sampling of blood
in such a manner would also help determine what, if
any, interactive effects exist between these factors
and the lactate responses to resistance exercise.
1.3.6 Training Status (Weight Trained vs
Endurance Trained)
The type of training experience is important in
modulating the acute lactate response to resistance
exercise. Brown and colleagues[86] compared the
 2006 Adis Data Information BV. All rights reserved.
73
responses among two trained groups (weight trained
and endurance trained), each performing three sets
of leg press movements to exhaustion. The lactate
response in the weight-trained group was signifi-
cantly elevated above the other group after the last
set and remained so throughout the 15-minute re-
covery period. Regan and Potteiger[94] reported a
similar response (weight trained > endurance
trained), examining blood lactate concentrations in
strength/power and endurance athletes at three dif-
ferent velocities, on an isokinetic dynamometer.
Such results are not surprising given that endurance
training is thought to reduce lactate accumulation
during exercise,[26,95] reflecting the adaptive re-
sponse of the body to this type of training. That is,
endurance athletes exhibit greater capillary supply
and density, and a greater percentage of type I fibres
than weight-trained athletes.[96,97] Given that train-
ing of this nature is also known to increase the
number and volume of mitochondria, increase oxi-
dative and decrease glycolytic enzyme activity,[98,99]
such differences provide endurance-trained muscle
with greater oxidative capacity (i.e. reduce lactate
production, increase lactate removal) than weight-
trained muscle. Central adaptations to endurance
training (e.g. increase haemoglobin and haematocrit
levels, increase stroke volume, greater fatty acid
metabolism)[95,100,101] would further inhibit the ac-
cumulation of lactate. Again, respective differences
in 1RM strength and lean muscle mass, being typi-
cally greater in resistance-trained individuals, would
also explain the greater responses found among
weight-trained athletes.
1.3.7 Nutrition
It would appear that nutritional strategies (CHO
and/or PRO) have little influence upon acute lactate
responses to resistance exercise.[56,60,102,103] Wil-
liams et al.[102] examined the effect of a PRO and
CHO supplement ingested immediately after the
performance of three different workouts (low, mod-
erate and high training volume). Supplementation
produced no differences in blood lactate in any
workout, from that observed in a placebo group.
Kraemer et al.[60] investigated the influence of PRO
and CHO supplementation, taken before and after
Sports Med 2006; 36 (1)
74
exercise, and repeated over 3 consecutive days with
exercise. Although no differences in lactate re-
sponses were found on day one, a lowered lactate
response was reported over days two and three with
supplementation. It was suggested that the lower
lactate responses might be due to a relative increase
in the proportion of lipid as a fuel source or greater
conversion of lactate into glycogen.[60] However, in
practice resistance exercise is not typically per-
formed in such a manner (i.e. 3 consecutive days of
the same programme). Therefore, any changes in the
metabolic environment occurring under these condi-
tions, may not reflect those likely to occur in the
‘real world’. Other possibilities include a reduction
in muscle glycogen levels, resynthesis of lactate
back to glycogen or increased clearance of lactate
via gluconeogenesis. Pre-training levels of glycogen
are another important consideration, as lactate pro-
duction may increase if muscle glycogen is in-
creased to supramaximal levels prior to exercise.[26]
Alternatively, low muscle glycogen levels may lead
to greater utilisation of lactate as a fuel source,
resulting in greater lactate removal.[104] Addressing
such issues is beyond the scope of this review.
2. Implications for Strength and
Power Development
From the data reviewed, it would appear that
hypertrophy schemes elicit relatively large increases
in blood lactate concentrations to a single training
session. Furthermore, such responses are greater
than that found across a single neuronal or dynamic
power session. This may be attributed to the specific
configuration of the various training variables and
subsequently, the relative contribution of energy
supply via glycolysis. Thus, where hypertrophy
schemes (controlled movements, moderate loads,
moderate repetitions, high total work, short rest peri-
ods) rely heavily on anaerobic glycolysis for energy
production, neuronal (explosive intent, heavy loads,
few repetitions, lower total work, long rest periods)
and dynamic power schemes (explosive and/or bal-
listic movements, light loads, moderate repetitions,
lower total work, moderate rest periods) involve
much less glycolytic activity. The shorter rest peri-
 2006 Adis Data Information BV. All rights reserved.
Crewther et al.
ods associated with hypertrophy schemes also re-
duce the ability of muscle to clear blood lactate
during exercise. Given these findings, it may be
speculated that the metabolic stimulus plays a
greater role in mediating strength changes through
morphological adaptation. Anecdotal evidence sup-
ports such a notion with bodybuilders often utilising
advanced training strategies (e.g. giant sets, drop
sets, pause training) as part of their training regime,
which are likely to produce large metabolic re-
sponses, contributing to resultant adaptation.
The different lactate responses observed appear
to be largely mediated by differences in strength,
muscle mass used and muscle composition. For
example, the amount of work (force × distance)
performed would appear an important factor deter-
mining lactate responses;[40,74,86] therefore, those
with greater 1RM strength would elicit greater work
at a given relative intensity (i.e. heavier loads) and
thereafter, produce more lactate than less strong
individuals. The amount of muscle mass employed
during movement is another consideration. Activi-
ties characterised by a large number of muscle
groups (i.e. high total muscle mass), such as squats
and deadlifts, would stimulate much higher blood
lactate concentrations than activities using smaller
quantities of muscle mass, such as bicep curls. By
analogy those individuals utilising a greater amount
of lean muscle mass, at a given relative intensity,
may also produce greater lactate responses. As indi-
cated throughout this review, the intracellular com-
position of muscle (e.g. enzyme activity, fibre distri-
bution, capillary density, mitochondria size and vol-
ume) is also important in regulating the production
and removal of lactate. Whilst the accumulation of
lactate appears to be influenced by various factors, it
is not yet known if the ability to increase the lactate
response would also result in greater training bene-
fits from the metabolic stimulus.
It would appear that nutritional strategies (CHO
and/or PRO) do not influence the acute lactate re-
sponse to a single bout of resistance exercise; how-
ever, over consecutive days of such exercise, a re-
duced lactate response may result from supplemen-
tation. Again, how this response may influence the
Sports Med 2006; 36 (1)
Possible Stimuli for Strength and Power Adaptation
training benefits afforded by the metabolic stimulus
remains highly speculative. Although CHO and
PRO would appear to inhibit the metabolic stimulus,
nutrition itself is a key component for weight train-
ing and resultant adaptation, particularly for ener-
getic requirements and muscle recovery and repair.
It is evident from the literature that the impor-
tance of the acute metabolic stimulus, in facilitating
strength and power adaptation, remains largely un-
known. This is highlighted by the lack of scientific
evidence surrounding those mechanisms that under-
lie the metabolic stimulus. Confounding our under-
standing is the fact that endurance-type schemes
(light loads, high total repetitions, short rest periods)
produce greater lactate responses than neuronal and
hypertrophy-type schemes,[32,33] which would sug-
gest that the metabolic stimulus may be more impor-
tant for eliciting endurance, rather than strength
adaptation. However, light-load high-repetition
training is another strategy often employed by
bodybuilders to induce muscle growth. Still, with
resistance exercise inducing numerous acute
mechanical, hormonal and metabolic responses, it is
likely that resultant adaptation is an integration of
these factors, rather than a single mechanism. What
role the metabolic stimulus plays in signalling those
processors involved in long-term adaptive change is
still speculative. As intimated throughout this re-
view, there are a number of areas in need of further
research and interactions to be addressed. Such an
analysis would enhance understanding in this area
and improve the prescription of resistance exercise
for strength and power development.
3. Conclusions
It is obvious from the data presented that the
current understanding of the metabolic stimulus and
its contribution to strength and power adaptation
remains largely unknown. The configuration of the
various training variables did impose a specific acti-
vation pattern in the lactate responses (i.e. hypertro-
phy schemes > neuronal > dynamic power
schemes); however, fewer studies have examined
neuronal and dynamic power schemes. Factors such
as age, sex, training experience and nutrition may
 2006 Adis Data Information BV. All rights reserved.
75
also influence the lactate response to resistance ex-
ercise and thereafter, adaptation. Still, the impor-
tance of these differences remains, as yet, unclear.
Those mechanisms underpinning muscular adapta-
tion, in relation to the metabolic stimulus, remain
highly speculative. Inconsistent findings and meth-
odological limitations within research (e.g. pro-
gramme design, sampling period, number of sam-
ples) also make interpretation difficult. More re-
search is also needed to examine the lactate
responses to different loading schemes, as well as
interactions across age, sex and training status, so
our understanding of the metabolic stimulus is im-
proved.
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this review. The authors have no conflicts of interest
that are directly relevant to the content of this review.
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Correspondence and offprints: Blair Crewther, HortRe-
search, Private Bag 92169, Auckland, New Zealand.
E-mail: BCrewther@Hortresearch.co.nz
Sports Med 2006; 36 (1)