REVIEW

CURRENT
OPINION Four birds with one stone? Reparative,
neuroplastic, cardiorespiratory, and metabolic
benefits of aerobic exercise poststroke
Michelle Ploughman and Liam P. Kelly

Purpose of review
Converging evidence from animal models of stroke and clinical trials suggests that aerobic exercise has
effects across multiple targets.
Recent findings
The subacute phase is characterized by a period of heightened neuroplasticity when aerobic exercise has
the potential to optimize recovery. In animals, low intensity aerobic exercise shrinks lesion size and reduces
cell death and inflammation, beginning 24 h poststroke. Also in animals, aerobic exercise upregulates
brain-derived neurotrophic factor near the lesion and improves learning. In terms of neuroplastic effects,
clinical trial results are less convincing and have only examined effects in chronic stroke. Stroke patients
demonstrate cardiorespiratory fitness levels below the threshold required to carry out daily activities. This
may contribute to a ‘neurorehabilitation ceiling’ that limits capacity to practice at a high enough frequency
and intensity to promote recovery. Aerobic exercise when delivered 2–5 days per week at moderate to
high intensity beginning as early as 5 days poststroke improves cardiorespiratory fitness, dyslipidemia, and
glucose tolerance.
Summary
Based on the evidence discussed and applying principles of periodization commonly used to prepare
athletes for competition, we have created a model of aerobic training in subacute stroke in which training
is delivered in density blocks (duration  intensity) matched to recovery phases.
Keywords
aerobic training, cardiorespiratory fitness, glucose tolerance, neuroplasticity, stroke rehabilitation

INTRODUCTION stroke. Described in a review article by Dirnagl

Stroke recovery and the limited window of
neuroplasticity
Research over the past 25 years convincingly shows
that the window of recovery poststroke is about
12 weeks. The Copenhagen Stroke Study, now over
20 years old, showed that in 420 patients with
stroke, best possible upper limb function was
achieved by 95% of patients within 9 weeks [1].
Recent work using new sophisticated robotic tech-
nology [2] in 113 people with first stroke from an
acute stroke unit showed very similar results. In
more mildly affected patients, upper limb sensori-
motor recovery was achieved quickly (in about
6 weeks) while moderate to severely affected
patients achieved most recovery within 12 weeks.
The stroke recovery timeline aligns with the seque-
lae of pathological and neuroplastic events after
et al. [3], ischemic stroke is characterized by initial
excitotoxicity followed by inflammation over days
and then apoptotic cell death of nearby tissue in the
penumbra. The window of neuroplasticity begins to
open a few days poststroke where, in animals with
ischemic stroke, the neuro-biological events have
been clearly described [4]. Timing is important. A
critical period exists in which growth-promoting
Faculty of Medicine, Memorial University, St. John’s, Newfoundland and
Labrador, Canada
Correspondence to Dr Michelle Ploughman, PT, PhD, Assistant Pro-
fessor, Physical Medicine and Rehabilitation, Recovery and Performance
Laboratory, L.A. Miller Center, 100 Forest Road, Faculty of Medicine,
Memorial University, St. John’s, NL, Canada A1A 1E5.
Tel: +1 709 777 2099; e-mail: Michelle.ploughman@med.mun.ca
Curr Opin Neurol 2016, 29:684–692
DOI:10.1097/WCO.0000000000000383

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KEY POINTS
 Poor cardiorespiratory fitness contributes to a
‘neurorehabilitation ceiling’, limiting the ability of the
subacute stroke patient to partake in neuromotor
practice at levels high enough to promote plasticity.
 In animals, early-initiated aerobic exercise (1–7 days
postischemia) shrinks lesion size and suppresses cell
death and inflammation whereas the AVERT trial
showed that intensive mobilization earlier than 24 h
poststroke was detrimental, supporting later training
onset.
 Moderate to high intensity aerobic exercise, beginning
1–7 days postischemia, increases perilesional levels of
BDNF and synapsin-I (building blocks for
neuroplasticity) while enhancing learning and memory
in animal models of stroke.
 Although more research is needed examining the
effects of aerobic exercise on executive function in
subacute clinical stroke, data from chronic stroke
suggests that higher intensities and combining with
cognitive training could be beneficial.
 We present a model of aerobic exercise to be tested in
subacute stroke in which the intervention is titrated
using the ‘training density’ concept, first described for
athletes and now modified to fit within the neuroplastic
window of recovery.
proteins such as brain-derived neurotrophic factor
(BDNF) are upregulated. This prime opportunity for
enhanced plasticity wanes as neurotrophic factors
become downregulated and growth inhibitory
proteins are upregulated essentially closing the win-
dow of neuroplasticity [4].
The mismatch between research and practice
With improvements in poststroke care, many stroke
patients in Europe, Asia, and North America receive
rehabilitative care promptly [5,6]. However, despite
links between intensity of therapy and degree of
functional improvement [7], in some centers there
is still a disconnect between the optimal dosage of
rehabilitation to capitalize on the neuroplastic
environment and what is actually delivered to the
stroke patient. Several research groups have con-
firmed, in United States, Europe, Canada, and
Australia that stroke patients receive a modest
amount of therapy (less than 2–3 h per day, 5 days
&
per week) that is of very low intensity [8,9 ,10,11].
Most patients are sedentary, alone in their rooms
with very little stimulation [8,10]. Furthermore,
compensatory movement using proximal muscle
groups [12], employing the less-affected side
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Four birds with one stone? Ploughman and Kelly
[13,14] or relying on external devices such as canes
and splints [15] are learned spontaneously or even
taught to patients sometimes to hasten discharge
[16]. Research in animals has shown that training of
the less impaired forelimb essentially ‘uses up’ the
plasticity that is available at the cost of less recovery
in the affected limb [17]. Early compensation using
the stronger side and low intensity levels of reha-
bilitative practice are some of the factors that likely
conspire against optimal recovery poststroke. There
is a need for innovation to promote further stroke
recovery.
Aerobic exercise as therapy
Although it is ubiquitous in everyday life, aerobic
exercise could be an intervention with robust effects
across multiple targets in stroke rehabilitation. For
example in aging humans with mild cognitive
impairment, aerobic exercise enhances brain health
and cognition [18]. In a study of 877 older people
participating in a stroke prevention project, after
adjusting for confounders, cardiovascular fitness
was predictive of better executive function [19].
Aerobic exercise improves cardiovascular fitness
and enhances capacity to partake in strenuous
activities without fatigue. In a cross-sectional study
of 265 stroke patients with first ischemic stroke, 40%
experienced fatigue and people who did not exercise
before stroke were four times more likely to experi-
ence poststroke fatigue [20]. This review examines
recent research on the benefits of aerobic exercise
across four domains focusing on subacute stroke
rehabilitation, i.e., brain repair, neuroplasticity/
neurological recovery, cardiorespiratory fitness,
and metabolic health. We examine whether similar
aerobic exercise parameters can affect these four
outcomes in time and space by extracting data from
research using FITT principles (Frequency, Intensity,
Type of exercise and Time) and adding a further
parameter peculiar to stroke ‘Initiation poststroke’
to make ‘FITTI’ (Fig. 1). We also present one training
model to employ aerobic exercise in the first
12 weeks of stroke using periodization method-
ology. As previously discussed by Page et al. [21],
this type of exercise training, which systematically
varies the intensity, frequency, and duration of
therapeutic exercise, may be beneficial in stroke
survivors to minimize the potential for a motor
recovery plateau. Based on the literature discussed
below, the proposed aerobic exercise model pro-
gressively increases the training density (intensi-
ty  volume/10) over the first 9 weeks according
to stage of recovery in order to prepare stroke sur-
vivors to be able to perform the recommended
150 min of moderate-to-vigorous intensity physical
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Trauma and rehabilitation

be employed. Exercise volume incorporates both

Repair Plasticity CR fitness Metabolic
Lesion size, Execu- Dyslipidemia,
the frequency and duration of each session to reflect
BDNF VO
cell death (solid) tive impaired glu- the total weekly exercise time. Using this model,
and inflam- Synapsin function cose tolerance
mation (outline) it is conceivable that aerobic exercise could be a
relatively simple yet potent method to maximize
Intensity (%max) Frequency (d\wk)

7
6 plasticity and recovery within the limited time
5
F 4 window of stroke recovery.
3
2
1
Aerobic exercise effects on brain repair
80
70 After stroke, excitotoxicity, oxidative stress, and
60 inflammation create a necrotic stroke core while a
I 50
40 cascade of events further damage nearby tissues [32].
30 There is an emerging body of evidence in animal
20
models of ischemic stroke that aerobic exercise
70 directly interacts with brain repair processes early
Time (min)

60
50 after stroke targeting several components such as
40 inflammatory cytokines, markers of oxidative stress,
30
20
and cell death [23]. In a systematic synthesis of
studies in animal models of ischemic stroke
12
(n ¼ 47), 20–30 min of early-initiated (1–3 days
Duration (wks)

9
6 postischemia), low intensity walking exercise insti-
4
T 3
tuted most days of the week reduced both lesion
2 volume (33 studies) and markers of cell death (11
1 studies). Although longer interventions (2–4 weeks)
<1
resulted in greater tissue rescue than shorter
duration, lower intensity exercise reduced lesion
Cont.

volume more than higher intensities (Fig. 1). Impor-

Type

T
tantly, all the studies included in the review
Int.

demonstrating positive benefits of aerobic exercise

90 began exercise 24–48 h after stroke (not before).
70
50
There have been no studies examining the repara-
30 tive effects of aerobic exercise in clinical stroke;
Initiation (days)

10 however, the AVERT trial may offer some insights

7 &&

I 6 on early exercise poststroke [33 ]. The AVERT trial,

5 which employed very early mobilization on a stroke
4
3
2 poststroke with higher frequency and longer
1
<1
Animal model
FIGURE 1. Parameters of aerobic exercise to affect
outcomes within the four domains (brain repair,
neuroplasticity/neurological recovery, cardiorespiratory (CR)
fitness, and metabolic health) according to FITTI principles. F
– frequency, I – intensity, T – time and duration, T – type
(continuous or intermittent), and I – initiation poststroke.
Data summarized from animal models (gray boxes) [23,24]
and clinical trials (black boxes) [24–28,29 ,30,31].
unit, showed that patients mobilized before 24 h
duration of out of bed therapy time had worse odds
of a favorable outcome measured by the modified
Clinical stroke
Rankin Scale compared to the usual care group [odds
ratio (OR) 0.73], irrespective of age, stroke severity,
tissue plasminogen activator administration, or
stroke type. Interestingly, further analysis of the
findings showed that in fact, higher frequency
(but not earlier intervention or longer duration)
was beneficial with 13% increase in odds for favor-
&&
able outcome for each out-of-bed session [34 ]. The
finding that shorter more frequent sessions were
&&

beneficial aligns with the optimal parameters

reported in animal models of ischemic stroke
activity weekly [22] upon discharge. In our model, discussed above (Fig. 1) and suggests that when
exercise intensity is described in terms of percentage translating a periodization aerobic exercise training
of peak oxygen consumption but heart rate reserve model from athletes to stroke patients, a develop-
[HRR; ((maximal heart rate  resting heart rate) - mental phase is required to prepare the individual
 target intensity) þ resting heart rate] could also for specific aerobic exercise training. Although the

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AVERT trial did not examine the mechanisms
explaining poorer outcome, stroke progression
and worsening of neurological deficit were the most
common adverse events in the early mobilization
group suggesting possible extension of stroke lesion.
The AVERT trial, as well as the consolidated findings
of animal studies, suggest that lower intensity,
higher frequency physical activity initiated more
than 24 h poststroke is likely beneficial while earlier,
more intense activity is not (Fig. 1).
Aerobic exercise effects on neuroplasticity
and neurological recovery
Neuroplasticity was first described in context of
stroke recovery in primates by Randolph Nudo in
a series of papers between 1996 and 2000 [35–38].
Work since that time has confirmed that a high
degree of task practice of the impaired limb(s) is
required to promote synaptogenesis and axonal
sprouting; important mechanistic underpinnings
of restoration of sensorimotor control poststroke
[4,39]. These structural changes are the result of
long-term potentiation-like process involving the
upregulation of BDNF and other trophic factors such
as insulin-like growth factor-I (IGF-I) [40]. In order
to determine if aerobic exercise positively affects
neuroplasticity, studies would have to associate
spatial and temporal aerobic exercise-induced
changes in a biomarker of neuroplasticity (such as
BDNF, synaptic, or dendritic markers or imaging)
with aerobic exercise-induced neurological recovery
that was maintained at follow-up (recovery of func-
tion as opposed to short-term performance improve-
ment). A recent review of the effects of aerobic
exercise on markers of neuroplasticity showed that
30 min of progressive moderate intensity aerobic
exercise instituted most days of the week beginning
1–7 days poststroke for 2–4 weeks most consistently
increased perilesional levels of BDNF (15 studies) in
animal models [24]. The same parameters at higher
intensities increased brain levels of synapsin, a
marker of synaptogenesis (15 studies) (Fig. 1). All
this work has been completed in animal models but
several research groups are measuring serum levels
of neurotrophins and the relationship to poststroke
& &
recovery [41 ,42 ]. Preliminary evidence suggest
&
that lower serum levels of BDNF [42 ] and presence
of BDNF polymorphisms [43,44] are associated with
poorer recovery of function and that intensive reha-
bilitation interventions that alter BDNF signaling
improve motor recovery [45].
In terms of the effects of aerobic exercise on
neurological outcomes, a recent systematic review
showed that low to moderate aerobic exercise (but
not vigorous intensity), delivered on its own early
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Four birds with one stone? Ploughman and Kelly
after stroke significantly improved spatial (six
studies) and working memory (three studies) and
lower limb recovery (22 studies) in animal models
&
of stroke [46 ]. In clinical trials (nine studies
>4 months poststroke), aerobic exercise consist-
ently improved lower limb measures of recovery,
which is not surprising since all of the aerobic
exercise interventions employed the lower limbs.
In contrast, the hemiplegic upper limb was resistant
to the effects of aerobic exercise (seven animal
studies and two clinical trials), even when delivered
&
within 4 weeks of stroke [46 ,47]. Executive function
is one outcome that holds promise since cognition is
sensitive to aerobic exercise in animals. However,
a review of five studies examining the effects of
aerobic exercise on executive function, all in
chronic stroke, showed mixed results. Cognition
was only improved with moderate to high intensity
exercise, three to five times per week for 8 weeks
when combined with cognitive training in chronic
stroke patients [48,49]. There were no control
groups and whether these improvements were due
to recovery or short-term performance enhance-
ment could not be determined because of the lack
&
of follow-up [46 ]. In a recent study of a progressive
intensity community-based exercise programme in
chronic ambulatory stroke patients (n ¼ 40), the
exercise group had less hippocampal atrophy and
more improvement in cognition at the end of the
programme compared with the control group
&
(stretching) [50 ]. In terms of FITTI parameters,
the programme was, F – three times per week;
I – 40–50% to 70–80% HRR with 10% increments;
T – 45–60 min for 19 weeks; T – group exercise
incorporating functional movements; and I –
greater than 6 months poststroke. Unfortunately
the longer-term benefits were not assessed. There
is more clinical research required to determine the
effects of aerobic exercise on neurological recovery
during the subacute phase of stroke.
Cardiorespiratory benefits of aerobic
exercise in subacute stroke
Cardiorespiratory fitness, measured using the ‘gold
standard’ maximal graded exercise testing and
expired gas analysis (peak aerobic capacity;
V̇O2peak), is extremely low during the subacute
phase of stroke [51]. V̇O2peak values are reported
to be between 8 and 15 ml kg1 min1 [25,26,52]
representing about 40–50% of age-matched and
gender-matched populations [51]. Converting these
values to metabolic equivalents (METS) [53], stroke
patients would be able to reach peak MET values
between 2.3 and 4.3 and are unlikely to be able to
sustain activities beyond 1.5–3 METS (65% of peak)
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Trauma and rehabilitation

Tang 2009 Mackay-

n = 41 Lyons 2013
Teixeira
da Cunha Duncan n = 50 # Threshold for iADL independence
Filho 2001 2003 n = 100 Billinger (65% of unadjusted 5.7MET)
n = 15 2012 n = 10

1.5 3 4.5 6 7.5 9 10.5 Stroke-adjusted MET**

# MET*
1 2 3 4 5 6 7 8 9 10

FIGURE 2. Cardiorespiratory fitness of stroke patients is below what is required for daily activities: #Instrumental daily
activities such as carrying groceries and housework require a peak of 5.7 metabolic equivalents (METS) and sustained values
65% of that (about 3.7 METS). One MET is approximately 3.5 ml oxygen kg1 body weight min1 [53]. V̇O2peak values
from five studies [25,26,28,59,62] were converted to METS then adjusted for the fact that stroke patients expend 1.5 times
the energy for walking (and likely other activities) compared with matched controls.

(Fig. 2). It is widely accepted that the threshold for
cardiorespiratory fitness needed to independently
perform typical activities of daily living (ADL) is
20 ml kg1 min1 [54], which represents a peak
MET level of 5.7 MET and sustained levels around
4 MET (Fig. 2). Such workloads are beyond the
capabilities of most people with subacute stroke
[26,51]. Also, considering that energy costs of walk-
ing are more than 1.5 times higher in stroke patients
[55,56], performing even light ambulatory activities
may require moderate to high levels of effort [55–
57] and the MET levels of ADL may need to be
adjusted to reflect the increased energy demand
(Fig. 2). Consequently, such low levels of cardiores-
piratory fitness may contribute to a ceiling for neu-
romotor practice, limiting both the number of
repetitions that can be performed within a session
and the total intensity at which they can be sus-
tained. For example, routine rehabilitation therapy
(light intensity) reaches 4.5 METS [58], which are
levels not achievable in patients with V̇O2peak
below 15 ml kg1 min1. Therefore, an exercise
strategy that is progressive in nature and modulates
the frequency and intensity of training according to
each patient’s physical status within subacute reha-
bilitation and also encourages neuromotor recovery
is needed (Fig. 3).
Studies examining the effects of aerobic exercise
show that exercise can be safely implemented in the
&&
subacute phase of stroke [25,28,29 ,59–61] as early
as 5 days after initial symptoms [26] in patients with
&&
mild [29 ] and moderate to severe [25,26,28,59,62]
impairment. Aerobic exercise was effectively incorp-
orated within routine rehabilitation [25,26,28,62]
using ergometer type exercise, 3–5 days per week,
over a 3–12-week period, at moderate-to-vigorous
intensity, lasting between 20 and 60 min per session
(Fig. 1). However, the training effect seems to be
influenced by aerobic exercise intensity with lower
training levels having less benefit [25,28,59,60] than
&&
moderate to vigorous intensity [26,29 ]. Those
studies employing higher intensity sessions also
demonstrated that improvements in V̇O2peak are
&&
maintained at 6 months [26,29 ] and 12 months
[26] follow-up compared with usual care, which
suggests ‘true recovery’ rather than an acute
response to the intervention.
Metabolic effects of aerobic exercise
poststroke
Impaired glucose tolerance (IGT), dyslipidemia, and
cardiorespiratory fitness are linked to the initial
occurrence of stroke and secondary stroke risk
&
[63,64 ]. In a large prospective study of 43 933
men, the risk of stroke increased by 6% for each
0.6-unit increase in fasting plasma glucose beyond
6.1 mmol/l [65]. Similarly, during 2.6 years of fol-
low-up after transient ischemic attack or minor
stroke, the incidence of stroke increased by two-fold
and three-fold in those with IGT (7.8–11.0 mmol/l)
and diabetic glucose tolerance (DGT; 11.1 mmol/l),
respectively, compared with those with normal glu-
cose levels [66]. Accordingly, several research groups
are employing cardiac rehabilitation strategies in
stroke survivors [67–69] to improve the metabolic
profile and combat the high prevalence of ischemic
heart disease in this group [70]. These studies report
significant reductions in cardiovascular risk scores
[67,68], improvements in cardiorespiratory fitness
[69], and even enhanced functional performance
[69] (Fig. 1). However, they mainly included chronic
stroke survivors who had completed conventional
stroke rehabilitation [68,69] or were mildly affected
and community living [67]. Recently, in a series of
studies including a randomized controlled trial
(RCT) [30,31,71], Wang and colleagues showed that
substituting 40 min of physical therapy with

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 Four birds with one stone? Ploughman and Kelly

Model of aerobic exercise in subacute stroke

(intensity* volume (time * frequency) / 10

25
Initial recovery General preparatory Specific preparatory phase
phase phase

Weekly training density

20

15

Volume
10

5 Intensity

0
1 2 3 4 5 6 7 8 9 10 11 12 13
Time since stroke (weeks)
.
Day Week Minute Intensity (% VO2peak) Phase
3–6 0 25 20% IRP
7–13 1 50 30% IRP
14–20 2 75 35% IRP
21–27 3 100 40% IRP
28–34 4 125 45% GPP
35–41 5 150 50% GPP
42–48 6 200 55% GPP
49–55 7 250 60% GPP
56–62 8 300 65% SPP
63–69 9 250 70% SPP
70–76 10 200 75% SPP
77–86 11 175 80% SPP
84–90 12 150 85% SPP

FIGURE 3. Model of aerobic exercise in subacute stroke. After a stroke, the Initial Repair Phase (IRP) spans the first 30 days
where the goal is to minimize physical deconditioning through frequent (1–3 times per day) short duration (5–10 min) and
light intensity (20–40% V̇O2peak ) aerobic exercise [e.g., weekly training density calculation ¼ 0.2  (10  10)/10 ¼ 2.0]. The
IRP takes into consideration evidence that very early mobilization (<24-h) may be detrimental while more frequent and short-
duration activity is beneficial [33 ,34 ]. The goal of the next 30 days, the General Preparatory Phase (GPP), is to build
&& &&

exercise tolerance by incorporating less frequent (4–6 sessions/week) but longer duration (30–60 min) aerobic exercise while
keeping exercise intensity in the low to moderate range (45–60% V̇O2peak ). Several studies have demonstrated that such
exercise is appropriate at this time poststroke [26,28,29 ,30,31,61] [e.g., weekly training density calculation&&

0.5  (5  40)/10 ¼ 10]. The last 30 days encompasses the Specific Preparatory Phase (SPP) as exercise intensity is now at a
level required to achieve significant improvements in cardiorespiratory fitness. For example, the SPP could include steady state
aerobic exercise (e.g., three sessions of 30–60 min at 65–80% V̇O2peak ) and one high-intensity interval training session (e.g.,
10 intervals of 2 min at 85–90% HRR and 10 intervals of 2 min 65% HRR) [e.g., weekly training density calculation
(0.7  (40  3)) þ (0.9  (10  2)) þ (0.65  (10  2)) ¼ 15.3].

moderate to vigorous intensity ergometry exercise medicine, and one 30 min session of ‘physical
(50–70% of HRR) at 2 weeks poststroke, among agents’ for a total of 210 min of therapy per day
severely affected patients, was feasible and safe (17.5 h of therapy per week) without metabolic
[30]. The addition of three sessions of aerobic exer- benefits [71]. Although not an aerobic exercise inter-
cise to routine therapy was effective in reducing vention per se, in a recent RCT employing progress-
fasting insulin and glucose tolerance with nonsigni- ive lower body resistance training three times per
ficant improvements in lipid profile [30,31]. It is week for 8 weeks, chronic and severely affected
important to note that the ‘usual care’ group in patients showed significant improvements in fast-
these studies received three 40 min sessions of ing insulin, 2-h plasma glucose, and lipid profile
&
physical therapy, two 15 min sessions of occu- [72 ]. Similar to exercise prescription to alter cardio-
pational therapy, one 30 min session of Chinese respiratory fitness, aerobic exercise intensity seems

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Trauma and rehabilitation
to have a profound effect on metabolic outcomes.
However, more research is required to examine the
effects of different types of exercise on metabolic
markers in subacute stroke.
A model of aerobic exercise in subacute
stroke
Based on the findings described above, we present a
conceptual model of aerobic exercise training
during subacute stroke rehabilitation applying
periodization methodology [73] to systematically
progress the duration and intensity of aerobic exer-
cise within blocks (Fig. 3) according to the stage of
recovery. This training framework is commonly
used to prepare elite athletes for competition and
&
has recently been validated in inactive [74 ] and
older adults [75]. The Initial Repair Phase (IRP) of
the model occurs within the first 30 days poststroke
when impairment levels are high. In this phase, the
focus is on frequent, short duration, and low inten-
sity activity aimed at preventing deconditioning.
Since the energy costs of activity are more than
1.5 times higher in stroke patients [55,56], adequate
training levels may be achieved using simple func-
tional activities. In the second stage, the General
Preparatory Phase (GPP), the focus is on building
tolerance for all types of activity while in the final
stage, the Specific Preparatory Phase (SPP), the aim is
to build aerobic capacity specifically. Such aerobic
exercise training methods have been recommended
for use during both cardiac [76] and stroke [77]
rehabilitation. We propose this model as a starting
point for future research using aerobic exercise in
subacute stroke.
CONCLUSION
The low intensity nature of conventional rehabili-
tation as well as low premorbid levels of cardio-
respiratory fitness likely contribute to physical
deconditioning poststroke [57]. Poor cardiorespira-
tory fitness, as mentioned above, contributes to a
‘neurorehabilitation ceiling’, limiting the ability of
the patient to partake in neuromotor practice at
levels high enough to promote plasticity (Fig. 2).
The benefits of aerobic exercise to improve cardio-
respiratory fitness and cardiovascular health, along
with the effects of aerobic exercise on brain repair
and neuroplasticity, at least in animal models, sup-
ports the use of aerobic exercise to, in effect, hit ‘four
birds with one stone’. However the parameters
required for each outcome seem to be a little differ-
ent. For example highly intensive protocols too
&& &&
early are not beneficial [33 ,34 ] whereas later
on, they are of substantial benefit across several
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outcomes (Fig. 1). We provide an initial model of
aerobic exercise training designed to be instituted
beginning about 3 days after stroke which is based
on the findings discussed here as well as established
athletic training principles described in sport
science (Fig. 3). The adapted ‘Model of aerobic
exercise in subacute stroke’, initially created for
achieving peak performance in elite athletes, would
need research and empirical support to determine if
it is effective for stroke survivors whose ultimate
goal is to regain independence and to get back to
life as they knew it.
Acknowledgements
None.
Financial support and sponsorship
M.P. is supported by the Canada Research Chairs Pro-
gram and the Research and Development Corporation,
NL, Canada. L.P.K. is supported by the Heart and Stroke
Foundation Canadian Partnership for Stroke Recovery,
the Keith Griffiths Scholarship Heart and Stroke Founda-
tion, and the Translational and Personalized Medicine
Imitative/NL SUPPORT, Memorial University.
Conflicts of interest
There are no conflicts of interest.
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Volume 29  Number 6  December 2016