Psychophysiology, 41 (2004), 563–574. Blackwell Publishing Inc. Printed in the USA.

Copyright r 2004 Society for Psychophysiological Research

DOI: 10.1111/j.1469-8986.2004.00176.x

Brain electrocortical activity during and after exercise: A

quantitative synthesis

JAMES B. CRABBE and ROD K. DISHMAN

Department of Exercise Science, University of Georgia, Athens, Georgia, USA

Abstract
Investigators of brain electrocortical responses to exercise have interpreted increased activity, or frontal hemispheric
asymmetry, in the alpha frequency band as indicative of relaxation or a change in affect. However, few studies
compared alpha activity with other frequencies and within or across hemispheres. To clarify the cumulative evidence in
this area, we provide a quantitative review of the effects of exercise on brain electrocortical activity according to
frequency bands and recording sites. Fifty-eight effects from 18 studies and 282 participants were retrieved. The mean
effect size was moderately large (0.54 SD, 95% CI: 0.43 to 0.65) but heterogeneous. Compared to before exercise, alpha
activity was greater immediately after and during exercise when expressed as absolute power but not as relative to
power in other frequency bands; delta, theta, and beta activity also increased (0.38 to 0.75 SD). Effects did not differ
significantly by recording sites. The cumulative evidence does not indicate that change in brain electrocortical activity
after exercise is specific to alpha activity or hemispheric site.
Descriptors: Electroencephalography, Hemispheric asymmetry, Meta-analysis, Physical activity, Review

People without clinical mood disorders rank exercise near the top
among the behaviors they use to self-manage their moods
(Thayer, Newman, & McClain, 1994). Although experimental
studies support that acute exercise transiently reduces self-rated
anxiety, tension, or negative affect (Landers & Petruzzello, 1994;
McAuley 1994) and increases positive affect (McAuley, 1994),
the effects are small with, as yet, unknown mechanisms. The
experimental methods used in many of the studies did not effec-
tively discount that the changes in mood observed during or after
acute exercise were influenced by experimental artifacts that can
bias participants’ responses to the transparent content of the self-
report measures used (Morgan, 1997). In contrast, studies of the
effect of acute exercise on brain electrocortical activity have been
evaluated as providing objective, biologically plausible evidence
that exercise influences affective states (e.g., Boutcher, 1993;
Boutcher & Landers, 1988; Petruzzello, Hall, & Ekkekakis,
2001; Petruzzello & Landers, 1994; Petruzzello, Landers, Hat-
field, Kubitz, & Salazar, 1991; Petruzzello & Tate, 1997).
Most studies and literature reviews of the effect of acute
exercise on brain electrocortical activity measured by electro-
encephalography (EEG) have emphasized, or have been
restricted to, reports of increased activity in the alpha frequency
This review was conducted by the first author in partial fulfillment of
the requirements for the Doctor of Philosophy degree at the University of
Georgia.
Address reprint requests to: James B. Crabbe, Ph.D., Stress and
Motivated Behavior Institute (SMBI) & NeuroBehavioral Research
Laboratory, New Jersey Health Care System, 385 Tremont Avenue, 129,
East Orange, NJ 07019 USA; E-mail: crabbe@njneuromed.org.
563
band (Kubitz & Pothakos, 1997). Their common premise has
been that increased alpha activity reflects a state of decreased
cortical activation indicative of fatigue, relaxation, or decreased
anxiety (Boutcher, 1993; Petruzzello et al., 1991). Recent inves-
tigations of brain electrocortical activity as a putative mechanism
underlying the effects of acute exercise on affective experience
have extended that premise and further restricted the focus to
interhemispheric asymmetry in frontal alpha activity (Petruzzello
et al., 2001; Petruzzello and Landers, 1994; Petruzzello & Tate,
1997), consistent with the theoretical view that alpha asymmetry
in anterior brain regions is a predominant feature of the neural
circuitry of human affective experience (Davidson, 2001). Our
impression after reading the extant literature in this area is that a
predominant focus on alpha activity or anterior recording sites
might lead to premature or wrong conclusions about the loci and
meaning of brain electrocortical responses to exercise.
As an initial step toward examining this issue, we provide in
this article a quantitative review of the published studies on brain
electrocortical activity in response to exercise. The goals of the
review are to describe the effects of exercise on alpha activity in
comparison with activity in other frequency bands and, when
possible, according to inter- and intrahemispheric variation in
those effects. Features of participants, the exercise stimulus, and
methods that might influence the effects of exercise on brain
electrocortical activity are also considered. The main purposes of
the review are to examine: (1) whether the extant literature pro-
vides evidence consistent with the premise that the effects of ex-
ercise on brain electrocortical activity are specific to the alpha
frequency band, (2) whether the effects differ according to inter-
and intrahemispheric sites, and (3) whether variations in effects
564
according to features of participants, exercise, and methods can
clarify the accumulated evidence and suggest directions for future
investigations designed to elaborate the meaning of brain elec-
trocortical responses to acute exercise.
Background
Our review tactic has been guided by key findings illustrated by
several seminal studies. The first study we know of that examined
the change in alpha activity from before to after exercise reported
that the increase in alpha activity was uncorrelated with level of
head trauma after a match in a group of 52 boxers (Beaussart,
Niguet, Gaudier, & Guislain, 1959). Pineda and Adkisson (1961)
speculated that the results of the Beaussart et al. study were
indicative of increased fatigue and that the brains of the boxers
were resting after the exertion of physical activity (Faure, 1951).
Pineda and Adkisson used a preexperimental, pre–post research
design and reported that alpha activity increased by about 20%
at the frontal cortex among 16 medical students who achieved a
mean maximal heart rate of 200 beats per minute during an
exercise bout that lasted 50 min. The increase in alpha activity
was strongest during the first 5–10 min after the end of exercise
and returned to baseline levels by about the 30th min of recovery
from exercise. Similar increases in alpha activity from before to
after exercise were subsequently reported at occipital or parietal
sites after cycling exercise at moderate intensities in studies of
single groups of participants without a control condition (Farm-
er et al., 1978; Kamp & Troost, 1978; Wiese, Singh, & Yeudall,
1983). In an extension of those early, uncontrolled studies,
Boutcher and Landers (1988) used a controlled, crossover design
to compare changes in brain electrocortical activity at temporal
sites after 20 min of running at an intensity of 85% of maximal
heart rate to a resting condition. In concordance with Pineda and
Adkisson’s (1961) results, alpha activity was increased immedi-
ately after exercise and returned to near baseline levels about
20 min after the end of exercise.
Further extending the methods of prior studies, Boutcher and
Landers (1988) reported a dissociation of changes in alpha ac-
tivity and state anxiety after exercise that was dependent upon
physical activity history. They speculated that increased alpha
activity was indicative of relaxation among trained runners but
fatigue among untrained runners. Shibata, Shimura, Shibata,
Wakamura, and Moritani (1997) also speculated that an increase
in alpha activity was evidence for a muscle relaxation effect of
exercise. They reported an increase in central alpha activity from
before to after walking for 20 min among seven elderly women
(mean age: 68.5 years) that was greatest at walking intensities
estimated by electromyography to be at or 20% above the level at
which additional motor units are recruited to compensate for
muscular fatigue.
Other studies indicated that the effects of exercise on brain
electrocortical activity were not limited to the alpha frequency
band. Youngstedt, Dishman, Cureton, and Peacock (1993) re-
ported increases in alpha and beta activity and a decrease in theta
activity at occipital sites after underwater cycling exercise at an
intensity of about 70% of aerobic power. The changes were
similar across hemisphere and were not associated with ratings of
anxiety. Kubitz and Pothakos (1997) found that activity in the
alpha and theta frequency bands, averaged across left and right
frontal regions, was increased from before to immediately after
exercise. Oda, Matsumoto, Nakagawa, and Moriya (1999) re-
ported increases in alpha and beta (13–30 Hz) activity and de-
creases in delta and theta activity after aerobic exercise in the
J.B. Crabbe and R. K. Dishman
water. They implied a causal link with a concomitant enhance-
ment of mood after the exercise, but correlations between the
changes in mood and alpha activity were not reported. Collec-
tively, these studies suggest that changes in brain electrocortical
activity in response to exercise are not specific to the alpha fre-
quency band and may be similar within and between hemi-
spheres. Moreover, with few exceptions (e.g., Petruzzello &
Landers, 1994) the aforementioned studies of exercise and alpha
activity either did not assess or observe a direct relationship
between changes in alpha activity and measures of fatigue,
relaxation, or affect. Also, inter- or intrahemispheric changes in
the alpha frequency band were not compared with other
frequencies (e.g., Petruzzello & Landers, 1994).
There are several theoretical reasons why failure to contrast
frontal alpha activity with activity in other frequency bands and
recording sites might lead to premature conclusions about the
meaning of increased alpha activity in response to exercise. First,
it seems premature to restrict the recording of electrocortical
activity after exercise to anterior brain regions. There is no
scientific consensus about the specific functional roles that
cortical regions and hemispheres, and their interactions, play in
the experience, expression, and modulation of emotion (Borod,
1992; Hellige, 1994; Tucker, 1984). Second, the topographical
distribution of alpha activity is not inversely related to the ac-
tivities of higher brain electrocortical frequencies in many con-
texts that elicit affective responses. For example, emotional
processing has been associated with increased beta activity, while
alpha activity did not change, in right temporal and parietal
regions (Ray & Cole, 1985). Third, the viewing of emotion-elic-
iting pictures has been accompanied by hemispheric asymmetries
in gamma (Muller, Keil, Gruber, & Elbert, 1999) and theta ac-
tivity (Aftanas, Varlamov, Pavlov, Makhnev, & Reva, 2001) in
anterior temporal regions, but no change in overall alpha
activity, measured at frontal sites. In addition, self-ratings of
positive affective experience during meditation were correlated
with increased theta activity, but not alpha activity, in the
anterior frontal region (Aftanas & Golocheikine, 2001). Hence,
it is unlikely that alpha activity alone provides a sufficient
indicator of the activity of cortical networks linked with
subcortical regions that may modulate pleasant and unpleasant
emotions (e.g., Lane et al., 1997).
Quantitative Review
To help clarify the cumulative evidence, we used standard meta-
analytic methods (Hedges & Olkin, 1985) to conduct a quan-
titative synthesis of the results from published studies that
examined the effect of exercise on brain electrocortical activity
measured up to 30 min after exercise. In most studies, postex-
ercise electrocortical activity was compared to the level of activity
measured in a single group of participants during a preexercise
resting state without a control condition for comparison. Only a
few studies compared the change in electrocortical activity after
exercise to a pre–post change measured in a resting control con-
dition. Nonetheless, we were able to examine pre- to postexercise
changes in alpha activity in all the studies included in the review.
Because alpha activity should be interpreted in relation to the
activity in other frequencies (Gale, 1987; Nunez, 1995), we ex-
amined whether the cumulative evidence from studies of brain
electrocortical activity in response to exercise was indicative of
changes that are specific to the alpha frequency band or to frontal
sites. Our examination of other frequency bands, that is, delta
( 1–3 Hz), theta (  4–7 Hz), and beta ( 13–30 Hz), as well as
Exercise and brain electrocortical activity
the low and high divisions of alpha and beta (  8–10 Hz and
11–13 Hz,  13–20 Hz and  21–30 Hz, respectively), was not
as extensive; about a third of the studies examined these other
frequencies. We correlated the effect sizes between frequency
bands among studies that measured multiple frequency bands
after exercise.
About half the studies reported recording alpha frequency
activity at specific sites or regions (i.e., International 10-20 Sys-
tem; Jasper, 1958), which permitted us to determine whether
there were regional and/or interhemispheric differences of the
effects of exercise. In a separate analysis, there were only enough
studies of electrocortical activity during exercise to conduct a
quantitative analysis of change in alpha activity compared to a
preexercise measure.
To clarify methodological features of the accumulated evi-
dence and guide future studies, we also examined several putative
moderators of electrocortical responses to exercise that varied
among the studies. These moderators included stimulus proper-
ties of exercise (i.e., intensity, duration, mode, posture, and
elapsed time after exercise cessation), characteristics of the par-
ticipants (i.e., age and sex), the manner in which electrocortical
activity was recorded (i.e., time of day, region or site, position of
the eyelids, and body position), referenced (i.e., ear lobes [A1
and/or A2], mastoid[s], or centrally [C3, C4, and/or Cz]) or ex-
pressed (i.e., absolute vs. relative power [the power of one fre-
quency band expressed as a percentage of the summation of
power in all examined frequency bands]), and the effect of study
design (i.e., pre–post comparison vs. comparison with a control
group or condition).
Method
We searched MEDLINE, PSYCINFO, and CURRENT CON-
TENTS PLUS for the period 1960 to April, 2003 using the key
words of exercise, physical activity, run, cycle, cycle ergometry,
treadmill, and walk, in conjunction with electroencephalo-
graphy, EEG, brain, brain activity, brain activation, electrocor-
tical, electrocortical activity, electrocortical activation, and brain
waves. We also conducted a manual search of the bibliographies
of the retrieved papers on these topics. Studies were considered
for inclusion if they assessed changes in brain electrocortical ac-
tivity measured by EEG in response to an acute bout of exercise
among participants who were healthy. Thus, cross-sectional
studies of groups differing in levels of fitness or exercise training
status were not reviewed (e.g., Dustman et al., 1990; Lardon &
Polich, 1996). Fifty-five abstracts and journal articles were
located and reviewed. Of the 55 studies that were retrieved, 18
provided enough data on alpha activity and enough English
language to discern and compute an effect size (ES) expressed as
Cohen’s d (Cohen, 1988; posttest minus pretest/pretest SD) or an
estimate of Cohen’s d by transforming a t value, exact p value or a
simple effect F ratio (Rosenthal, 1994). Some studies provided
coherence or asymmetry scores, but no raw data were presented
and, hence, could not be used in our analysis (e.g., Mott, Dyer &
Kubitz, 1995). An asterisk (n) in the reference list indicates stud-
ies that did not meet the inclusion criteria for our analysis but
may otherwise add to the knowledge base regarding the effect of
exercise on brain electrocortical activity.
Fifty-eight effect sizes (k) were derived from the 18 studies
that tested 21 separate groups and involved 282 participants (see
Table 1). When possible, separate ESs were derived from frontal,
temporal, central, parietal, and occipital regions according to the
565
International 10-20 system. Five studies presented data from an
exercise condition compared to a rest control condition (Boutcher
& Landers, 1988; Fernhall & Daniels, 1984; Mimasa, Hiyashi,
Shibata, Yoshitake, & Moritani 1996; Mimasa, Matusumoto, &
Moritani, 1990; Youngstedt et al., 1993) and rendered 11 effect
sizes. For these studies, we assessed the change in EEG activity
from before to after exercise, and this effect was subtracted from
changes in EEG activity from before to after rest. The remaining
studies provided data comparing postexercise data with preex-
ercise data only, without a comparison condition to control for
the passage of time that ranged from 15 min to several hours.
Two other studies (Kubitz & Mott, 1996; Kubitz & Pothakos,
1997) used a rest control condition for comparison, but the EEG
recordings from this condition were confounded by the use of a
‘‘relaxation’’ manipulation. Also, the EEG assessments 5–10
and 11–25 min after exercise in the Kubitz and Pothakos study
were not used because vigilance tasks were performed during
these times.
Some data from several other studies were not used or were
collapsed across groups. Youngstedt et al. (1993) reported data
from a condition of cycling exercise in cold water; these data were
not used because of the novelty of the condition. Similarly, data
from the hyperthermia condition in the Nielsen, Hyldig, Bids-
trup, Gonzalez-Alonzo, and Christoffersen (2001) study were
not used. Also, the data from three groups in a study by Beh,
Mathers, and Holden (1996) were collapsed because levels of
exercise dependency were formed using scores from an unvali-
dated index.
Statistical software (DSTAT, version 1.11; Johnson, 1989)
was used to compute ES adjusted for sample size (weighted es-
timator d1; Hedges & Olkin, 1985, pp. 110–113), tests of het-
erogeneity, 95% confidence intervals (CI) around the mean ES,
and to compare mean ESs between levels of moderators. Meta
5.3 software (Schwarzer, 1993) was used to compute sampling
error variance using a random effects model. Heterogeneity was
indicated if Q (the sum of squares of each effect about the
weighted mean effect; Hedges & Olkin, 1985, p. 123) reached a
statistical significance level of po.05 and when sampling error
accounted for less than 75% of the observed variance (Hedges &
Olkins, 1985, pp. 191–200). To estimate the hypothetical impact
of null findings from unpublished or unretrieved studies on the
aggregated effect size estimate (i.e., the ‘‘file drawer’’ problem),
we computed a ‘‘fail safe’’ n to estimate of the number of ad-
ditional null effects that would attenuate the observed estimate
but retain a small cumulative effect of .20 SD (Orwin, 1983).
Differences between moderators were determined using the QB
statistic (i.e., the difference between Q computed within each
moderator level and Q computed across moderator levels; John-
son, 1989, p. 106; Hedges & Olkins, 1985, p. 257) tested at an
alpha level of po.01 to constrain the Type I error rate. Mod-
erators reasoned a priori to have a putative effect on alpha ac-
tivity after exercise are presented in Table 2. Only two effects were
reported for parietal sites, so they were collapsed with eight ef-
fects for central sites to increase statistical power. A moderator
analysis of ESs of frequency bands other than alpha was not
performed because there were too few effects. Nevertheless, ESs
were correlated (Pearson r) with several key continuous variables
(e.g., time elapsed after exercise cessation). Intercorrelations
were computed among ESs derived from studies that reported
results for concurrent measures of multiple frequency bands.
We conducted two other more limited quantitative analyses in
addition to examining changes in EEG frequency activity from
Table 1. Characteristics of Studies Used in the Meta-Analysis of Change in Alpha Activity from Pre- to Postexercise
566

Age Peak HR Duration Electrode reference Electrode EEG analysis Research Time elapsed Effect
Study/Group n Sex (m) (m) Mode (min) scheme region(s) method design (min) size (d)
Pineda & Adkisson (1961) 16 FM 28 200 Run 50 A1 A2 linked F Absolute Pre–Post 10.5 0.87
Pineda & Adkisson (1961) 16 FM 28 200 Run 50 A1 A2 linked O Absolute Pre–Post 10.5 0.30
Kamp & Troost (1978) (younger) 10 FM 25 130 Cycle NR C1 C2 A1 A2 same side PO Absolute Pre–Post 1 0.46
Kamp & Troost (1978) (older) 10 FM 57 130 Cycle NR C1 C2 A1 A2 same side PO Absolute Pre–Post 1 0.18
Farmer et al. (1978) (type A) 6 M 20 160 Cycle 6 NR O Absolute Pre–Post 6 3.72
Farmer et al. (1978) (type A) 6 M 20 200 Cycle 6 NR O Absolute Pre–Post 6 8.48
Farmer et al. (1978) (type B) 6 M 20 160 Cycle 6 NR O Absolute Pre–Post 6 0.50
Farmer et al. (1978) (type B) 6 M 20 200 Cycle 6 NR O Absolute Pre–Post 6 2.29
Krause, Ullsperger, Beyer, and Gille (1983) 4 M 33.7 NR Iso 4.5 A1 C Absolute Pre–Post 0.5 1.82
Krause et al. (1983) 4 M 33.7 NR Iso 4.5 A1 O Absolute Pre–Post 2.5 1.45
Krause et al. (1983) 4 M 33.7 NR Iso 4.5 A1 C Absolute Pre–Post 0.5 0.97
Krause et al. (1983) 4 M 33.7 NR Iso 4.5 A1 O Absolute Pre–Post 2.5 0.73
Fernhall & Daniels (1984) 36 M NR NR Run 30 NR T Absolute Control NR 2.48
Boutcher & Landers (1988) (trained) 15 M 29.9 161 Run 20 Mastoids same side T Absolute Control 4.5 1.62
Boutcher & Landers (1988) (trained) 15 M 29.9 161 Run 20 Mastoids same side T Absolute Control 11 0.95
Boutcher & Landers (1988) (trained) 15 M 29.9 161 Run 20 Mastoids same side T Absolute Control 18 0.61
Boutcher & Landers (1988) (trained) 15 M 26.7 161 Run 20 Mastoids same side T Absolute Control 4.5 3.21
Boutcher & Landers (1988) (trained) 15 M 26.7 161 Run 20 Mastoids same side T Absolute Control 11 0.85
Boutcher & Landers (1988) (trained) 15 M 26.7 161 Run 20 Mastoids same side T Absolute Control 18 0.61
Mimasa et al. (1990) 7 M 20.5 148 Cycle 20 NR NR Absolute Control NR 1.41
Youngstedt et al. (1993) 11 M 26 154 Cycle 20 A1 A2 same side O Relative Control 13 0.82
Youngstedt et al. (1993) 11 M 26 154 Cycle 20 A1 A2 same side O Relative Control 23 0.60
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side F Absolute Pre–Post 7 0.31
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side T Absolute Pre–Post 7 0.02
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side F Absolute Pre–Post 12 0.33
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side T Absolute Pre–Post 12 0.00
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side F Absolute Pre–Post 22 0.11
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side T Absolute Pre–Post 22 0.17
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side F Absolute Pre–Post 32 0.09
Petruzzello & Landers (1994) 19 M 22.7 163 Run 30 Mastoids same side T Absolute Pre–Post 32 0.13
Kubitz & Mott (1996) 18 M 23.4 160 Run 15 Cz FT Absolute Pre–Post 9 0.11
Mimasa et al. (1996) 8 M 23 133 Cycle 30 NR P Absolute Control NR 0.48
Stock et al. (1996) 10 M 25.6 157 Iso 30 Cz F Absolute Pre–Post 6 0.44
Stock et al. (1996) 10 M 25.6 157 Iso 30 Cz T Absolute Pre–Post 6 0.66
Stock et al. (1996) 10 M 25.6 157 Iso 30 Cz C Absolute Pre–Post 6 0.58
Stock et al. (1996) 10 M 25.6 157 Iso 30 Cz P Absolute Pre–Post 6 1.02
Stock et al. (1996) 10 M 25.6 157 Iso 30 Cz O Absolute Pre–Post 6 0.22
Beh et al. (1996) 36 FM 19 NR NR 45 Cz O Relative Pre–Post 4.5 0.10
Shibata et al. (1997) 7 F 68.5 94 Walk 20 NR C Absolute Pre–Post 7.5 0.68
Shibata et al. (1997) 7 F 68.5 100 Walk 20 NR C Absolute Pre–Post 7.5 1.85
Shibata et al. (1997) 7 F 68.5 110 Walk 20 NR C Absolute Pre–Post 7.5 1.32
Kubitz & Pothakos (1997) 14 FM 21.7 153 Cycle 15 Cz FT Absolute Pre–Post 4 0.56
Mechau et al. (1998) 19 FM 42.4 130 Run 6 Cz FTCPO Absolute Pre–Post 4 0.67
Mechau et al. (1998) 19 FM 42.4 140 Run 12 Cz FTCPO Absolute Pre–Post 4 1.17
Mechau et al. (1998) 19 FM 42.4 153 Run 18 Cz FTCPO Absolute Pre–Post 4 1.16
Mechau et al. (1998) 19 FM 42.4 161 Run 24 Cz FTCPO Absolute Pre–Post 4 0.95
Mechau et al. (1998) 19 FM 42.4 175 Run 30 Cz FTCPO Absolute Pre–Post 4 0.98
Mechau et al. (1998) 19 FM 42.4 175 Run 30 Cz FTCPO Absolute Pre–Post 15 0.10
Mechau et al. (1998) 19 FM 42.4 175 Run 30 Cz FTCPO Absolute Pre–Post 30 0.04
J.B. Crabbe and R. K. Dishman

Oda et al. (2001) 8 M 23 89 Aqua 60 A1 A2 (x) C Relative Pre–Post 12.5 1.14

Exercise and brain electrocortical activity 567

size (d)

Key: Repeated assessments (e.g., multiple assessments of time elapsed or electrode region) in the same group are in bold; n is the total number of participants in each study/group, F: female, M: male, FM: both

EEG data were expressed, ‘‘absolute’’ indicates that alpha activity was not expressed relative to activity in other frequency bands, and ‘‘relative’’ indicates that alpha activity was expressed as a percentage of
Duration: the time spent in the exercise mode; Electrode reference scheme: the placement of the reference (supposedly nonactive) electrode site according to the International 10-20 System, A: ear lobe, C:

activity in the traditional EEG frequency range (1–30 or 40 Hz); Research design is either Pre–Post, indicating that changes in alpha activity are expressed relative to a preexercise resting state, or control, which
indicates that changes in alpha activity were expressed relative to a preexercise resting state in addition to being compared to changes from a Prerest to a Postrest condition; Time elapsed: time since the cessation
sexes studied; Peak HR: the mean peak heart rate (in beats per minute) achieved during the exercise bout; Mode: the manner in which exercise was conducted, Aqua: Standing water aerobics; Iso: isometric;

central; Electrode region(s): the location of EEG sites according to the International 10-20 system, F: frontal, T: temporal, C: central, P: parietal, O: occipital, EEG analysis method: the fashion in which the
Effect before to after exercise. In the first, we sought to assess changes

0.57
0.67
0.83
0.83
0.84
0.98
0.98
1.31
from preexercise levels in alpha activity during exercise. Five
studies reported alpha activity data during exercise. Those stud-
ies provided 21 ESs from 68 participants. Data recorded during
Time elapsed

rest periods within the exercise condition (e.g., Mechau, Mucke,

Weiss, & Liesen, 1998) were not included. Other frequency bands
(min)
17.5
0.5
0.5
0.5
0.5
0.5
0.5
0.5
were not analyzed because too few studies examined them during
exercise.
In a subsequent analysis we compared change in alpha ac-
tivity after exercise according to brain region and hemisphere.
Research

Pre–Post
Pre–Post
Pre–Post
Pre–Post
Pre–Post
Pre–Post
Pre–Post
Pre–Post
design

Eight studies of 165 participants reported site-specific alpha ac-

tivity after exercise, yielding 63 ESs. We coded these ESs as left
frontal (F7, F3), right frontal (F4, F8), left temporal (T5, T3),
right temporal (T4, T6), left central (C3), right central (C4), left
EEG analysis

parietal (P3), right parietal (P4), and left occipital (O1), right
method

Absolute
Absolute
Absolute
Absolute
Absolute
Absolute
Absolute
Relative

occipital (O2), and midline (Pz, Cz, and Fp).

Results
Electrode
region(s)

Brain electrocortical activity in alpha and other frequencies was

increased when measured during or after exercise. The effects
were moderately large and statistically significant. However,
C
F
F
F
F
F
F
F

when alpha activity was assessed relative to activity in other fre-

quency bands an increase was not evident. Moderator analyses
Electrode reference

revealed that alpha activity increased the most after shorter bouts
of exercise, immediately after exercise, and when the exercise
scheme

Mastoids linked
Mastoids linked
Mastoids linked
Mastoids linked
Mastoids linked
Mastoids linked
Mastoids linked

effect was compared to change after a rest condition (i.e., con-

of the exercise bout; d: sample size adjusted effect size; NR: data not reported or indeterminable from publication.

trolled experimental design). Alpha activity was also increased

A1 A2 (x)

more after exercise when testing occurred in the morning or when

the time of day was controlled, with closed eyelids, and when
body posture approximated a supine position. The effects of ex-
ercise on alpha activity did not differ according to hemisphere
Duration

nor reference scheme.

(min)
60

10
12
20
25
36
2
5

Alpha Activity after Exercise

The mean ES for EEG alpha activity after an exercise bout was
Mode
Aqua
Cycle
Cycle
Cycle
Cycle
Cycle
Cycle
Cycle

0.54 SD, 95% CI: 0.43 to 0.65 (see Figure 1). The fail safe n was
96 effects. Heterogeneity was indicated; variance explained by
sampling error was 19.7%, Q (57) 5 174.39, po.001. There were
Peak HR

outliers (positive skewness 5 3.91 and kurtosis 5 21.28). Fur-

(m)

140
142
147
147
150
151
155

thermore, ES was negatively correlated with sample size (Pearson

89

r 5 .28, p 5 .03). Removing the influence of three outliers from

26.3
26.3
26.3
26.3
26.3
26.3
26.3
Age

two studies (Boutcher & Landers, 1988; Farmer et al., 1978)

(m)
23

minimized the skewness (0.37) and kurtosis (0.32) but did not
appreciably change the correlation between effect size and sam-
Sex
M
M
M
M
M
M
M
M

ple size (r 5 .30, p 5 .03) or the mean effect size (0.50 SD, 95%
CI: 0.39 to 0.61). Hence, all effects were retained in subsequent
n
8
7
7
7
7
7
7
7

moderator analyses. Table 2 provides the mean ES and 95% CI

for each level of the moderators. Effects of exercise on alpha
activity did not differ according to recording sites.

Activity in Other Frequency Bands after Exercise

The mean ES for delta activity after exercise was 0.50 SD (95%
CI 0.32 to 0.68), derived from six studies of 88 participants
yielding 17 ESs. The fail safe n was 26 effects. Effects were het-
erogeneous, Q(16) 5 43.23, po.001. The mean ES for theta ac-
Nielsen et al. (2001)
Nielsen et al. (2001)
Nielsen et al. (2001)
Nielsen et al. (2001)
Nielsen et al. (2001)
Nielsen et al. (2001)
Nielsen et al. (2001)

tivity after exercise was 0.53 SD (95% CI 0.36 to 0.70), derived

Oda et al. (2001)

from eight studies of 113 participants and 20 ESs. The fail safe n
Study/Group

was 33 effects. Effects were heterogeneous, Q(19) 5 70.50,

po.001. The results for alpha activity measured concurrently
with other frequency bands were similar to the result derived
from the larger analysis of only alpha activity after exercise. The
568
1 (r  .76, po.01); theta and high beta were inversely correlated
0.8
Effect Size 95% CI
0.6
0.4
0.2
0 regions were not statistically different either. Notably, left frontal
delta
theta
alpha-1
alpha-2
beta-1
beta-2
beta-c
ALPHA
Figure 1. Effect size 95% confidence intervals (CI) from studies that
recorded multiple frequency bands concurrently for activity after
exercise. The number of effect sizes (k) used in the analyses: delta,
k 5 17; theta, k 5 20; alpha-1, k 5 12; alpha-2, k 5 12; beta-1, k 5 13,
beta-2, k 5 13. Beta-c is the ES 95% CI from studies that measured the
13–30 Hz range, effectively beta-1 and beta-2 Hz ranges (k 5 21). For
comparison, the upper case ALPHA (far right bar) represents the ES and
95% CI from all the studies that measured alpha frequency (k 5 58).
mean ES was 0.75 SD (95% CI 0.54 to 0.97) for low alpha
activity and 0.57 SD (95% CI 0.36 to 0.78) for high alpha activity
computed from 12 ESs and 29 participants from two studies. The
fail safe ns were 33 and 22 effects for low and high alpha activity,
respectively. Effects were judged to be homogeneous for both
low, Q(11) 5 17.31, p 5 .099, and high, Q(11) 5 13.51, p 5 .261,
alpha activity.
The mean ES for beta activity after exercise was 0.38 SD
(95% CI 0.23 to 0.53). This effect was derived from studies that
measured only the full beta range and the mean low and high beta
combined from studies that made a distinction in beta frequen-
cies. From 10 studies, 28 ESs were derived that involved 138
participants. The fail safe n was 25 effects. Effects may have been
heterogeneous, Q(27) 5 41.06, p 5 .067. The mean ES for low
beta activity after exercise was 0.70 SD (95% CI 0.50 to 0.89) and
for high beta activity it was 0.38 SD (95% CI 0.18 to 0.56). These
effects were derived from three studies involving 13 ESs and 65
participants. The fail safe ns were 33 and 12 null effects for low
and high beta activity, respectively. Effects were heterogeneous
for low beta, Q(12) 5 24.60, p 5 .017, but homogeneous for high
beta, Q(12) 5 10.06, p 5 .611.
Activity in alpha and beta frequency bands (including low
and high divisions) was inversely correlated with the amount of
time elapsed since exercise cessation (low alpha: r 5 .57, p 5
.05; high alpha: r 5 .77, po.01; low beta: r 5 .71, po.01;
high beta: r 5 .65, p 5 .02; beta: r 5 .48, p 5 .01). Delta ac-
tivity was positively correlated with time elapsed; theta activity
was uncorrelated (delta: r 5 .37, p 5 .17; theta: r 5 .05, p 5 .86).
Generally, changes in brain electrocortical activity after exercise
were not correlated with participant age, peak exercise intensity
(e.g., HR), or exercise duration. Exceptions were that delta ac-
tivity was correlated with age (r 5 .59, p 5 .01), peak intensity
(r 5 .60, p 5 .01), and duration (r 5 .75, po.01); low and high
beta activity were inversely correlated with exercise intensity
J.B. Crabbe and R. K. Dishman
with exercise duration (r 5 .60, po.04). Changes in activity of
all frequency bands from before to after exercise were directly
correlated (Table 3).
Alpha Activity during Exercise and Hemispheric Analyses
The mean of the 21 ESs for alpha activity during exercise was
0.41 SD (95% CI: 0.24 to 0.58). The fail safe n was 22 effects.
Effects were heterogeneous, Q(20) 5 36.20, p 5 .015. The mean
ES from the hemispheric analysis for EEG alpha activity was
similar to that from the main analysis (ES 5 0.49 SD, 95% CI:
0.40 to 0.59). Heterogeneity was indicated, Q(62) 5 183.32,
po.001. Post hoc contrasts revealed no statistically significant
differences between regions, likely because there were so few ESs
for each site. On an a priori basis, right and left homologous
(ES 5 0.32 SD, 95% CI: 0.10 to 0.54) was not different from
right frontal (ES 5 0.11 SD, 95% CI: 0.15 to 0.36), w2 5 1.5,
p 5 .22; left temporal (ES 5 0.53 SD, 95% CI: 0.29 to 0.7) was
not different from right temporal (ES 5 0.59 SD, 95% CI: 0.34
to 0.85), w2 5 0.11, p 5 .74. Finally, changes in alpha activity
after exercise did not differ according to hemisphere. The mean
of 32 ESs from the left hemisphere (0.49 SD, 95% CI: 0.35 to
0.63) was not different from the mean of the 23 ESs from the
right hemisphere (0.46 SD, 95% CI: 0.31 to 0.62), and neither of
these means were different from the mean of the eight ESs de-
rived from the midline (0.62 SD, 95% CI: 0.34 to 0.90), w2so0.9,
ps4.35, a priori.
Discussion
Brain electrocortical activity in the alpha frequency band was
increased by one-half standard deviation when measured up to
30 min after an acute bout of exercise. This is a moderately large
effect judged by statistical guideposts (Cohen, 1988), which may
be practically meaningful. Though absolute alpha activity was
increased after exercise when compared to resting levels or to
changes after a nonexercise control condition, the cumulative
evidence from the few studies that expressed alpha activity rel-
ative to total power showed no evidence of an effect of exercise
that was specific to alpha activity. Moreover, studies that re-
ported changes after exercise in other frequency bands measured
concurrently with alpha activity reported increases in all fre-
quency bands that were similar in size as the increase in absolute
alpha activity. Hence, the cumulative evidence does not yet sup-
port that the effects of acute exercise on brain electrocortical
activity are specific to alpha frequencies. Future studies should
report a broad spectrum of frequencies prior to interpreting
changes in the alpha band as having special significance for neu-
ral processing in response to exercise.
Changes in alpha activity did not vary significantly between
regions (frontal, temporal, central/parietal, and occipital). This
observation has implications for future studies of exercise based
on theoretical models that emphasize anterior cortical regions in
the modulation of affective experience (e.g., Petruzzello et al.,
2001; Petruzzello & Tate, 1997). Though the increased alpha
activity measured at frontal sites was not statistically different
from increases measured at other regional sites, the number of
effects for each site did not permit a statistically powerful test of
regional differences. The number of effects would need to be
roughly doubled to provide a statistical power of .80 to detect a
moderately large difference in effects among sites of .50 SD at an
Exercise and brain electrocortical activity 569

Table 2. Alpha Activity After Exercise, Showing Moderators, Number of Effects (k), Mean Effect Sizes (d), and 95% Confidence
Intervals (CI) for Each Level, and Statistically Significant Differences Between Moderator Level(s)

Moderator and level k d 95% CI Contrasts p value

Percent of estimated maximal heart rate at peak intensity
a. o82% 29 0.633 0.459–0.808
b. 482% 23 0.452 0.303–0.601
c. not reported 6 0.630 0.271–0.990
Duration
a. o22 min 30 0.869 0.696–1.043 ab o.001
b. 422 min 26 0.319 0.177–0.461
Mode
a. cycle 18 0.653 0.406–0.899
b. run 25 0.493 0.354–0.631
c. isometric 9 0.710 0.355–1.065
Posture
a. sitting 28 0.623 0.429–0.816
b. standing 29 0.552 0.416–0.688
Intensity variation
a. incremental test 8 0.848 0.504–1.191
b. steady state 40 0.512 0.376–0.647
c. variable 10 0.485 0.274–0.696
Elapsed time
a. o6 min 22 0.829 0.645–1.012 ac 5 .001
b. 6–10.5 min 17 0.545 0.330–0.760
c. 410.5 min 16 0.154 0.035–0.382
Time of day
a. am 14 0.647 0.453–0.844
b. pm 4 0.067 0.534–0.400 bc o.001
c. controlled 6 1.123 0.789–1.457 cd 5 .003
d. not reported 34 0.421 0.273–0.569
Region
a. frontal 13 0.287 0.057–0.518
b. temporal 12 0.699 0.483–0.915
c. central and parietal 10 0.936 0.590–1.281
d. occipital 11 0.232 0.039–0.503
e.  two regions 7 0.602 0.392–0.813
Position of eyelids
a. open 8 0.064 0.290–0.161 ab o.001
b. closed 36 0.645 0.504–0.786 ad o.001
c. not reported 12 1.092 0.796–1.3880
Body position
a. supine 9 0.881 0.532–1.230 ac 5 .003
b. recumbent 15 0.501 0.314–0.687 cd 5 .010
c. seated 19 0.223 0.031–0.415
d. not reported 14 0.749 0.526–0.971
Reference scheme
a. ear lobes 10 0.393 0.082–0.705 ad 5 .002
b. central 15 0.499 0.319–0.679 bd o.001
c. mastoids 21 0.408 0.238–0.579 cd o.001
d. not reported 12 1.266 0.947–1.584
Age
a. o23.4 years 18 0.189 0.012–0.367 ab 5 .005
b. 23.4–30 years 24 0.647 0.468–0.826 ac o.001
c. 430 years 15 0.779 0.562–0.996
Sex
a. female 3 1.224 0.557–1.891
b. male 40 0.536 0.396–0.676
c. both 15 0.493 0.317–0.669
Method of EEG analysis
a. absolute 50 0.595 0.479–0.711 ab 5 .009
b. % total power 8 0.170 0.124–0.465
Study design
a. controlled 11 0.880 0.619–1.140 ab 5 .005
b. uncontrolled 47 0.467 0.348–0.586
Publication format
a. abstract 5 2.089 1.541–2.637 ab o.001
b. journal 53 0.475 0.365–0.585

alpha of .01. Nonetheless, the pattern of effect sizes across would be less than those in the temporal and central/parietal sites
regions suggests that were differences to be detected among the (ES  .70 to .93). Such a difference would be consistent with our
regions, the increases in alpha activity at frontal sites (ES  .29) concern that recent investigations (e.g., Petruzzello et al., 2001;
570 J.B. Crabbe and R. K. Dishman

Table 3. Correlation Matrix of Different Frequency Bands

Frequency theta alpha 1 alpha 2 alpha beta 1 beta 2 beta

mean ES r r r r r r r
95% CI p p p p p p p
k k k k k k k
Delta .88 .74 .69 .47 .19 .34 .39
0.50 SD .01 .01 .01 .06 .53 .26 .12
0.32–0.68 17 12 12 17 13 13 17
Theta .76 .78 .25 .36 .45 .07
0.53 SD .01 .01 .29 .23 .12 .76
0.36–0.70 12 12 20 13 13 20
Alpha 1 .78 .95 .53 .74 .61
0.75 SD .01 .01 .07 .01 .03
0.54–0.97 12 12 12 12 12
Alpha 2 .93 .65 .69 .68
0.57 SD .01 .02 .01 .01
0.36–0.78 .12 12 12 12
Alpha .67 .78 .69
0.55 SD .01 .01 .01
0.39–0.70 13 13 28
Beta 1 .91 .96
0.70 SD .01 .01
0.50–0.89 13 13
Beta 2 .93
0.38 SD .01
0.18–0.56 13
Beta
0.38 SD
0.23–0.53

k: number of effects compared.

Petruzzello & Tate, 1997) have prematurely focused on changes
in alpha activity at frontal sites, to the exclusion of considering
other sites. Future studies should examine a broad topography of
cortical networks before presuming a premier role for specific
brain regions in neural responses to exercise.
Variations in effect size across the studies we reviewed suggest
several moderating variables that could guide future studies
designed to better understand circumstances in which exercise
may have stronger affects on brain electrocortical activity. They
may also inform methodological advances in future studies. The
large mean effect for an increase in alpha activity reported in
studies conducted in the morning may be partly explained by the
circadian and wake-dependent nature of alpha activity (Aesch-
bach et al., 1997). All of the 14 effects resulting from studies
conducted in the morning (Mechau et al., 1998; Pineda &
Adkisson, 1961; Stock et al., 1996) were derived using a single
group, pre–post design (i.e., a no-exercise control condition was
not used). Thus, the passage of time, and not the exercise ma-
nipulation, may have accounted for the elevation of alpha ac-
tivity in these studies. The large mean effect when time of day was
controlled was computed from six effects reported in a single
study (Boutcher & Landers, 1988) that used a resting control
condition, effectively countering the aforementioned methodo-
logical concern, though the specific time of day in this study was
not mentioned. Testing time of day was also related to body
position during EEG recording (r 5 .50). However, the larger
effects obtained when participants were in supine or semirecum-
bent postures during recording may have been confounded by
pre–post morning tests or by use of a closed eyelids protocol,
which was also associated with supine or semirecumbent posi-
tions (r 5 .53).
The increase in alpha activity after exercise did not vary ac-
cording to participants’ sex, mode, posture, or the mode and
intensity of exercise. Larger increases in alpha activity among
older participants are likely explained by confounding associa-
tions of age with method of data reduction. Studies of older
participants were more likely to express alpha activity relative to
power in other frequency bands (e.g., Shibata et al., 1997).
A few studies of brain electrocortical activity after exercise
(Crabbe, Smith, & Dishman, 1999; Petruzzello et al., 1994, 2001;
Petruzzello & Tate, 1997) adopted contemporary theoretical
models that conceptualize two major dimensions of affective ex-
perience: pleasantness and unpleasantness (Davidson, 1998;
Lang, Bradley, & Cuthbert, 1998). Consistent with these models,
some nonexercise studies have shown that the left or right frontal
cortex is predominantly activated (i.e., alpha activity is decrea-
sed) during the respective induction of pleasant or unpleasant
affect (Davidson, Ekman, Saron, Senulius, & Friesen, 1990;
Davidson, Marshall, Tomarken, & Henriques, 2000).
However, the cumulative evidence from the exercise studies
reviewed herein suggests that there is not only a change in frontal
brain electrocortical activity after exercise, but an effect is also
evidenced in the temporal, central, and parietal regions.
Furthermore, the cumulative results indicate no intrahemispheric
shift in alpha activity after exercise. For example, in one report, a
reduction in anxiety 10 min after exercise was accompanied by
decreased left frontal alpha activity 5 min after exercise (Pet-
ruzzello et al., 1994), but another study found that frontal alpha
asymmetry measured at rest or in response to moderately intense
exercise was unrelated to emotional responding after exercise,
despite a reduction in anxiety (Crabbe, Smith, & Dishman,
1999). Although it has been assumed that exercise is an emotion
elicitor (Petruzzello & Tate, 1997; Petruzzello et al, 2001), this has
been shown not to be precisely the case; exercise elicits an increase
in feelings of arousal but does not change affective valence
(Crabbe, Smith, & Dishman, 1999). Moreover, our quantitative
Exercise and brain electrocortical activity
analysis indicates that alpha activity was most elevated when
measured immediately and up to about 6 min after the cessation
of exercise. The transience of the effect of exercise on alpha ac-
tivity suggests conceptual and methodological challenges for
studies that examine mood or affective responses to emotion-
eliciting stimuli at later periods after exercise has ended.
Generalized attentional (Breus & O’connor, 1998) or arousal
(Magnie et al., 2000) effects of exercise might influence brain
electrocortical activity in several frequencies and loci, and it is
plausible that brain cortical systems are altered generally in re-
sponse to the increased metabolic arousal that uniquely accom-
panies physical exertion (Dishman, 1998). Several authors have
speculated that hypothalamic modulation of increased metabo-
lism during exercise might influence electrocortical activity. Re-
cently Nielsen et al. (2001) showed that the ratio of alpha activity
to beta activity in the frontal region was directly related to in-
creases in esophageal temperature, which is proportional to in-
creased metabolism, during  35 min of cycling exercise. Alpha
activity tended to increase immediately and stay elevated during
exercise as a percentage of baseline (i.e., preexercise resting state),
but beta increased immediately and then subsided. The Nielsen
group speculated that hypothalamic nuclei involved with tem-
perature regulation might modulate beta activity during exercise.
It has also been suggested that increased alpha activity might
be positively related to increased neural traffic from somatosen-
sory afferents (Youngstedt et al., 1993). This idea is consistent
with the cumulative evidence reported herein of increased alpha
activity measured at central and temporal sites that overlay por-
tions of the sensorimotor cortex that receive afferent feedback
during exercise. Other research has implicated feedback to cor-
tico-thalamic tracts from sympathetically mediated increases in
epinephrine and norepinephrine. Stock et al. (1996) showed a
correlation of plasma norepinephrine with low alpha and low
beta activity (r 5  .70) after resistance exercise. Norepinephrine
levels increase proportionally with increasing intensity of exer-
cise and are associated with mechanoceptive and nociceptive
responses to exertion that might influence brain electrocortical
activity.
Alpha activity also might be increased because of cortical
inhibition by subcortical and brain-stem activation associated
with cardiovascular regulation during exercise (Koriath, Lind-
holm, & Landers, 1987; Lacey & Lacey, 1978). For instance,
cortical oscillations in the alpha frequency band are inversely
related to metabolism in the thalamus of healthy adults (Larson
et al., 1998; Lindgren et al., 1999). The thalamus also is inter-
connected with the insular cortex, which is involved in cardio-
vascular control during exercise (Williamson, McColl, &
Mathews, 2003; Williamson, McColl, Mathews, Ginsburg, &
Mitchell, 1999). Heller and colleagues have reported that
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Studies that did not meet the inclusion criteria for our analysis but may
otherwise add to the knowledge base regarding the effect of exercise on
brain electrocortical activity.
(Received September 10, 2002; Accepted December 15, 2003)