Psychophysiological markers of burnout
Hypothalamic-pituitary-adrenal axis (HPA) measures
Most studies searching for a biomarker of burnout have used HPA axis measures
[21]. Despite its involvement in
other processes (e. g., fighting illness or infection), the HPA axis is best
known as a stress regulation system; and when a stressor is perceived, it is
activated by the limbic part of the brain (e. g., amygdala) and results in the
sequential release of corticotropin hormone from the hypothalamus,
adrenocorticotropic hormone from the pituitary gland, and cortisol from the
adrenal cortex [22]. This release of
hormones into the blood mobilizes substrates for energy metabolism, supplying
the body with the energy required to actively cope with the stressor [23]. As the end-product of the HPA
axis, most research has focused on cortisol, largely through saliva samples but
less commonly via blood (serum), hair, or urine [24]. Cortisol levels often increase in
response to a stressor [25] and tend
to follow a diurnal pattern in which they steadily increase in the second half
of the night, peak shortly after waking (i. e., within 30 to 60 minutes), and
then gradually decrease across the day [26]. Due to this diurnal rhythm, and the fact that cortisol levels
are affected by many factors (e. g., diet, sleep) [27], there are complexities in
measuring it, and various approaches have been used including collecting single
(e. g., pre-work) or multiple (e. g., cortisol awakening response) morning
samples, and samples taken serially across the day (e. g., afternoon, evening)
[21].
Research linking burnout with salivary cortisol assessed via one-off morning
samples has revealed mixed results [22]. While some studies have shown null effects [e. g., 28] or a
negative association [e. g., 29, 30], more than half of these studies found that
burnout was associated with elevated morning cortisol [e. g., 31, 32, 33, 34].
For example, well-powered studies by Deneva et al. [33] and Wingenfeld et al. [34] found that burnt-out medical
professionals (303 doctors and 279 nurses, respectively) had higher morning
cortisol than their colleagues. However, in both studies, cortisol samples were
taken at the start of a workday (i. e., at approximately 7 am) and thus did not
reflect, or account for, waking levels or time. This makes the findings
difficult to interpret given cortisol’s diurnal rhythm (e. g., the typical
increase observed 30 to 60 minutes after waking) and that various uncaptured
factors could have impacted cortisol concentrations in the time between waking
and arriving at work (e. g., ambient light level, anticipation of the day ahead,
caffeine consumption) [35]. Indeed,
variations in sample timing and a lack of control for confounding factors likely
explains the mixed findings across studies employing single morning samples. For
instance, samples were reportedly taken at 7 AM in two studies [30]
[34], 8 AM in two studies [28]
[32], between 6 AM and 8
AM in one study [33], and at an
unspecified time in two studies [29]
[31]. Given these
issues, expert consensus guidelines strongly advise against one-off morning
samples, instead recommending multiple morning samples (e. g., to assess the
cortisol awakening response) while controlling for crucial confounding factors
like time of awakening [35].
The cortisol awakening response, defined as the rapid rise in cortisol levels
that typically occurs in the morning after waking (usually within 30 to 60
minutes), has been the subject of much research and can be assessed in numerous
ways (e. g., from area-under-the-curve metrics to change scores) [36]. The findings from research
assessing burnout in relation to the cortisol awakening response have also been
equivocal [36], with studies reporting
null effects [e. g., 37], positive associations [e. g., 38], or negative
associations [e. g., 39]. Indeed, these mixed findings are likely due, at least
in part, to inconsistencies in how the awakening response has been assessed. For
example, while Sjors and Jónsdóttir [39] utilized change scores (i. e., difference between awakening and
15 minutes later), McCanlies et al. [37] and Traunmuller et al. [38] used area-under-the-curve metrics (i. e., ground and increment)
from a greater number of samples (e. g., awakening and 15, 30, and 45 minutes
later). Despite the unclear results, it is worth noting that one of the more
rigorous (e. g., confounding factors such as awakening time, cigarette smoking,
drug use, etc. were controlled for in the analyses and/or protocol) and largest
datasets collected to date by Marchand and colleagues [40]
[41]
[42] reported that
higher burnout was related to a blunted cortisol awakening response (i. e., less
change from waking to 30 minutes after waking) in a sample of 401 Canadian
day-shift workers. Indeed, this finding mirrors the conclusion from an earlier
meta-analysis by Chida and Steptoe [43], as well as sport-based research linking salivary cortisol to a
concept related to burnout, overtraining syndrome [e. g., 44]. As such, the
cortisol awakening response might be worth examining in future work alongside
other potential biomarkers (e. g., diurnal cortisol).
Further to research centered on morning cortisol, studies have investigated if
burnout impacts salivary cortisol secretion across the rest of the day (e. g.,
afternoon, evening) [21]. Overall, the
findings on diurnal cortisol have been mixed, with some studies reporting null
effects [e. g., 45], and others revealing a positive [e. g., 46] or negative
[e. g., 47] association. Again, this is likely due, at least in part, to
variations in how and when diurnal cortisol was assessed. For instance, studies
differed in whether they analyzed diurnal cortisol via one-off samples (e. g.,
at the end of a work shift) [46], a
single metric (e. g., diurnal slope from awakening to bedtime) [37], or multiple samples while
factoring in morning cortisol levels (e. g., waking, 30 minutes later, 11 AM, 3
PM, and 8 PM) [45]. However, despite
the equivocal results, it is worth noting that when focused solely on studies
using non-clinical samples of a relatively large size (i. e., ≥ 200
participants) that measured burnout in a manner most consistent with athlete
burnout (i. e., via Maslach Burnout Inventory; MBI) [48], a clearer picture emerges. Indeed,
Marchand et al. [41] collected
salivary cortisol from 401 Canadian workers at awakening, 30 minutes later, 2
PM, 4 PM, and bedtime, and found that higher burnout (and particularly
exhaustion) was linked with lower cortisol in the afternoon and evening, with
the largest effect at bedtime. Similarly, among 197 police officers, McCanlies
et al. [37] found that greater
exhaustion and cynicism were associated with less diurnal cortisol secretion,
with samples collected at lunchtime, dinner, and bedtime. In contrast,
Wingenfeld et al. [34] found that
burnt-out nurses had higher salivary cortisol than colleagues across all samples
(i. e., 11:30 AM, 5:30 PM, and 8 PM). This conflicting finding, which mirrors
research linking hypercortisolism with depression – a condition thought to
overlap with burnout [36] – could be
due to methodological differences between studies (e. g., populations).
Many reviews published to date have concluded that there is no single compelling
HPA axis-related marker of burnout, attributing this to the high methodological
heterogeneity and weaknesses inherent in the literature (but it might be that
burnout is not reflected in any HPA-axis measures) [21]. First, the way in which burnout
has been conceptualized has varied between studies [36]. For example, while some studies
have used Maslach’s [48]
multidimensional definition (i. e., emotional exhaustion, cynicism, personal
inefficacy) [49], others have explored
burnout via the dimensions (e. g., cognitive weariness, emotional exhaustion,
physical fatigue; [50]) developed by
Shirom and Melamed [e. g., 51]. Second, studies have differed in how they have
treated burnout data [52], either
analyzing it in a continuous fashion [e. g., 41] or, most often, grouping
participants using cut-points that differ from study-to-study [e. g., 53].
Third, the population has varied greatly between studies [24], ranging from non-clinical (e. g.,
teachers) to clinical (e. g., patients with exhaustion disorder; [54]) samples. Fourth, studies have
differed in when biomarker data was collected (e. g., 15, 30, 45, or 60 minutes
after waking) [36], and if they
controlled statistically for confounding factors (e. g., age) [21]. Fifth, most studies have used
small samples and cross-sectional designs, which limit statistical power and
causal understanding [22]. Given these
issues, future work evaluating HPA-axis related markers of burnout should strive
for greater methodological homogeneity (e. g., in burnout questionnaire use) and
employ stronger methods (e. g., longitudinal study designs). Unfortunately, the
few studies that have been conducted in sport also suffer from the issues noted
above (e. g., small sample sizes; see [Table 1]).
Table 1 A summary of studies linking burnout with
salivary or serum cortisol and HRV in athletic
samples.
Authors (Year)
|
Study Design
|
Sample (n)
|
BO Measure
|
Sample Timing
|
Key Results
|
Effect Sizes
|
Main Limitations
|
Davis et al. (2018)
|
Cross-sectional
|
82 athletes (55 male, 27 female;
M
age
=20 years)
|
ABQ
|
Salivary cortisol sampled at 7–9 am, 10–11 am, 1–3pm, or 6–8
pm based on training timing Also, before, immediately
after, and 20 minutes after, a physical test *No
other biomarkers assessed
|
BO was not significantly associated with change in
cortisol
|
r=0.10
|
Small sample size Cross-sectional or snapshot
design Did not assess BO dimensions, only a global
score Unclear precisely when cortisol was
sampled No control for confounding factors
|
Dobson et al. (2020)
|
Repeated measures observational
|
13 female swimmers (M
age
=19
years)
|
ABQ at beginning of season, in period of overload training,
and after a taper (11 weeks between each measure)
|
Resting lnRMSSD assessed for 10 minutes in supine position at
three time points via Finapres (lnRMSSD from last 5 minutes
used in analyses) *HR also assessed
|
BO was highest in tapering period and lnRMSSD was lowest in
overload period Change in BO not significantly
associated with change in lnRMSSD *Change in BO also
not significantly associated with change in HR
|
Not available
|
Small sample size Did not assess BO dimensions, only a
global score Equipment used to assess HRV was not
ECG-based No control for confounding factors
|
Landolt et al. (2019)
|
Cross-sectional
|
32 professional jockeys (14 male, 18 female;
M
age
=19 years)
|
MBI
|
Salivary cortisol sample at awakening and 30 minutes after in
low- and high-stress period of season *sAA-AR also
assessed
|
No significant associations between BO dimensions and CAR
apart from positive relationship between cynicism and CAR in
high-stress period *Professional inefficacy
significantly associated with sAA-AR
|
r between BO dimensions and CAR in low stress period
ranged from 0.06 to 0.27
r between BO
dimensions and CAR in high stress period ranged from 0.22 to
0.37
|
Small sample size Cross-sectional or snapshot
design Did not assess athlete BO or a global BO
score No control for confounding factors
|
Martin et al. (2022)
|
Longitudinal
|
40 NCAA swimmers (17 male, 23 females;
M
age
= 20 years)
|
ABQ
|
Serum cortisol at beginning and end of a 6-week training
period, no specific time of day stated *CK, MG, and
testosterone also assessed
|
BO was positively associated with change in the ratio of
testosterone to cortisol, which was mostly driven by a ↓ in
cortisol *BO not significantly associated with change
in CK or MG
|
r=0.34
|
Small sample size Did not assess BO dimensions, only a
global BO score Unclear precisely when cortisol was
sampled in blood No control for confounding
factors
|
Monfared et al. (2021)
|
Cross-sectional
|
42 youth athletes (14 males, 28 females;
M
age
= 15 years)
|
ABQ
|
Salivary cortisol sample 30 minutes before and immediately
before practice, but no specific time of day
stated *BVP, GSR, and RR also assessed
|
Significant positive association between BO and change in
cortisol *BO not significantly associated with GSR,
but negatively associated with BVP and RR
|
β=0.24
|
Small sample size Cross-sectional or snapshot
design Did not assess BO dimensions, only a global BO
score Unclear precisely when cortisol was
sampled No control for confounding factors
|
Souza et al. (2018)
|
Case-control
|
12 BO and 12 control soccer and futsal players (gender not
stated but M
age
= 21 years)
|
ABQ
|
Salivary cortisol sample at 8 am *DHEA-S and
testosterone also assessed
|
No significant differences in salivary cortisol between
groups *No significant differences in DHEA-S or
testosterone between groups
|
d=0.32
|
Small sample size Cross-sectional or snapshot
design Failure to sample at multiple time
points No control for confounding factors
|
Notes: ABQ, athlete burnout questionnaire; BO, burnout; BVP, blood
volume pulse; CAR, cortisol awakening response; CK, creatine kinase;
DHEA-S, dehydroepiandrosterone sulphate; GSR, galvanic skin response;
HR, heart rate; lnRMSSD, natural log of RMSSD; MBI, Maslach burnout
inventory; MG, myoglobin; NCAA, national collegiate athletic
association; RMSSD, root mean square of successive differences of r-to-r
intervals; RR, respiration rate; sAA-AR, Salivary alpha-amylase
awakening responses.
Like the research noted outside of sport, the few studies conducted in sport have
revealed mixed results. Indeed, most research has reported null effects between
athlete burnout and cortisol [e. g., 55]. For instance, Souza et al. [28] split soccer players into burnt out
and control groups based on ABQ scores and found no significant between-group
differences in morning salivary cortisol (assessed via one sample at 8 AM).
Similarly, among professional jockeys, Landolt et al. [56] found few significant associations
between burnout dimensions assessed via the MBI and cortisol awakening response,
with only a positive relationship emerging between cynicism and the cortisol
awakening response during a high-stress period of the season. Monfared et al.
[57] also reported a significant
positive correlation, with higher burnout (measured via the ABQ) associated with
greater increases in salivary cortisol from 30 minutes to immediately before
training in 42 youth athletes. Finally, in a study with 40 collegiate-level
swimmers, Martin et al. [58] collected
serum cortisol samples at the beginning and end of a six-week training block and
found that burnout was significantly and positively associated with a change in
testosterone to cortisol ratio, an effect that was mostly driven by a reduction
in cortisol concentrations. Thus, to date, no single compelling HPA-axis related
biomarker has emerged from the literature focused specifically on athletic
populations.
In summary, the results of research linking burnout with HPA-axis measures
(e. g., cortisol) have been relatively unclear. However, some of the largest and
more rigorous studies have hinted that biomarkers such as elevated morning
(i. e., pre-work) cortisol levels, a blunted cortisol awakening response, and
diminished salivary cortisol secretion in the afternoon and evening (e. g., at
bedtime) might warrant further investigation [41]. It therefore remains for future
research to assess these physiological markers alongside other indices (e. g.,
HRV).
Autonomic nervous system (ANS) metrics
Many studies searching for a biomarker of burnout have used ANS metrics [21]. The ANS plays a pivotal role in
maintaining balance in key regulatory functions (e. g., metabolism,
temperature), and is an important system that enables the body to react flexibly
and effectively in response to stressors [59]. The ANS has two main branches: the sympathetic nervous system
(SNS) which aids the rapid mobilization of energy to actively combat a stressor
(i. e., fight vs. flight response), and the parasympathetic nervous system (PNS)
which facilitates energy conservation and restoration following a stressor [60]. These two systems are normally in
dynamic balance, but chronic stress results in the SNS persistently dominating
the PNS, thereby placing excessive demands on the body and inhibiting energy
conservation and recovery [61]. This
stress-related ANS imbalance (i. e., SNS hyperactivity and PNS hypoactivity) has
most commonly been examined via HRV, defined as variations in the time intervals
between successive heart beats [62].
Both ANS branches impact HRV via the sinoatrial node, with SNS and PNS activity
accelerating and decelerating heart rate, respectively [63]. Due to differences in chemical
signaling at the sinoatrial node, the PNS can modulate heart rate via the vagus
nerve on a shorter timescale than the SNS (i. e., milliseconds versus seconds),
meaning that high-frequency changes in HRV offer a relatively purer measure of
PNS activity, while low-frequency changes reflect a mixture of SNS and PNS
activity [64].
Research linking burnout with low-frequency HRV parameters has revealed equivocal
results [52]
[59]. Indeed, while some studies have
reported null effects [e. g., 38], others have found positive [e. g., 65] or
negative [e. g., 66] associations. For instance, Thielmann et al. [67] performed a 24-hour
electrocardiogram (ECG) recording with 414 employees working with patient or
child populations and found no differences between low, moderate, and high
burnout groups in low-frequency HRV. While May et al. [68] used a similar 24-hour ECG
recording protocol with 88 female undergraduate students, they found that higher
burnout was associated with greater low-frequency HRV after controlling for
depression symptomology. In contrast, Lennartsson et al. [69] found that low-frequency HRV,
assessed over a 300-second recording session in a supine position, was lower in
a clinical burnout group compared to non-clinical high and low burnout groups.
This unclear pattern of results could be due to low-frequency HRV metrics
reflecting a blend of SNS and PNS activity, which contrasts with high-frequency
HRV metrics that more purely indicate PNS activity (or vagal tone) [70]. Indeed, given the less clear
physiological origin of low-frequency HRV (e. g., baroreflex activity, mix of
SNS vs. PNS activity), researchers are encouraged to focus more on metrics
linked to PNS activity [70].
Studies relating burnout with HRV metrics reflective of PNS activity have also
revealed mixed findings [21]
[59]. Indeed, studies using indices from
the frequency-domain (e. g., high-frequency HRV) have either reported null
effects [e. g., 71], positive associations [e. g., 29], or negative associations
[e. g., 72]. However, frequency-domain HRV measures are susceptible to the
influence of movement and respiration [59]
[73], which might have
clouded the results. To combat this, some studies have assessed only time-domain
HRV metrics reflective of PNS activity (e. g., root mean square of successive
differences; RMSSD) [70]. For
instance, well-powered and high-quality studies have emerged from the Dresden
Burnout Study [74]. In the first,
Kanthak et al. [75] measured HRV among
410 healthy adults during three conditions (i. e., an emotionally arousing
situation, a recumbent recovery period, and seated rest) and found that higher
burnout (and especially exhaustion) was associated with lower RMSSD in most
conditions after controlling for covariates (e. g., age). Subsequently, among
167 healthy adults, Wekenborg et al. [76] found that lower RMSSD during seated rest predicted higher
burnout (and particularly exhaustion) 12 months later after accounting for
covariates (e. g., gender). Finally, in a longitudinal study of 378 healthy
adults, Wekenborg et al. [77] found
that lower RMSSD predicted higher exhaustion, but not vice versa (or global
burnout), after controlling for covariates (e. g., body mass index). Thus, RMSSD
might offer a promising biomarker of burnout, and particularly the dimension of
emotional exhaustion [78].
Although RMSSD may potentially mark burnout, when looking at the burnout-HRV
literature overall, the findings have been mixed, likely due to high
methodological heterogeneity (but possibly because burnout is not reflected in
ANS-related indices) [52]. First, the
way in which burnout has been assessed has varied between studies [21]. Indeed, while the MBI has been
used most [e. g., 79], other instruments such as the Copenhagen burnout
inventory [80] have also been used
[e. g., 66]. Second, HRV recording equipment has differed across studies [81], ranging from gold-standard ECG
devices [e. g., 82] to chest- or wrist-worn sensors [e. g., 83] and mobile
applications using photoplethysmography [e. g., 84]. Third, the time periods
used to record HRV data has varied [59], with most studies using 24-hour recordings [e. g., 38] but some
using shorter measurement periods during rest [e. g., 85] or work-related tasks
[e. g., 86]. Fourth, a vast array of HRV metrics has been used across studies,
often with little justification [52].
For example, May et al. [68] found a
negative association between burnout and very low-frequency HRV, with limited
consideration of the metrics’ physiological origin (e. g., thermoregulation)
[70]. Fifth, most studies have
used absolute HRV values that do not account for participants’ normative values
and, as such, have not explored other promising metrics (e. g., HRV coefficient
of variation) [59]. Finally, many
studies have been cross-sectional with small samples, thereby limiting causal
understanding [21]. Given these
issues, future work examining ANS-related indices of burnout should strive for
greater methodological homogeneity (e. g., in equipment use) and utilize
stronger methods (e. g., larger sample sizes). Unfortunately, there is a dearth
of research on burnout and HRV in sport, and what studies do exist, suffer from
similar issues (see [Table 1]). For
example, in a rare study, Dobson et al. [87] found no link between burnout and RMSSD among 13 female
swimmers.
In summary, the results of studies searching for an ANS-related indicator of
burnout (e. g., HRV) have been equivocal. However, the most well-powered and
rigorous studies imply that indices of PNS hypoactivity such as lower RMSSD
during seated rest might hold some promise [e. g., 75,76]. Future research
therefore needs to further assess this biomarker while taking into consideration
the key issues central to this complex field of study.
Considerations for future research
While this review will help the selection of biomarkers for further investigation
(e. g., bedtime salivary cortisol; [41]), such decisions should be theoretically grounded. Given that
burnout is theorized to develop when there is a persistent mismatch between
situational demands and personal coping resources [78], the biopsychosocial model (BPSM)
of challenge and threat might offer a neat theoretical framework to explore
potential biomarkers [88]. Indeed,
according to the BPSM, a threat appraisal, where an individual feels that
situational demands exceed their coping resources, is associated with a distinct
physiological profile [89].
Specifically, compared to a challenge appraisal (i. e., when coping resources
are deemed to match or exceed situational demands), a threat appraisal is marked
by lower vagally-mediated HRV (e. g., RMSSD) and higher cortisol at rest [90]. Moreover, in response to an
acutely stressful event (e. g., sporting competition), a threat appraisal
results in cardiovascular reactivity characterized by relatively lower cardiac
output (i. e., amount of blood ejected by the heart per minute) and higher total
peripheral resistance (i. e., net constriction in the blood vessels) [89]. Thus, the BPSM could help
researchers select and integrate potential biomarkers of burnout in future
investigations, resulting in studies that are more theoretically underpinned.
However, it should be noted that other frameworks exist [12], some of which go beyond
stress-based explanations and offer additional causes of athlete burnout (e. g.,
unidimensional identity).
In addition to the predictions of the BPSM [91], other pertinent frameworks could guide future research on
burnout biomarkers. Indeed, borrowing from models of allostatic load [92], a common hypothesis is that the
early stages of burnout are marked by higher HPA-axis and ANS activity (e. g.,
hypercortisolism and SNS hyperactivity) [21], while over time these systems become exhausted due to prolonged
or recurrent stress, resulting in more severe burnout being marked by lower
HPA-axis and ANS activity (e. g., hypocortisolism and lower PNS activity) [36]. Thus, future research should
assess if different biomarkers are needed to detect athletes at varying stages
of burnout. To help with this feat, researchers could draw on initial conceptual
models that suggested that burnout dimensions develop sequentially (i. e.,
emotional exhaustion → cynicism → professional inefficacy) [93]. As well as testing these
theory-driven predictions, future work could explore if burnout biomarkers are
more likely to emerge in response to challenges (e. g., intense exercise) [22]. Indeed, research has hinted that
burnout may be marked by hypocortisolism in response to acute stress [e. g.,
94], a response that differs from the typical increase in cortisol seen in
reaction to a stressor [25].
As noted previously, the literature exploring burnout biomarkers has been
hampered by cross-sectional designs and small samples [21]. Thus, future research should use
longitudinal designs with larger samples [22]. Historically, this has been difficult given the expensive,
time-consuming, laboratory-based, and expertise-reliant nature of biomarker
testing (e. g., cortisol) [95].
However, new technology is emerging (e. g., microsensors) that might help
researchers determine if biomarkers (e. g., cortisol, HRV) are useful in
identifying burnt out athletes [96].
For example, due to learnings from the COVID-19 pandemic, companies are
developing rapid assay-based tests that could, in the future, enable accurate,
reliable, and cost-effective assessments of cortisol in day-to-day life [97]. While many of these diagnostic
tests are only at the proof-of-concept stage, technology already exists that
allows for the valid and expedient measurement of vagally-mediated HRV (e. g.,
camera-based photoplethysmography via applications such as HRV4Training) [98]. This technology might offer an
effective way of integrating burnout biomarker testing into practice given that
athletes are used to wearing devices (e. g., heart rate monitors) to supply
sport scientists with data (e. g., related to physical training load). Although
sport may provide an excellent “natural laboratory” to assess burnout biomarkers
(e. g., cortisol, HRV), more research is needed into the acceptability of such
testing and how it might integrate with existing practices (e. g., well-being
monitoring) [99]. There is also a risk
that, due to the relatively high cost of this technology (vs. self-report
measures), such biomarker testing is only available to support elite
professional athletes operating at the highest levels in their sport, with
lower-level and talented youth athletes missing out.
As mentioned previously, high methodological heterogeneity has hindered burnout
biomarker research [36]. Future work
therefore needs to be more consistent in the methods used to assess burnout
(e. g., conceptualization, measurement) and physiological markers (e. g.,
equipment, sample timing). Regarding the former and in line with past
recommendations [100], future studies
that examine burnout as a health problem in athletes should use a definition
where exhaustion is central [e. g., 50] and use questionnaires that align with
this conceptualization (e. g., SMBQ) [13]. That said, given recent research showing that athlete burnout is
on the rise predominately due to increases in sport devaluation and a reduced
sense of accomplishment (vs. emotional and physical exhaustion) [9], future investigations might also
wish to use other additional questionnaires (e. g., ABQ) [14]. Furthermore, to encourage more
complex approaches (e. g., experience sampling methods), researchers could
develop expedient single-item measures (e. g., “Right now I feel exhausted”)
[49]. Also, rather than dividing
athletes into groups (e. g., high vs. low) using arbitrary cut-points or median
splits, future work should examine associations between burnout and biomarkers
continuously and report findings for global burnout as well as its subdimensions
[7]. Indeed, this is important
given that some biomarkers (e. g., RMSSD) have been more strongly linked to
certain dimensions (e. g., exhaustion) [77]. While uniformity in physiological recording is
biomarker-dependent, future research should use valid and reliable equipment
(e. g., ECG devices for vagally mediated HRV), comparable measurement times and
methods (e. g., cortisol samples taken via passive drool upon awakening, 30
minutes after waking, 2 PM, 4 PM, and bedtime), and similar metrics in analyses
(e. g., RMSSD). As well as striving for greater homogeneity in the methods
utilized, future work should strictly adhere to best-practice guidelines [70]
[101].
Future burnout biomarker research can also be improved by more routinely
controlling for confounding factors [21], either by accounting for covariates in protocols (e. g., asking
participants not to consume caffeine two hours before measuring vagally mediated
HRV) [70], or controlling for them
statistically (e. g., adjusting for awakening time when assessing cortisol)
[101]. Confounders of particular
interest are likely to include age, gender, physical fitness, sleep time, and
stage of season [36]. For age,
research has shown that HRV declines with age, particularly for metrics
reflecting PNS activity (e. g., RMSSD) [102]. Moreover, for gender, studies have suggested that chronically
stressed females may display larger increases in cortisol upon awakening than
males [e. g., 103]. Furthermore, for physical fitness, research has shown that
highly fit athletes have higher resting HRV than less fit athletes [e. g., 104].
Additionally, for sleep, research has suggested that shorter sleep times may be
associated with lower cortisol at awakening [e. g., 105]. Finally, for stage of
season, research has shown that RMSSD might be higher among athletes during
periods of overload training than at other times (e. g., tapering) [87]. Thus, to confidently link certain
biomarkers to athlete burnout, future research needs to better account and
control for important confounding factors [21]. Indeed, one crucial factor, which is central to most sport
contexts, is the exercise associated with training and competition. Given that
many biomarkers are impacted acutely by exercise (e. g., cortisol) [106], it is possible that physiological
indices measured at rest and away from training or competition temporally
(e. g., at bedtime) might hold most promise in identifying athlete burnout.
In summary, the key considerations for future research on physiological markers
of athlete burnout include: (1) ensuring the selection of biomarkers is
underpinned by empirical evidence, pertinent theory, and takes into account
stage of burnout development; (2) using technology that enables biomarker data
to be collected longitudinally from large samples; (3) adopting more homogenous
methods in the assessment of burnout and physiological parameters; and (4)
routinely controlling for confounding factors (see [Table 2]). The final point is
particularly important given the myriad of factors that can impact biomarkers
such as cortisol and HRV (e. g., diet, illness, medication) [35]
[70]. If the factors listed above are adequately considered, a clearer
picture should emerge of any physiological indices of athlete burnout.
Table 2 Key considerations for future research on
biomarkers of athlete burnout.
Ensure selected biomarkers are:
|
-
Evidence-based (i. e., aligned with previous
research)
|
-
Theoretically grounded (e. g., BPSM of challenge and
threat)
|
-
Appropriate for burnout stage (i. e., early versus
latter stages)
|
Use technology that enables:
|
-
Researchers to use stronger study designs (e. g.,
longitudinal)
|
-
Data to be collected from larger samples (i. e., ≥
200 participants)
|
-
Cost-effective and efficient data acquisition (e. g.,
HRV4Training)
|
Adopt consistent methods when:
|
-
Measuring burnout via self-report (e. g., ABQ and
SMBQ)
|
-
Assessing biomarkers (e. g., timing of saliva
samples)
|
-
Analysing physiological data (e. g., ECG signals for
HRV)
|
Control for confounding factors, such as:
|
-
Chronological age
|
-
Biological sex or gender
|
-
Physical fitness
|
-
Sleep time and/or quality
|
-
Stage of season (e. g., tapering)
|
-
Exercise or physical activity
|