Brain and Cognition 80 (2012) 338–351

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Brain and Cognition

journal homepage: www.elsevier.com/locate/b&c

Differential effects of differing intensities of acute exercise on speed and accuracy

of cognition: A meta-analytical investigation
Terry McMorris ⇑, Beverley J. Hale
Chichester Centre of Applied Sport and Exercise Sciences, University of Chichester, College Lane, Chichester, West Sussex PO19 6PE, United Kingdom

a r t i c l e i n f o a b s t r a c t

Article history: The primary purpose of this study was to examine, using meta-analytical techniques, the differential
Accepted 3 September 2012 effects of differing intensities of acute exercise on speed and accuracy of cognition. Overall, exercise dem-
Available online 11 October 2012 onstrated a small, significant mean effect size (g = 0.14, p < 0.01) on cognition. Examination of the com-
parison between speed and accuracy dependent variables showed that speed accounted for most of the
Keywords: effect. For speed, moderate intensity exercise demonstrated a significantly larger mean effect size than
Central executive those for low and high intensities. For speed of processing during moderate intensity exercise, central
Catecholamines
executive tasks showed a larger effect size than recall and alertness/attention tasks; and mean effect size
Brain derived neurotrophic factor
Prefrontal cortex
for counterbalanced or randomized studies was significantly greater than for studies in which a pre-exer-
Response time cise followed by during or post-exercise protocol was used. There was no significant difference between
Arousal mean effect sizes when testing took place post-exercise compared to during exercise for speed but accu-
racy studies demonstrated a significantly larger mean effect size post-exercise. It was concluded that
increased arousal during moderate intensity exercise resulted in faster speed of processing. The very lim-
ited effect on accuracy may be due to the failure to choose tests which are complex enough to measure
exercise-induced changes in accuracy of performance.
Ó 2012 Elsevier Inc. All rights reserved.

1. Introduction II errors could not be dismissed. To some extent, the problems of

Early studies examining the effect of exercise on cognition were
atheoretical (e.g., Gutin & Di Gennaro, 1968; McAdam & Wang,
1967). The first to offer a theoretical rationale was Davey (1973),
who reasoned that exercise was a stressor which would induce
changes in arousal levels. He, therefore, drew on Yerkes and
Dodson’s (1908) arousal–performance interaction theory to
hypothesize an inverted-U effect of acute exercise on cognitive
performance, with moderate intensity exercise inducing signifi-
cantly better performance than low and high intensities. While
meta-analyses (Etnier et al., 1997; Lambourne & Tomporowski,
2010) have shown small but significant mean effects sizes for an
acute exercise effect on cognition, narrative reviewers (Brisswalter,
Collardeau, & Arcelin, 2002; McMorris & Graydon, 2000; Tompo-
rowski, 2003; Tomporowski & Ellis, 1986) have failed to find evi-
dence for an inverted-U effect. The conclusions reached by the
reviewers were based on probability data. However, McMorris
(2009b) urged caution with regard to dismissing the inverted-U
effect, as he pointed out that, in most studies, sample sizes were
very small and effect sizes suggested that the possibility of Type
⇑ Corresponding author. Address: 63 Four Winds Court, Hartlepool TS26 0LP,
United Kingdom.
E-mail address: t.mcmorris@chi.ac.uk (T. McMorris).
small sample sizes can be overcome by the use of meta-analytical
techniques, which allow the investigation of hypotheses based on
effect sizes rather than probabilities. Hence the use of meta-
analytical techniques in the present study. However, a recent
meta-analysis (McMorris, Sproule, Turner, & Hale, 2011) raised
an issue which may affect the present study. Those authors exam-
ined the effect of acute, moderate intensity exercise on working
memory tasks and found that speed and accuracy of processing
were differentially affected. Speed showed a large effect size which
demonstrated facilitation, while accuracy demonstrated a small
effect size which signified a detrimental effect.
An obvious possibility, if speed of cognition improved while
accuracy deteriorated, is that a speed-accuracy trade-off occurred.
McMorris et al. (2011) ruled this out after examining studies in
which P3 latency and response time were both measured. In nor-
mal circumstances, the individual classifies and evaluates the stim-
uli, and then chooses the response, as well as preparing the
movement. If an individual decides to increase speed at the
expense of accuracy, the response and motor preparation are pre-
determined regardless of stimulus classification and evaluation.
Response time involves speed of stimulus classification and evalu-
ation, response selection and motor preparation (Kutas, McCarthy,
& Donchin, 1977), while P3 latency only measures speed of stimu-
lus classification and evaluation. Therefore, if decreases in P3

0278-2626/$ - see front matter Ó 2012 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.bandc.2012.09.001
 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
latency are mirrored by decreases in response time, this would
suggest that these changes are due to exercise-induced increases
in arousal (Yanagisawa et al., 2010). However, if there are changes
in response time but not P3, it would appear that response selec-
tion and motor preparation had taken place before stimulus classi-
fication and evaluation. In other words, speed is favored over
accuracy. McMorris et al. (2011) found that none of the research
they examined showed changes in response time but not P3. More-
over, results for tasks which do not measure speed plus accuracy,
e.g. random number generation, and reading span and operation
span, showed similar results for accuracy as did those tasks in
which a speed-accuracy trade off is possible, e.g. flanker task and
Stroop color test. Furthermore, several studies have demonstrated
significantly faster speed of processing with no detrimental effect
on accuracy of processing (e.g., Arcelin, Brisswalter, & Delignières,
1997; Davranche & McMorris, 2009; Delignières, Brisswalter, &
Legros, 1994; Joyce, Graydon, McMorris, & Davranche, 2009;
McMorris & Graydon, 1996a, 1996b, 1997).
Based on Cooper’s (1973) assertion that acute exercise induces
increases in brain concentrations of the catecholamines neuro-
transmitters, dopamine and norepinephrine, McMorris et al.
(2011) claimed that the increased neurotransmitter concentrations
would have a positive effect on speed of processing but possibly
induce neural noise in areas of the brain involved in accuracy of
processing working memory tasks. Although they proffered this
explanation with regard to moderate intensity exercise and work-
ing memory tasks only, observation of the literature covered for
the present study suggested that a similar effect may be occurring
when analysis is extended to all intensities of exercise and all types
of cognitive task. Therefore, an initial examination of whether
exercise would have differential effects on speed and accuracy of
processing was undertaken. It was decided that if, as hypothesized,
there were a significant difference between effect sizes when speed
was the dependent variable compared to when accuracy was the
dependent variable, further statistical analyses would be under-
taken for the two variables separately.
Based on the theories that moderate intensity exercise induces
increases in arousal (Davey, 1973) and brain neurotransmitter con-
centrations (Cooper, 1973), it was hypothesized that, for speed, ef-
fect sizes as a result of acute, moderate intensity exercise would
demonstrate significantly larger effect sizes than those induced
by low and heavy intensity exercise. Given that the results of
McMorris et al.’s (2011) meta-analysis question the beneficial
effects of moderate intensity exercise on accuracy data, no
directional hypothesis was proposed. However, both cognitive-
energetical (e.g., Kahneman, 1973; Sanders, 1983) and neuroen-
docrinological theories (Cooper, 1973; McMorris, 2009a) would
suggest a hypothesis that different intensities of exercise would re-
sult in significantly different effect sizes. If the claims of McMorris
et al. (2011) are correct, it is most likely that low intensity exercise
would induce the largest effect size. In a previous meta-analysis,
Etnier et al. (1997) tested for an inverted-U effect between short
duration (2–15 min), moderate intensity; longer duration
(>15 min), moderate intensity; light exercise; and ‘‘difficult’’ exer-
cise (p. 262), which presumably means heavy, but showed no sup-
port for the hypothesis. Exact details of what constituted each of
the categories are not provided.
In the present study, we used Borer’s (2003) classification of
low, moderate and heavy exercise, and the intensities used in the
acute exercise-cognition research to determine the exercise inten-
sities. Moderate intensity exercise was determined as being
between 40% and 79% maximum power output (W _ MAX ) or equiva-
lent. If W_ MAX values were not presented but percent volume of
maximum oxygen uptake (VO2MAX) or percent maximum heart
rate were given, the conversion formulae of Arts and Kuipers
(1994) were applied. For other indicators of intensity, e.g. percent
339
heart rate reserve, percent maximum aerobic power, percent ven-
tilatory threshold and percent lactate threshold power, the exer-
cise physiology and exercise endocrinology literatures were
examined to ascertain whether or not the intensity would be with-
in the 40–79% W _ MAX limits. It should be noted that there is an ele-
ment of subjectivity using this method. Measures <40% W _ MAX were
_
deemed to be light exercise and P80% W MAX heavy.
1.1. Moderator variables
Moderator variables were determined following examination of
the theoretical and empirical literature. The first moderator
variable to be examined was timing of testing (during versus
post-exercise). Given that the half-life of catecholamines in the
periphery is only 3 min, some authors have argued that effects
would only be seen during exercise or for a very short period of time
following exercise (Dietrich, 2003; McMorris & Graydon, 2000).
Lambourne and Tomporowski (2010), however, showed higher
effect sizes for post-exercise testing than for testing during exer-
cise. It should be noted that they did not carry out any statistical
comparisons between during and post-exercise effect sizes. More-
over, Joyce et al. (2009) showed improved cognitive performance
on a Stop-signal task as much as 50 min following cessation of exer-
cise. Therefore, we decided to examine the hypothesis that testing
during exercise would differ from testing following exercise.
The second moderator variable to be examined was task com-
plexity (central executive tasks versus recall and attention/alert-
ness tasks). Several authors (Dietrich, 2003; Luft, Takase, &
Darby, 2009; McMorris & Graydon, 2000) have claimed that com-
plex tasks are more likely to be affected by exercise than more sim-
ple tasks. The argument that complex tasks will be more
susceptible to both positive and negative affects of acute exercise
is based on the interaction between central executive tasks, brain
function and stress. Central executive tasks require more in the
way of prefrontal cortex activation than other tasks (Leh, Petrides,
& Strafella, 2010) and the prefrontal cortex is more sensitive to
stress than other areas of the brain (Arnsten, 2009; Ramos &
Arnsten, 2007). Exercise is commonly used as a stressor in animal
and human studies (e.g., Can et al., 2012; Kirschbaum, Scherer, &
Strasburger, 1994; Tian, Nie, Tong, & Baker, 2012), therefore these
authors hypothesized that central executive tasks would be more
susceptible to the effects of exercise than would the more simple
recall and attention/alertness tasks.
The possibility of a ceiling effect on some more simple tasks,
such as simple reaction time or even choice reaction time, cannot
be ruled out, while working memory tasks have been shown to
be significantly affected by acute, moderate intensity exercise
(McMorris et al., 2011). Baddeley (1986) divided working memory
into the central executive and two short-term memory compo-
nents. While McMorris et al. (2011) examined all working memory
tasks, in this study we decided to examine central executive tasks
only because these tasks are thought to be the most susceptible to
effects of stress (Barbas, 2000; Ramos & Arnsten, 2007). We com-
pared these to the other tasks used, recall or short-term memory,
visual search, reaction time, soccer decision making, simple arith-
metic and coincidence anticipation. Such tasks require limited pre-
frontal cortex activity and are more concerned with attention and
alertness (Dietrich & Audiffren, 2011; Rektor et al., 2003). We
hypothesized that central executive tasks would demonstrate a
larger mean effect size than the recall and attention/alertness
tasks.
The third moderator variable to be examined was a protocol is-
sue, the use of counterbalancing/randomization of testing (coun-
terbalanced/random testing versus pre-exercise testing followed
by during or post-exercise testing). Research methods texts all rec-
ommend counterbalancing or randomization but many studies in
340 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
this field have tested using the same order (pre-exercise followed
by during or post-exercise) throughout the experiments. The pos-
sibility of a learning or habituation effect is obvious. Some authors
(e.g., McMorris & Graydon, 1996a, 1996b, 1997) carried out preli-
minary, reliability studies on their cognitive tests to show that
pre-/post-exercise testing would not affect results, while others
(e.g. Brisswalter, Arcelin, Audiffren, & Delignières, 1997; Collar-
deau, Brisswalter, & Audiffren, 2001; Delignières et al., 1994) have
used tests in which there is no feedback, presumably believing that
this removes the necessity to counterbalance or randomize. As a
large number of studies have used the same order, we felt that it
was necessary to compare mean effect sizes for studies using coun-
terbalanced/randomized designs compared to those using pre-
exercise followed by during or/post-exercise testing and we
hypothesized that the latter would show larger mean effect sizes.
Other possible moderator variables were considered, especially
fitness level which might interact with neuroendocrine responses
to exercise and cognitive perceptions of distress, but there were
not enough studies measuring these variables and meeting the cri-
teria for inclusion to warrant examination by meta-analysis.
2. Materials and methods
A literature search using the computer data bases PsycArticles,
PsycINFO, Pubmed, SportsDISCUS and Web of Knowledge was
undertaken. Key words used in the searches were combinations
of ‘‘acute’’, ‘‘exercise’’, ‘‘cognition’’, ‘‘cognitive function’’, ‘‘cognitive
performance’’, ‘‘reaction time’’, ‘‘response time’’, ‘‘accuracy’’, ‘‘error’’,
‘‘working memory’’, ‘‘short-term memory’’, ‘‘long-term memory’’,
‘‘memory’’, ‘‘recall’’, ‘‘executive function’’, ‘‘central executive’’, ‘‘odd-
ball’’, ‘‘visual search’’, ‘‘attention’’, ‘‘anticipation’’, ‘‘coincidence antici-
pation’’, ‘‘decision making’’, ‘‘flanker task’’, ‘‘Simon task’’, ‘‘Sternberg
test’’, ‘‘Wisconsin card sorting task’’, ‘‘Tower of London’’ and ‘‘Tower
of Hanoi’’. In addition, reference lists from empirical reports and re-
views were examined. Studies were included if they were per-
formed on healthy individuals; the exercise intervention required
the activation of large muscle groups; repeated measures, with-
in-subject design, was used; data were provided showing the
intensity of the exercise with reference to a maximum or thresh-
old; exercise intensity was based on objective measures; the range
_ MAX or equiv-
of measures for a specific intensity was not P10% W
alent; and the dependent variables were objective. Studies includ-
ing pharmacological treatments were not included.
Most studies provided more than one effect size and the depen-
dent variables were either speed of response or accuracy/errors. In
order to limit bias, one effect size per study was calculated from
those studies in which either speed or accuracy were the only
dependent variable and where only one exercise intensity was
undertaken. Some studies examined both dependent variables
and we wished to test the hypothesis that effect sizes, with speed
as the dependent variable, would be significantly different from
those where accuracy was the dependent variable. Similarly, some
studies measured more than one exercise intensity and we wished
to compare these. Therefore, it was decided to calculate separate
effect sizes for speed and accuracy at each intensity. This unfortu-
nately biases the importance of these studies (see Borenstein,
Hedges, Higgins, & Rothstein, 2009, pp. 226–227). Therefore, fol-
lowing an initial analysis, a sub-group comparison was undertaken
in which effect sizes from studies which only measured either
speed or accuracy at one exercise intensity (one effect size in our
initial analysis) were compared to the effect sizes from studies
which measured both speed and accuracy, and/or at more than
one exercise intensity (more than one effect size in the initial anal-
ysis). Following this a sub-group analysis between speed and accu-
racy effect sizes was undertaken. If the comparison between
dependent variable type, speed versus accuracy, was significant,
all further analyses would be undertaken separately for speed
and accuracy.
The first analyses, with speed and accuracy data separate, were
comparisons between effect sizes for low, moderate and heavy
exercise, regardless of whether they came from studies that exam-
ined one, two or three intensities. There were 10 effect sizes for
low intensity, 39 for moderate and 17 for heavy exercise, for speed:
and 12, 28, and 16 for low, moderate and heavy, respectively, for
accuracy. Following this, three moderator variables were exam-
ined. The moderator variables identified were timing of testing
(during versus post-exercise); task complexity (central executive
task versus recall and attention/alertness tasks); and counterbal-
ancing of testing (counterbalanced/random testing versus pre-
exercise testing followed by during or post-exercise testing).
2.1. Data analyses
Where means and SDs were available, effect sizes were calcu-
lated using Cohen’s d formula for matched pairs (see Borenstein
et al., 2009, pp. 28–30). Where means and SDs were only provided
graphically, an initial attempt was made to estimate their values
but inter-and intra-experimenter reliability were unsatisfactory,
therefore these data were not included. Where means and SDs
p
were not available, d was calculated from t (d = 2t/ (df)). As accu-
racy data were sometimes reported with accuracy as the depen-
dent variable and sometimes with error as the dependent
variable, all effect sizes were transposed to show changes in accu-
racy, i.e. positive effect sizes indicate better accuracy. Similarly,
where speed of responding was the dependent variable, effect sizes
were multiplied by 1 so that positive effect sizes demonstrated
an improvement in performance. Each individual d was then trans-
formed to the bias-corrected standardized mean difference,
Hedges’ g, by applying the correction factor J (J = 1  (3/4df  1))
and this was used to calculate a mean effect size using the ran-
dom-effects model. Orwin’s (1983) Fail-safe N was calculated
when the mean effect size g was P0.02. Results of the Q test for
homogeneity were calculated and reported as was s2, which is a
measure of absolute variance whereas Q is a measure of relative
variance (Borenstein et al., 2009, p. 121). Where sub-group analy-
ses were undertaken with two groups, effect sizes for each group
were compared using a Z-test on the differences with a random-ef-
fects model, with separate estimates of s2 for each sub-group
(Borenstein et al., 2009, pp. 149–186). Where there were three
sub-groups, an omnibus measure of Q based on analysis of variance
was calculated with a random-effects model, with separate esti-
mates of s2 for each subgroup (see Borenstein et al., 2009, pp.
169–170), and post hoc Z-tests on the differences, with the Bonfer-
roni correction factor. The proportion of variance explained by the
moderator variable, R2, was calculated (Borenstein et al., 2009, pp.
179–183).
3. Theory
The first to proffer a theoretical underpinning for an acute exer-
cise-cognition interaction was Davey (1973), who hypothesized an
inverted-U effect as he saw exercise as a stressor, which would in-
duce increases in arousal as intensity rose. In line with Yerkes and
Dodson’s (1908) theory, he claimed that moderate intensity exer-
cise would induce optimal cognitive performance, while low and
high intensities would have negative effects. Other researchers
(e.g., Arcelin et al., 1997; Delignières et al., 1994) drew on later
arousal–performance interaction theories such as those of
Kahneman (1973) and Sanders (1983). These theorists also hypoth-
esized an inverted-U effect, although they claimed that it was
 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
possible for performance at low levels of arousal to be as good as at
moderate levels if cognitive effort were able to allocate sufficient
resources to the task. During high levels of arousal, however, neu-
ral noise would make it impossible for effort to allocate sufficient
resources to the task.
More recently, Dietrich (Dietrich, 2003; Dietrich & Audiffren,
2011) put forward the reticular activation hypofrontality theory.
According to this theory, during moderate intensity exercise acti-
vation of the reticular system will increase alertness and arousal
leading to improved performance of well-learned and habitual
tasks. However, heavy exercise requires greater activation of the
premotor cortex and supplementary motor area, therefore, if exer-
cise intensity is to be maintained, these areas will be activated at
the expense of the prefrontal cortex, hence poorer cognitive perfor-
mance of tasks requiring prefrontal cortex activation. McMorris
(2009a) agreed with Dietrich except that he claimed that, during
heavy exercise, it will be the limbic system that is activated at
the expense of the prefrontal cortex due to increased anxiety.
Closely linked to these theories is the catecholamines hypothe-
sis, first proposed by Cooper (1973), which states that during, and
even immediately before, exercise the hypothalamus and brain-
stem initiate action of the sympathoadrenal system. This results
in the release of catecholamines at the postganglionic cells of those
neurons that require activating or inhibiting. As exercise increases
in intensity from low to moderate there is also release of epineph-
rine and, to a lesser extent norepinephrine, into the blood from the
adrenal medulla. Peripherally, catecholamines play important roles
in the organism’s ability to undertake exercise, while centrally
dopamine and norepinephrine activate the primary motor cortex,
premotor cortex and supplementary motor area during exercise.
It has long been thought that there is an interaction between
the release of catecholamines into the periphery and increases in
brain concentrations. Despite the presence of the blood–brain bar-
rier, there is a direct effect of peripheral epinephrine and norepi-
nephrine on synthesis and release of norepinephrine in the brain.
Peripheral epinephrine and norepinephrine activate b-adrenore-
ceptors on vagal afferent nerves, which runs from the abdomen
through the chest, neck and head, and terminates in the nucleus
tractus solitarii within the blood–brain barrier. Noradrenergic cells
in the nucleus tractus solitarii project into the locus coeruleus and
stimulate norepinephrine synthesis and release to other parts of
the brain (Miyashita & Williams, 2006). There is also feedback to
the hypothalamus via the thalamus, reticular activation system
and limbic system, concerning stress on the cardiorespiratory sys-
tem, pain and glycogen depletion. This triggers a response by the
hypothalamus, which results in increased release of catechola-
mines peripherally and possibly centrally. Release centrally may
well also be due to the individual perceiving the situation as being
unpredictable and/or one in which he/she is not in control (Mason,
1975a, 1975b), which has been shown to induce the release of cat-
echolamines in plasma in humans (Sothmann, Hart, Horn, & Gus-
tafson, 1991) and in the brain in animals (Wann, Audet, &
Anisman, 2010).
Animal studies provide some evidence for exercise-induced in-
creases in brain concentrations of dopamine and norepinephrine,
the norepinephrine metabolite 3-methoxy 4-hydroxyphenylglycol,
and the dopamine metabolites 3,4-dihydroxyphenylacetic acid and
4-hydroxy 3-methoxyphenylacetic acid, also known as homovanil-
lic acid (see Meeusen and De Meirleir (1995) and Meeusen, Piacen-
tini and De Meirleir (2001) for reviews). Increased activity of
tyrosine hydroxylase, the rate limiter for catecholamines synthesis,
has also been shown during exercise in rodents (Hattori, Naoi, &
Nishino, 1994; Morgan, Yamamoto, & Freed, 1984). In humans,
Dalsgaard et al. (2004), examining norepinephrine and epinephrine
concentrations in cerebrospinal fluid (CSF) by lumbar puncture,
demonstrated exercise-induced increases in CSF concentrations
341
of norepinephrine only. The authors concluded that the CSF in-
crease in norepinephrine concentrations was probably due to
activity in the locus coeruleus. This may have been the result of va-
gal/nucleus tractus solitarii pathway activation by circulating cat-
echolamines. The locus coeruleus has extensive connections to
most other parts of the brain (Miyashita & Williams, 2006).
Increases in brain concentrations of catecholamines during and
following moderate intensity exercise should theoretically facili-
tate cognition. During and following low intensity exercise perfor-
mance will be inhibited due to limited activation in the relevant
brain areas. During and following heavy exercise, the much larger
increases in catecholamines will lead to neural noise, which will
inhibit performance (Arnsten & Goldman-Rakic, 1985). It should
be noted, however, that high concentrations of brain catechola-
mines have been shown to enhance memory consolidation by
the hippocampus in rats (Hopkins & Johnston, 1988). In humans,
this may only apply to emotionally charged information (Payne
et al., 2007; Qin, Hermans, van Marle, & Fernández, 2012). Further
complicating matters is the fact that exercise P80% VO2MAX in-
duces increases in plasma concentrations of the stress hormones,
adrenocorticotropin hormone (ACTH) and cortisol (De Vries, Ber-
nards, De Rooij, & Koppeschaar, 2000; Hill et al., 2008; McMorris,
Davranche, Jones, Hall, & Minter, 2009). Rodent studies have
shown evidence of acute exercise-induced increases in brain con-
centrations of corticosterone (Droste et al., 2008) and increased
corticotropin releasing factor messenger ribonucleic acid (mRNA)
expression in the brain (Hand et al., 2002; Jiang et al., 2004: Yan-
agita et al., 2007) following acute exercise. Corticotropin releasing
factor, ACTH and cortisol interact with norepinephrine and dopa-
mine in the brain, resulting in increased catecholamines neuro-
transmitter synthesis and release, hence increasing the potential
for neural noise.
Although theoretically moderate intensity exercise appears to
be beneficial, there is a problem with regard to moderate intensity
exercise. The intensity at which increases in brain catecholamines
concentrations begin is a contentious issue. Chmura, Nazar, and
Kaciuba-Uscilko (1994) argued that the point at which exercise
would induce an improvement in cognition would be at, or shortly
after, peripheral plasma concentrations of norepinephrine and epi-
nephrine began to rise exponentially. Green, Hughson, Orr, and
Ranney (1983) termed the points at which plasma concentrations
of norepinephrine and epinephrine show significant increases,
the norepinephrine threshold and the epinephrine threshold. Im-
proved cognition has been shown at, or just after, these thresholds
were reached (Chmura et al., 1994; McMorris et al., 1999) but find-
ings are not unequivocal (McMorris et al., 2003, 2000). It is gener-
ally thought that, although there are huge inter-individual
variations (Urhausen, Weiler, Coen, & Kindermann, 1994), intensity
needs to be 75+% VO2MAX (Podolin, Munger, & Mazzeo, 1991),
which according to Arts and Kuipers (1994) equates to 65+%
W_ MAX , before the thresholds are reached. This intensity is, of
course, much higher than the lower end of the moderate intensity
criteria chosen for this study. Our choice was based on the range
classified by Borer (2003) to be of intermediate intensity (50–80%
VO2MAX) and the fact that several authors have used intensities be-
low the thresholds and shown significant effects on cognition
(Delignières et al., 1994; Fontana, Mazzardo, Mokgothu, Furtado,
& Gallagher, 2009; Joyce et al., 2009).
The success of exercise below the norepinephrine and epineph-
rine thresholds to induce improved cognition may be because
peripheral measures are not good indicators of central changes. In-
creased psychological stress due to perception of the task as being
unpredictable and/or one in which the person does not feel in con-
trol, or anxiety about the exercise, especially if it is to continue for
any length of time, would result in increased central concentrations
of dopamine and norepinephrine (Mason, 1975a, 1975b; Mason
342 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
et al., 1973). The duration of the exercise is another issue when
intensity is below the catecholamines thresholds. Even though par-
ticipants may begin exercising below the threshold, if it continues
long enough they may find that they have passed the threshold.
Chmura, Kristztofiak, Ziemba, Nazar, and Kaciuba-Uścilko (1998)
found that participants exercising at 75% of their lactate threshold
(the norepinephrine and epinephrine thresholds correlate highly
with the lactate threshold (Podolin et al., 1991)) demonstrated a
significant increase in lactate concentrations in the blood and sig-
nificant increases in plasma epinephrine and norepinephrine con-
centrations after 20 min. Winter et al. (2007), using an exercise
regimen designed to have participants work for 40 min at an exer-
cise intensity that would not elicit blood lactate concentrations of
>2 mmol l1, also demonstrated significant increases in plasma epi-
nephrine and norepinephrine concentrations. Therefore, exercise
may begin below the threshold but eventually exceed it.
While the theories outlined above may provide logical ratio-
nales for an acute exercise-cognition interaction they would sug-
gest that both speed and accuracy of processing would be
affected in the same way. As we saw in Section 1, McMorris et al.
(2011) found that moderate intensity exercise had a positive effect
on speed of processing but a negative one on accuracy of working
memory tasks. Having ruled out a speed-accuracy trade-off (see
Section 1), the authors claimed that increased neurotransmitter
concentrations would have a positive effect on speed of processing
but possibly induce neural noise in areas of the brain involved in
accuracy of processing working memory tasks. This is based on
Yerkes and Dodson’s (1908) theory. Yerkes and Dodson argued that
complex tasks require lower levels of arousal for optimal perfor-
mance than do more simple tasks. In fact, they claimed that very
simple tasks may need high levels arousal for performance to be
optimal. This argument assumes that changes in speed and accu-
racy are caused by the activity of different parts of the brain.
McMorris et al. (2009) claimed that this may be the case in tasks
like the flanker and Simon tasks where the task is cognitive but
the response is motoric, relying on premotor cortex and basal gan-
glia activation, while accuracy is dependent on anterior cingulate
cortex and dorsolateral prefrontal cortex activity (Ochsner,
Hughes, Robertson, Cooper, & Gabrieli, 2009; Wittfoth, Kuster-
mann, Fahle, & Herrmann, 2008). McMorris et al. (2009) showed
that exercise-induced increases in plasma norepinephrine concen-
trations were related to different effects on speed and accuracy in a
flanker task.
Another possible reason for different results for speed and accu-
racy of processing is that tasks requiring recall and/or learning may
be affected less by catecholamines and more by an interaction be-
tween acute exercise and brain concentrations of the protein, brain
derived neurotrophic factor (BDNF), as they depend on neuroplas-
ticity. Acute exercise induces increased concentrations of BDNF.
The binding of BDNF to the tropomyosin-related kinase-B receptor
initiates a number of intracellular signaling cascades, including cal-
cium/calmodulin kinase II (CaMKII) and mitogen-activated protein
kinase (MAPK), resulting in the phosphorylation of cyclic adeno-
sinemonophosphate (cAMP)-response element binding protein
(CREB) (Binder & Scharfman, 2004). While CaMKII, MAPK and CREB
play major roles in the individual’s adaptation to exercise, these
signaling pathways are also essential for neurogenesis and neuro-
plasticity, and hence learning and memory. Their effect as a result
of acute exercise is unlikely to be immediate because the cascades
initiated by BDNF are downstream and therefore take time. So the
effect of BDNF is most likely to take place post-exercise. Interest-
ingly, Lambourne and Tomporowski (2010) found that recall tasks
showed significantly larger effect sizes than processing tasks fol-
lowing exercise but not during exercise.
Several studies have shown that bouts of acute exercise have in-
duced significant increases in serum or plasma BDNF concentrations
(Ferris, Williams, & Shen, 2007; Goekint et al., 2008; Tang, Chu, Hui,
Helmeste, & Law, 2008; Winter et al., 2007). However, non-signifi-
cant effects were shown by other authors (Laske et al., 2010; Ströhle
et al., 2010). As BDNF crosses the blood–brain barrier (Sartorius
et al., 2009) peripheral concentrations are indicative of brain con-
centrations. In all cases the increase was transient and soon returned
to baseline levels, but as it is the downstream CaMKII, MAPK and
CREB activity that is the key issue, the transient nature of the BDNF
concentrations is not an issue. Indeed, exercise-induced increases in
BDNF concentrations in the brain have interested researchers exam-
ining the use of exercise as an aid for cognition in individuals suffer-
ing from Parkinson’s disease (Ahlskog, 2011) and multiple sclerosis
(Cardinal, Wilson, Giesser, Drain, & Sicotte, 2008; Gold et al., 2003).
The delayed actions of BDNF may mean that the positive effects
of exercise continue following cessation of activity. This is one of
the moderator variables to be examined. There are also sound rea-
sons for expecting task complexity to prove to be a significant
moderator. The complex tasks in this study were those which have
been described as being central executive tasks (Baddeley, 1986;
Miyake, Friedman, Emerson, Witzki, & Howerter, 2000). These
tasks activate mainly the prefrontal cortex but also draw on infor-
mation recalled from other parts of the brain (see Barbas (2000)
and Leh et al. (2010) for reviews). Central executive tasks appear
to be more readily affected by stress than other types of task
(Arnsten, 2009; Ramos & Arnsten, 2007). There is evidence that
when stress levels are high, the prefrontal cortex is taken off-line
(Arnsten, 2009, 2011).
Miyake et al. (2000) described the central executive processes
as involving several functions including shifting between tasks or
mental sets; inhibition of prepotent responses; updating and mon-
itoring working memory representations, which involves the re-
moval of redundant information and replacing it with new,
relevant information; planning; and the coordination of multiple
tasks. Leh et al. (2010) provided other examples, e.g. abstract
thinking, cognitive flexibility and selecting relevant sensory infor-
mation. The tasks delegated to the central executive category in
this study demonstrated at least one of the processes outlined by
Miyake et al. and/or Leh et al. Inhibition of prepotent responses
is central to the go/nogo, flanker, Stroop, random number genera-
tion, oddball, stop-signal and Simon tasks. Random number gener-
ation also requires updating and monitoring of working memory
processes, as does the paced auditory serial addition task. The
Sternberg task requires memory encoding, and updating and mon-
itoring of working memory processes. The switch visual attention
task used by Pesce and colleagues (Cereatti, Casella, Manganelli,
& Pesce, 2009; Pesce, Capranica, Tessitore, & Figura, 2002, 2003;
Pesce, Casella, & Capranica, 2004; Pesce, Cereatti, Casella, Caldari,
& Capranica, 2007a; Pesce, Tessitore, Casella, Pirritano, & Capra-
nica, 2007b) requires the shifting of mental sets. The Wisconsin
card sorting task involves the shifting of mental sets, and updating
and monitoring of working memory representations. The Tower of
Hanoi test requires planning and cognitive flexibility.
Moreover, positron emission tomography (PET) and functional
magnetic resonance imaging (fMRI) studies have shown that areas
of the brain known to be involved in central executive activity (see
Barbas (2000), Leh et al. (2010), and van den Wildenberg et al.
(2010) for reviews) are activated by random number generation
(Jahanshahi, Dirnberger, Fuller, & Frith, 2000), oddball (Huettel &
McCarthy, 2004), Wisconsin card sorting task (Henaff, Bayle,
Krolak-Salmon, & Fonlupt, 2010), flanker task (Ochsner et al.,
2009), Simon task (Wittfoth et al., 2008), Sternberg test (Marvel
& Desmond, 2010), Stroop color test (Leung, Skudlarski, Gatenby,
Peterson, & Gore, 2000), paced auditory serial addition task
(Cardinal et al., 2008), Tower of Hanoi (Fincham, Carter, van Veen,
Stenger, & Anderson, 2002), go/nogo (Goya-Maldonado et al., 2010)
and stop-signal (Li Huang, Constable, & Sinha, 2006) tasks. We
 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
could not find any direct evidence of parieto-occipatal activation
for the task used by Coles and Tomporowski (2008), however
Galati, Pelle, Berthoz, and Commiteri (2010) showed evidence of
such activity using a similar task. While similar tasks to that of
Pesce and colleagues (Cereatti et al., 2009; Pesce et al., 2002,
2003, 2004, 2007a, 2007b) have shown activation of the parietal
lobes and left dorsolateral prefrontal cortex (Hedden & Gabrieli,
2010). Although similarity does not equate to being synonymous,
it would not appear unreasonable to conclude that these tasks
are most likely to activate areas of the brain that have been shown
to be activated during performance of central executive tasks.
The recall and alertness/attention tasks are generally thought of
as being more simple. Although the tasks involved with reaction
time (simple and choice reaction time) are primarily controlled
by the prefrontal cortex, less neural activity is demonstrated than
during the performance of complex tasks (Bares, Rektor, Kanovsky,
& Streitova, 2003) and the basal ganglia also play an important role
(Rektor et al., 2003). Recall/short-term memory tasks require hold-
ing information in the visuospatial sketchpad (visual information)
or the phonological loop (verbal information) (Baddeley, 1986).
fMRI research has shown that the phonological loop involves the
lateral frontal and inferior parietal lobes of the left hemisphere,
while the visuospatial loop seems to be situated in the parieto-
occipatal region of both hemispheres, although it is more active
in the right hemisphere (Barbas, 2000; Leh et al., 2010). Visual
search and coincidence anticipation depend on the primary visual
cortex and the superior colliculus (Anderson & Rees, 2011). Verbal
fluency is heavily dependent on Broca’s area (Caplan, Alpert,
Waters, & Olivieri, 2000), while simple arithmetic is controlled
by the parietal lobe (Hamid, Yusoff, Mukari, & Mohamad, 2011).
There is no evidence as to brain areas concerned in the soccer deci-
sion making tests (McMorris & Graydon, 1996a, 1996b, 1997;
McMorris et al., 1999). McMorris (2009b) reported that the soccer
players, who were his participants, simply recalled what they had
been taught by their coaches and provided an automatic response.
So they are probably of little difference to the visual search tasks.
Given that the prefrontal cortex plays a lesser role in such tasks,
one would expect that the effect of moderate intensity exercise
will be less for these studies than for the central executive tasks.
4. Results
The literature reviewed yielded 53 articles which met the crite-
ria for inclusion, eight of these included more than one study. Five
of these articles reported two experiments using the same partici-
pants in each experiment, therefore only one effect size was calcu-
lated per article. In the other three articles, two experiments were
reported but which used different participants, and different exer-
cise intensities and/or cognitive tasks. The experiments were trea-
ted as separate studies. Córdova, Silva, Moraes, Simo }es, and
Nóbrega (2009) reported one experiment but the design was such
that there were three different groups each with different partici-
pants and each exercising at different intensities. These were trea-
ted as three separate studies. There were 25 studies where effect
sizes were calculated for both the speed and accuracy dependent
variables. For speed (k = 66), there were 31 studies in which effect
sizes were calculated for one intensity, 13 where two intensities
were included and three where there were three intensities. For
accuracy (k = 57), there were 20 studies in which effect sizes were
calculated for one intensity, eight where two intensities were in-
cluded and seven where there were three intensities. In total, there
were 124 effect sizes and 2270 participants. The types of tasks and
exercise intensities used in the speed and accuracy studies can be
seen in Tables 1 and 2, respectively.
343
4.1. Initial analyses
In the overall analysis, including both the speed and accuracy
dependent variables, effect sizes were heterogeneous
Q(122) = 472.93 (p < 0.001), s2 = 0.29. The mean effect size was sig-
nificant, g = 0.14 (Z = 2.80, p < 0.01), variance 0.003, SE = 0.05, and
95% confidence interval (CI) 0.04–0.24. The fail-safe N was not cal-
culated as g < 0.20. Forty-two effect sizes were negative, there was
one zero and 81 positive. Sub-group analyses comparing effect
sizes where one effect size from a single study were calculated
with those studies where there was more than one effect size
found no significant between group differences. Sub-group analy-
ses for speed and accuracy showed a significant difference between
the two variables (Meandiff = 0.26, SE = 0.10, Zdiff = 2.60, p = 0.01,
R2 = 0.98). Mean effect size for accuracy was non-significant
(g = 0.04, SE = 0.06), while speed demonstrated a significant mean
effect size (g = 0.30, Z = 3.75, p < 0.001, variance = 0.01, SE = 0.08,
CI = 0.14–0.46). Effect sizes were heterogeneous (Q(65) = 301.37,
p < 0.001, s2 = 0.37 and the fail-safe N was 1220.
Sub-group comparison of mean effect sizes for low, moderate
and high intensity exercise demonstrated no significant differences
for accuracy, with all exercise intensities demonstrating non-sig-
nificant mean effect sizes ranging from g = 0.14 to g = 0.09. For
speed, low and high intensity exercise showed non-significant
mean effect sizes barely above zero but moderate intensity exer-
cise demonstrated a significant mean effect size (g = 0.50,
Z = 4.82, p < 0.001, variance 0.01, SE = 0.10, CI 0.30–0.70). Effect
sizes were heterogeneous (Q(38) = 150.19, p < 0.001, s2 = 0.30).
There was a significant effect of intensity (Qbet = 9.08, p < 0.02,
R2 = 0.98). Post hoc Zdiff tests with the Bonferroni correction factor
found no significant differences (p > 0.017) between high and low
intensity effect sizes, but mean effect sizes for moderate intensity
were significantly different to those for low (Meandiff = 0.50,
SE = 0.22, Zdiff = 2.28, p < 0.017) and high intensities
(Meandiff = 0.50, SE = 0.20, Zdiff = 2.51, p < 0.017).
4.1.1. Moderator variables
For accuracy, only the timing of testing (during versus post-
exercise) showed any significant effect. Testing post-exercise dem-
onstrated a significant mean effect size (g = 0.17, Z = 1.70, p < 0.05,
variance 0.01, SE = 0.10, CI 0.03 to 0.37), while the mean effect
size for during exercise was non-significant (g = 0.08, SE = 0.08).
There was a significant difference between the means
(Meandiff = 0.25, SE = 0.13, Zdiff = 1.98, p < 0.05, R2 = 0.97).
For speed, examination of the moderator variables was under-
taken with results for speed of processing for moderate intensity
exercise only, as this was the only condition to elicit significant ef-
fect sizes. The moderator variable, the timing of testing (during
versus post-exercise), failed to show a significant effect (p > 0.05).
Testing during exercise demonstrated a significant mean effect size
(g = 0.48, Z = 3.72, p < 0.001, variance 0.02, SE = 0.13, CI 0.23–0.73),
as did post-exercise testing (g = 0.53, Z = 3.37, p < 0.001, variance
0.02, SE = 0.16, CI 0.22–0.84).
Examination of the task complexity (central executive task ver-
sus recall and attention/alertness tasks) moderator variable dem-
onstrated a significant effect (Meandiff = 0.46, SE = 0.17,
Zdiff = 2.28, p < 0.01, R2 = 0.96). Central executive tasks showed a
significant mean effect size (g = 0.77, Z = 4.70, p < 0.001, variance
0.03, SE = 0.16, CI 0.45–1.09). The other tasks, which were made
up of recall and attention/alertness type tasks, also showed a sig-
nificant mean effect size (g = 0.31, Z = 2.64, p = 0.01, variance
0.01, SE = 0.12, and 95% CI 0.08–0.54).
The effects of counterbalancing of testing (counterbalanced/
random testing versus pre-exercise testing followed by post-exer-
cise testing) were significant (Meandiff = 0.63, SE = 0.20, Zdiff = 3.47,
p < 0.001, R2 = 0.92). The mean effect size for counterbalanced/
344 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351

Table 1
Participants’ demographics, exercise intensities, cognitive tests and time of testing, for speed of processing studies.

Authors N M/F Age years Exercise intensity Design Test Test time Effect size (g)
(Intensity)
Arcelin et al. (1997) 22 MF 23.78 (4.81) 60% MAP Pre/post CRT During 0.59 (Mod)
Bard and Fleury (1978) 16 M N/R 100% Fatigue CB Visual Post 0.20 (Heavy)
search CA
Brisswalter et al. (1995) 10 M N/R 50% VO2MAX 6 min Pre/post SRT During 1.03 (Mod)
Brisswalter et al. (1997) 20 M 23.50 (1.65) 20%, 40%, 60%, 80% MAP Pre/post SRT During 1.93 (Low)
1.53 (Mod)
1.21 (Heavy)
Cereatti et al. (2009) 24 M 15.75 (1.6) 60% HRRES CB SVA During 2.35 (Mod)
Coco, Di Corrado, Calogero, Perciavalle, and 17 M 20.8 (2.21) Fatigue Pre/post ACT Post 0.91 (Heavy)
Maci (2009)
Collardeau et al. (2001) 11 N/R 26.5 (4.8) VT 40 and 60 min Pre/post CRT During and 0.47 (Mod)
post
Córdova et al. (2009) Test 1 12 F 65.9 (3.6) 60% TLA Pre/post SRT TOH Post 0.11 (Low)
Test 2 12 F 63.8 (4.9) 90% TLA 0.49 (Mod)
Test 3 12 F 63.1 (8.7) TLA 20 min 0.01 (Mod)
Davranche, Burle, Audiffren, and 12 MF 27 (4) 50% MAP CB CRT During 0.56 (Mod)
Hasbroucq (2005)
Davranche and McMorris (2009a) 12 M F 32 (9.0) VT CB Simon During 0.39 (Mod)
Davranche, Hall, and McMorris (2009a) 14 M F 30 (8) 50% MAP 20 min CB Flanker task During 0.40 (Mod)
Davranche, Audiffren, and Denjean (2006) 11 M F 23.9 (3.9) 90% VT 17 min CB CRT During 1.05 (Mod)
Delignières et al. (1994) 20 M F 23.3 (5.50) 20, 40, 60, 80% VO2MAX Pre/post CRT During 0.01 (Low)
0.22 (Mod)
0.02 (Heavy)
Féry, Ferry, Vom Hofe, and Rieu (1997) 13 30% VO2MAX, Fatigue 0.04 (Low)
0.05 (Heavy)
Fontana et al. (2009) 32 M 21.13 (1.62) 40%, 60%, 80% VO2MAX Pre/post SDM Post 0.26 (Low)
0.44 (Mod)
Guizani et al. (2006) 12 N/R 19.10 (2.99) 20%, 40%, 60%, 80% Pre/post SRT CRT During 0.31 (Low)
VO2MAX6 min
0.66 (Mod)
0.36 (Heavy)
Heckler and Croce (1992) 18 F 38.2 (6.1) 70% HRMAX 20 min CB Arithmetic Pos 0.60 (Mod)
Hogervorst, Riedel, Jeukendrup, and Jolies 15 M 24.9 (7.9) 75% WMAX Pre/post SRT CRT SCT Post 0.28 (Mod)
(1996)
Joyce et al. (2009) 10 MF 23 (2) 40% MAP 30 min CB Stop-signal During and 0.35 (Mod)
post
Kamijo et al. (2004a) 12 M 22–23 Fatigue Random Nogo/go Post 0.07 (Heavy)
Kamijo et al. (2004b) 12 M 22–23 Fatigue CB SRT Post 0.07 (Heavy)
Kamijo et al. (2009) 24 M 21.8 (0.6)/65.5 30%, 50% VO2MAX 20 min CB Flanker task Post 0.13 (Low)
(1.5)
0.77 (Mod)
Kashihara and Nakahara (2005) 6 M 23.5 (0.6) TLA 10 min CB CRT Post 0.89 (Mod)
McMorris and Graydon (1996a) 20 M 21.10 (1.65) 70%, 100% WMAX Pre/post SDM During 0.57 (Mod)
0.80 (Heavy)
McMorris and Graydon (1996b) Exp 1 10 M N/R 70%, 100% WMAX Pre/post SDM During 0.39 (Mod)
0.82 (Heavy)
McMorris and Graydon (1996b) Exp 2 20 M N/R 70%, 100% WMAX Pre/post SDM During 0.18 (Mod)
0.43 (Heavy)
McMorris and Graydon (1997) Exp 1 12 M 20.80 (1.34) 70%, 100% WMAX Pre/post Visual During 0.05 (Mod)
search
0.64 (Heavy)
McMorris and Graydon (1997) Exp 2 12 M 20.80 (1.78) 70%, 100% WMAX Pre/post SDM During 0.28 (Mod)
0.38 (Heavy)
McMorris, Swain, Lauder, Smith, and Kelly 12 M 21.04 (2.12) TLA CB SDM Post 0.21 (Mod)
(2006)
McMorris et al. (2009) 24 M 24.32 (7.1) 50%, 80% WMAX CB Flanker task During 0.78 (Mod)
1.30 (Heavy)
McMorris and Keen (1994) 12 MF 18–22 70%, 100% WMAX Pre/post SRT During 0.20 (Mod)
0.70 (Heavy)
McMorris et al. (1999) 9 M 22.0 (2.4) TE, WMAX Pre/post SDM During 0.47 (Mod)
0.70 (Heavy)
McMorris et al. (2003) 9 M 22.2 (2.10) 70%, 100% WMAX Pre/post NC-CRT During 0.16 (Mod)
0.34 (Heavy)
McMorris et al. (2000) 12 M 20.00 (2.00) TE, WMAX CB SDM Post 0.14 (Mod)
0.21 (Heavy)
O’Leary et al. (2011) 36 MF 21.8 (1.6) 60% HRMAX 20 min CB Flanker task Post 0.05 (Low)
Ozyemisci-Taskiran et al. (2008) 11 N/R N/R 70% HRMAX 20 min Pre/post ERT Post 0.53 (Mod)
Pesce and Audiffren (2011) 100 MF 16–24 and 65– 60% HRRES 20–24 min CB CRT During 1.13 (Mod)
74
Pesce et al. (2002) 16 MF 19–40 60% VO2MAX CB SVA During 1.30 (Mod)
Pesce et al. (2007b) 48 M 16–19 60% HRRES CB SVA During 1.15 (Mod)
Pesce et al. (2004) 42 MF 22.20 (4.25) 60% HRRES CB SVA During 0.89 (Mod)
Pesce et al. (2003) 16 MF 19–40 60% VO2MAX CB SVA During 1.17 (Mod)
 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351 345

Table 1 (continued)

Authors N M/F Age years Exercise intensity Design Test Test time Effect size (g)
(Intensity)
Pesce et al. (2007a) 25 MF 66.25 (4.65) 60% HRRES CB SVA During 0.15 (Mod)
12 min
Pontifex and Hillman (2007) 41 MF 20.2 (1.6) 60% VO2MAX 6.5 min CB Flanker task During 0.01 (Mod)
Stroth et al. (2009) 33 MF 14.2 (0.5) 60% HRMAX 20 min Random Flanker task Post 0.96 (Low)
Yanagisawa et al. (2010) 20 MF 21.5 (4.8) 50% VO2MAX CB SCT Post 2.14 (Mod)

Note: Test included switch costs but these were not included in meta-analyses: CB = counterbalanced: Random = randomized: Mod = moderate: VO2MAX = maximum volume
of oxygen uptake: MAP = maximum aerobic power: WMAX = maximum power output: M = male: F = female: N/R = not recorded: VT = ventilatory threshold: TLA = lactate
threshold: TE = epinephrine threshold: HRRES = heart rate reserve: HRMAX = maximum heart rate: Exp = experiment: CRT = choice reaction time: SRT = simple reaction time:
SVA = switch visual attention: TOH = Tower of Hanoi: ACT = attention and concentration task: NC-CRT = non-compatible choice reaction time: SDM = soccer decision making:
SCT = Stroop color test: ERT = electromyographical reaction time.

Table 2
Participants’ demographics, exercise intensities, cognitive tests and time of testing for accuracy studies.

Authors N M/F Age years Exercise intensity Design Test Test time Effect size (g)
(Intensity)
Ando, Kokubu, Yamada, and Kimura 12 M 25.3 (3.1) 40%, 60%, 80% VO2MAX CB Flanker task During 0.09 (Low)
(2011)
0.07 (Mod)
0.40 (Heavy)
Arcelin et al. (1997) 22 MF 23.78 (4.810 60% MAP Pre/post CRT During 0.10 (Mod)
Audiffren, Tomporowski, and 16 MF 21.13 (0.87) 90% VT 35 min CB RNG During and 0.47 (Mod)
Zagrodnik (2009) post
Bard and Fleury (1978) 16 M N/R 100% Fatigue CB Visual Post 0.17 (Heavy)
search CA
Brisswalter et al. (1997) 20 M 23.50 (1.65) 20%, 40%, 60%, 80% MAP Pre/post SRT During 0.78 (Low)
0.70 (Mod)
0.84 (Heavy)
Coco et al. (2009) 17 M 20.8 (2.21) Fatigue Pre/post ACT Post 0.71 (Heavy)
Coles and Tomporowski (2008) 18 MF 22.2 (1.6) 60% VO2MAX 30 min Pre/post visual STM Post 0.11 (Mod)
Collardeau et al. (2001) 11 N/R 26.5 (4.8) VT 40 and 60 min Pre/post CRT During and 0.12 (Mod)
post
Córdova et al. (2009) Test 1 12 F 65.9 (3.6) 60% TLA Pre/post VF Post 1.07 (Low)
Test 2 12 F 63.8 (4.9) 90% TLA 0.97 (Mod)
Test 3 12 F 63.1 (8.7) TLA 20 min 0.58 (Mod)
Davranche et al. (2006) 11 MF 23.9 (3.9) 90% VT 17 min CB CRT During 0.84 (Mod)
Del Giorno, Hall, O’Leary, Bixby, and 30 MF 20.2 (1.1) 75% VT and VT 25 min Pre/post WCST During and 0.01 (Low)
Miller (2010) post
0.28 (Mod)
Delignières et al. (1994) 20 MF 23.3 (5.50) 20%, 40%, 60%, 80% Pre/post CRT During 0.10 (Low)
VO2MAX
0.25 (Mod)
0.21 (Heavy)
Fontana et al. (2009) 32 M 21.13 (1.62) 40%, 60%, 80% VO2MAX Pre/post SDM Post 0.04 (Low)
0.22 (Mod)
0.40 (Heavy)
Griffin et al. (2011) 30 M 22 (2.0) 100% VO2MAX Pre/post SCT Post 0.79 (Heavy)
Guizani et al. (2006) 12 N/R 19.10 (2.99) 20%, 40%, 60%, 80% Pre/post SRT CRT During 0.10 (Low)
VO2MAX 6 min
0.03 (Mod)
0.07 (Heavy)
Heckler and Croce (1992) 18 F 38.2 (6.1) 70% HRMAX 20 min CB Arithmetic Post 0.09 (Mod)
Hillman et al. (2009) 20 MF 9.6 (0.7) 65% HRMAX 20 min Pre/post Flanker task Post 1.34 (Mod)
Isaacs and Pohlman (1991) 12 M 24.40 (4.00) 25%, 40%, 75%, 100% Random CA During 0.07 (Low)
VO2MAX
0.30 (Mod)
1.13 (Heavy)
Joyce et al. (2009) 10 MF 23 (2) 40% MAP 30 min CB Stop-signal During and 0.02 (Mod)
post
Kamijo et al. (2009) 24 M 21.8 (0.6)/65.5 30%, 50% VO2MAX 20 min CB Flanker task Post 0.59 (Low)
(1.5)
0.03 (Mod)
Kashihara and Nakahara (2005) 6 M 23.5 (0.6) TLA 10 min CB CRT Post 0.97 (Mod)
Lambourne, Audiffren, and 19 MF 21.37 (0.92) 90% VT 40 min CB PASAT During and 0.15 (Mod)
Tomporowski (2010) post
McMorris and Graydon (1996a) 20 M 21.10 (1.65) 70, 100% WMAX Pre/post SDM During 0.07 (Mod)
0.00 (Heavy)
McMorris and Graydon (1996b) Exp 1 10 M 20.60 (1.51) 70, 100% WMAX Pre/post SDM During 0.02 (Mod)
0.27 (Heavy)
McMorris and Graydon (1996b) Exp 2 20 M N/R 70, 100% WMAX Pre/post SDM During 0.71 (Mod)
0.22 (Heavy)

(continued on next page)

346 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351

Table 2 (continued)

Authors N M/F Age years Exercise intensity Design Test Test time Effect size (g)
(Intensity)
McMorris and Graydon (1997) Exp 2 12 M 20.80 (1.78) 70, 100% WMAX Pre/post SDM During 0.69 (Mod)
0.75 (Heavy)
McMorris et al. (2009) 24 M 24.32 (7.1) 50%, 80% WMAX CB Flanker task During 0.45 (Mod)
1.32 (Heavy)
McMorris et al. (1999) 9 M 22.0 (2.4) TE, WMAX Pre/post SDM During 0.36 (Mod)
0.10 (Heavy)
O’Leary et al. (2011) 36 M F 21.8 (1.6) 60% HRMAX 20 min CB Flanker task Post 0.22 (Low)
Pontifex and Hillman (2007) 41 M F 20.2 (1.6) 60% VO2MAX 6.5 min CB Flanker task During 0.82 (Mod)
Stroth et al. (2009) 33 M F 14.2 (0.5) 60% HRMAX 20 min Random Flanker task Post 0.11(Low)
Themanson and Hillman (2006) 28 M F 20.35 (2.05) 83% HRMAX 30 min CB Flanker task Post 0.15 (Mod)
Travlos and Marisi (1995) 20 M 23 (3) 40%, 50, 60% VO2MAX CB plus RNG During 0.06 (Low)
10 min control
0.08 (Mod)
0.18 (Heavy)

Note: CB = counterbalanced: Random = randomized: VO2MAX = maximum volume of oxygen uptake: MAP = maximum aerobic power: WMAX = maximum power output:
M = male: F = female: N/R = not recorded: Mod = moderate: VT = ventilatory threshold: TLA = lactate threshold: TE = epinephrine threshold: HRMAX = maximum heart rate:
RNG = random number generation: Exp = experiment: WCST = Wisconsin Card Sorting Task: PASAT = paced auditory serial addition test: CRT = choice reaction time:
SRT = simple reaction time: VF = verbal fluency: STM = short-term memory: SDM = soccer decision making: SCT = Stroop color test: CA = coincidence anticipation.

randomized studies was g = 0.80 (Z = 5.96, p < 0.001, variance 0.02,
SE = 0.13, CI 0.54–1.06). For studies using a pre-/during or post-
exercise order, the mean effect size (g = 0.17, SE = 0.12) was small
and non-significant (p > 0.05).
5. Discussion
The results for the initial, overall meta-analysis show a positive
and significant, small effect size. Although significant, the effect
size is well below the criteria set by Cohen (1988) as signifying a
small effect size. This result could be said to be statistically signif-
icant but practically insignificant. This is similar to Lambourne and
Tomporowski’s (2010) findings for results during exercise, but
slightly smaller than those post-exercise. Etnier et al. (1997) also
found a small mean effect size. However, examination of the re-
sults for the analyses comparing speed and accuracy of processing,
and those examining the inverted-U effect paint a different picture
and show both statistical and practical significance. The hypothesis
that speed of processing would show a larger mean effect size than
accuracy was borne out by the analysis, with speed demonstrating
a moderate, positive mean effect size, while accuracy showed a
non-significant, mean effect size approaching zero. Lambourne
and Tomporowski (2010) found that, for results during exercise, ef-
fect sizes for tasks that measured processing speed actually dem-
onstrated a negative effect. However, Lambourne and
Tomporowski did not include dependent variables such as inspec-
tion time in visual search tasks or speed of recall in memory tasks
as representing speed of processing. In the present study such
tasks were considered to measure speed of processing. That accu-
racy results showed no significant effect was a little surprising and
is in contrast with the findings of McMorris et al. (2011), who
found a moderate effect size demonstrating a detrimental effect
on performance. This was, however, only examining working
memory tasks and only for moderate intensity exercise. To fully
understand our results we need also to examine the results testing
the hypotheses concerning the inverted-U effect.
For speed of processing, it was hypothesized that effect sizes as
a result of acute, moderate intensity exercise would be signifi-
cantly higher than those induced by low and high intensity exer-
cise. This was strongly supported by the data with moderate
intensity exercise showing a positive, moderate mean effect size,
while low and heavy exercise demonstrated effect sizes close to
zero. These results are similar to those found by McMorris et al.
(2011), who demonstrated a large mean effect size for the effect
of moderate intensity exercise on working memory tasks. For accu-
racy, it was hypothesized that different intensities of exercise
would result in significantly different mean effect sizes. This was
not supported by the data. All three intensities showed results
close to zero. These result were different to those of McMorris
et al. (2011) for the effect of moderate intensity exercise on work-
ing memory tasks. The results for accuracy and the inverted-U
effect are similar to those of Etnier et al. (1997), who found no
significant differences in effect sizes between short duration (2–
15 min), moderate intensity; longer duration (>15 min), moderate
intensity; light exercise; and heavy exercise. However, these
authors combined speed and accuracy data and used different
intensity categories.
The findings outlined above show that speed and accuracy of
processing appear to have been affected differently by acute exer-
cise, with accuracy being unaffected while speed demonstrated an
inverted-U effect. The results for speed of processing can be ex-
plained by Davey’s (1973) exercise-arousal-cognition interaction
theory. Davey perceived low intensity exercise as being synony-
mous to low arousal, moderate intensity as equalling moderate
arousal and heavy exercise as inducing high levels of arousal.
Therefore, based on Yerkes and Dodson’s (1908) arousal–
performance theory, an inverted-U effect would be expected. The
results can also explained, to some extent, by Dietrich’s reticular
activation hypofrontality theory (Dietrich, 2003; Dietrich & Audif-
fren, 2011). According to Dietrich, during moderate intensity exer-
cise, activation of the reticular system will increase arousal leading
to improved performance of well-learned and habitual tasks. How-
ever, heavy exercise requires greater activation of the premotor
cortex and supplementary motor area, therefore, if exercise
intensity is to be maintained, these areas will be activated at the
expense of the prefrontal cortex, hence poorer cognitive perfor-
mance of tasks requiring prefrontal cortex activation. The catechol-
amines hypothesis (Cooper, 1973; McMorris, Collard, Corbett,
Dicks, & Swain, 2008) also provides a rational explanation for the
speed data. Increases in brain concentrations of the neurotransmit-
ters dopamine and norepinephrine, during and following moderate
intensity exercise, should theoretically facilitate cognition. During
and following low intensity exercise speed will be slower due to
less activation in the relevant brain areas. During and following
heavy exercise, the much larger increases in catecholamines will
lead to neural noise, which will inhibit performance.
It is easy to see that, during moderate intensity exercise, in-
creased arousal, catecholamines neurotransmitters availability in
the brain or increased reticular formation activation would facili-
tate speed of processing, but it is difficult to see why accuracy
 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
would not be affected. McMorris et al. (2011) argued that for work-
ing memory tasks, even moderate intensity exercise may induce
neural noise that would be detrimental to the performance of these
complex tasks. However, we found no significant difference be-
tween effect sizes for accuracy data for central executive tasks
compared to recall and attention/alertness tasks. Moreover, if
moderate intensity exercise induces neural noise that negatively
affects accuracy of performance, one would have expected that
low intensity exercise would induce optimal performance, in line
with Yerkes and Dodson’s (1908) assertion that complex tasks re-
quire lower levels of arousal. Observation of the results for accu-
racy in the individual studies suggest a much more mundane
reason for accuracy measures showing no significant effects. In
tasks such as the flanker task, Simon task, soccer decision making
tasks and reaction time, there were very few errors made. This
strongly suggests a ceiling effect. This is probably due to the way
these tests have been designed. These tests measure performance
through speed of processing, which is seen as being indicative of
ease of processing. The accuracy measures are only there to ensure
that the participants remain honest and continue to process the
problem fully. Basically it is to safeguard against a speed-accuracy
trade-off. It could be argued that if we wish to really test the effect
of acute exercise on accuracy of cognition, we need to use different
cognitive measures. This is similar to claims made by Etnier and
Chang (2009), who felt that the tasks were not complex enough.
The central executive tasks examined in this analysis, processes
like inhibition (Stroop color test, random number generation, oper-
ation span, reading span, oddball, Simon tasks), updating and mon-
itoring of working memory processes (random number generation,
paced auditory serial addition task), shifting of mental sets
(Wisconsin card sorting task, switch visual attention tests), while
demanding may not be complex enough to actually test accuracy
of cognition. They are not as complex as planning, abstract think-
ing, cognitive flexibility or selecting relevant sensory information.
Research needs to be carried out on these more complex processes.
Evidence also exists to show that learning can be positively af-
fected by acute exercise (Winter et al., 2007), while Lambourne
and Tomporowski (2010) showed larger effect sizes, though still
small, for memory tasks compared to speed of processing tasks,
when testing took place post-exercise. The effect of acute exercise
on learning and memory may be due to exercise-induced increases
in brain concentrations of BDNF and the resulting CaMKII, MAPK
and CREB intracellular signaling cascades, which are essential for
neuroplasticity. Recent research (Griffin et al., 2011) demonstrated
improved memory, which coincided with increased serum BDNF
concentrations, following exercise to exhaustion. There were no
significant effects on a Stroop test, which we might expect
following our results. Winter et al. (2007) found that changes from
pre-exercise BDNF serum concentrations demonstrated a small
but significant correlation with changes in performance on a
language task. However, Ferris et al. (2007) found no significant
correlations between BDNF concentrations and performance on
the Stroop test.
5.1. Timing of testing (during versus post-exercise)
There were no significant differences in mean effect sizes for
speed, when testing took place during or post-exercise. Both condi-
tions showed significant, moderate mean effect sizes. For accuracy,
testing post-exercise demonstrated a very small mean effect size,
one below that which Cohen (1988) classed as being small. It
was, however, significant and differed significantly to the mean ef-
fect size for testing during exercise, which was almost zero. This
moderator variable was included because several authors (e.g.,
Dietrich, 2003; McMorris & Graydon, 1996a, 1996b, 1997) have
claimed that testing during exercise would result in greater effects
347
than testing post-exercise. The arguments for this have been based
on the half-life of catecholamines peripherally, which is 3 min.
This fails to take into account that the key issue is central concen-
trations of catecholamines not peripheral. Eisenhofer, Kopin, and
Goldstein (2004) reported the half-life of brain catecholamines as
being in the range of 8–12 h, while Kadzierski, Aguila-Mansilla,
Kozlowski, and Porter (1994) stated that the half-life of tyrosine
hydroxylase mRNA was 14 ± 1 h.
Another factor that has not been taken into account is the pos-
sible effect of exercise-induced increases in BDNF, which were out-
lined in the previous section. The BDNF-induced activity of CaMKII,
MAPK and CREB occur downstream from the increased synthesis
and release of BDNF and are therefore most likely to be seen
post-exercise. This activity is necessary for neuroplasticity to take
place and may account for the fact that, for accuracy, testing
post-exercise resulted in a larger mean effect size than did testing
during exercise. However, one should be very cautious when inter-
preting these data. The mean effect size was very small and it is
probably fair to say that these results merely supply a prima facie
case for an acute exercise effect and further research is required.
5.2. Task complexity (central executive tasks versus recall and
attention/alertness tasks)
There was no significant difference, for accuracy, between the
mean effect size for central executive tasks compared to that for re-
call and attention/alertness tasks. Even though the overall mean ef-
fect size for accuracy was around zero, we expected central
executive tasks to show a small but significant mean effect size
rather than the non-significant g = 0.05, which was found. The
present results may differ from those of McMorris et al. (2011)
due to the fact that the central executive is only one part, albeit
the main part, of working memory but is more likely to be due
to differences in the criteria for inclusion in the two meta-analyses.
In the present study, protocols which used heart rate without ref-
erence to a criterion point, e.g. maximum heart rate, were not in-
cluded but they were in the McMorris et al. (2011) study.
Perhaps more importantly, where performance was measured dur-
ing and post-exercise within the same study, two effect sizes were
calculated by McMorris et al. (2011). This increases the importance
of those studies in the analyses.
For speed of processing, the mean effect size for central execu-
tive tasks was significantly larger than for recall and attention/
alertness tasks. The variance explained was very high. The recall
and attention/alertness tasks showed a small, significant mean ef-
fect size. The central executive tasks, however, demonstrated a
large effect size. It was not as large as that found by McMorris
et al. (2011) for working memory tasks. The difference in results
between the two studies may be due to the facts outlined above
regarding accuracy data but with an added factor. In the present
study only one effect size was calculated for those studies where
two experiments were carried out but by the same participants
and using similar tests in both experiments (Pesce et al., 2002,
2003, 2004, 2007a, 2007b), whereas McMorris et al. (2011) calcu-
lated separate effect sizes for reach experiment. All except one of
these studies show large effect sizes and the calculation of two ef-
fect sizes per study would greatly exaggerate the mean effect size.
These results were as expected based on the claims that central
executive tasks are more susceptible to changes in arousal (Arnsten,
2009; Ramos & Arnsten, 2007) and catecholamines concentrations
(Chrousos, 2009) than the more simple tasks. It should be noted,
however, that few authors have actually examined prefrontal cortex
activity during or following exercise, while undertaking testing on
central executive tasks. Event related potential research (e.g.,
Hillman et al., 2009; Kamijo, Nishihira, Higashiura, & Kuroiwa,
2007; Nakamura, Nishimoto, Akamatu, Takahashi, & Maruyama,
348 T. McMorris, B.J. Hale / Brain and Cognition 80 (2012) 338–351
1999; Pontifex & Hillman, 2007) has shown changes in P3 and N2
amplitudes during performance of a flanker task (Eriksen & Eriksen,
1974) following moderate intensity exercise, but not unequivocally.
N2 amplitude reflects activity in the anterior cingulate cortex, which
plays an important role in inhibition of prepotent responses (Barbas,
2000). P3 amplitude is described by Kok (2001) as being a measure of
processing during working memory performance. Yanagisawa et al.
(2010), using functional near infra-red spectroscopy, found a rela-
tionship between increased dorsolateral prefrontal cortex activation
and response time on a Stroop color test following exercise. Thus,
there is some support for the claim that central executive tasks are
more readily affected by acute exercise is due to the role of the pre-
frontal cortex in such tasks.
5.3. Counterbalancing of testing (counterbalanced/random testing
versus pre-exercise testing followed by during or post-exercise testing)
There was no significant difference between counterbalanced/
random testing and pre-exercise testing followed by during or
post-exercise testing, for accuracy. However, for speed of process-
ing, mean effect sizes in counterbalanced/random testing studies
were significantly larger than in pre-exercise testing followed by
during or post-exercise testing studies. The former demonstrated
a large, significant mean effect size and the latter a small and
non-significant mean effect size. Moreover, the variance explained
was very high. This was the opposite to what had been
hypothesized.
Research textbooks recommend counterbalancing or randomi-
zation in order to control for learning/habituation effects. The use
of pre-exercise testing followed by testing during or post-exercise
opens up the possibility, some might say probability, of a learning/
habituation effect. This would naturally result in larger effect sizes
from the pre- followed by during or post-exercise studies. That the
opposite occurred is very surprising. Certainly in some of the stud-
ies examined in the meta-analysis, authors with pre-/during exer-
cise testing designs used cognitive tests that had been shown to be
reliable in test/re-test conditions (McMorris & Graydon, 1996a,
1996b, 1997; McMorris et al., 1999). Others used tests in which
feedback is not available (Arcelin et al., 1997; Brisswalter, Durand,
Delignieres, & Legros, 1995; Brisswalter et al., 1997; Delignières
et al., 1994; Hillman et al., 2009; Ozyemisci-Taskiran, Gunendi,
Bolukbasi, & Beyazova, 2008), which would at least limit any learn-
ing/habituation effect. From our results it would look as though
these methods have been successful.
This does not explain, however, why mean effect sizes, where
counterbalancing or randomization were used, were the larger.
This could be due to the nature of the pre- followed by during or
post-exercise designs. In such studies participants undertook the
pre-exercise test just before they began exercising. At this stage
they knew that they were very soon going to undertake exercise.
Moreover, in many of these studies exercise was to be incremental
to exhaustion or to an intensity P80% VO2MAX (Brisswalter et al.,
1995, 1997; Delignières et al., 1994; McMorris & Graydon, 1996a,
1996b, 1997; McMorris et al., 1999). In such cases it is common
to see pre-exercise increases in plasma catecholamines concentra-
tions as a result of anticipation of stress (Mason et al., 1973). This is
in line with Mason’s (1975a, 1975b) notion of psychologically-in-
duced increases in stress. For example, McMorris et al. (2009)
showed that pre-exercise plasma concentrations of catecholamines
demonstrated a significant linear increase from rest to 50% maxi-
mum aerobic power (MAP) and onto 80% MAP despite the fact that,
in all cases, the participants were resting. Thus in the supposed
‘‘control’’, pre-exercise condition the participant may actually be
performing above their real resting, control capacity. As a result
the true effect on cognitive performance between rest and moder-
ate intensity exercise would not be seen.
6. Conclusions
Overall acute exercise demonstrated a small but significant
mean effect on cognition but examination of the comparison
between speed and accuracy dependent variables showed that
it was the former that accounted for 98% of the variance. For
speed of processing, an inverted-U effect was shown, with mod-
erate intensity exercise inducing significantly improved perfor-
mance, with a moderate effect size. Examination of the
moderator variables found that central executive tasks showed
a larger effect size than recall and alertness/attention tasks. Sim-
ilarly, counterbalancing or randomizing cognitive testing induced
larger effect sizes than using a pre-exercise followed by during
or post-exercise testing protocol. However, timing of testing
(post-exercise compared to during exercise) had no significant
effect. For accuracy, the only significant mean effect size found
was that when testing took place post-exercise compared to dur-
ing exercise but this was very small and could only be said to
demonstrate a trend. It was concluded that increased arousal
during moderate intensity exercise, probably due to increased
brain concentrations of the neurotransmitters dopamine and
norepinephrine resulted in faster speed of processing. The almost
non-existent effect on accuracy data may well be due to the fail-
ure to choose tests which are complex enough to measure exer-
cise-induced changes in performance.
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