RESEARCH ARTICLE
Inter-Individual Variability in the Adaptive
Responses to Endurance and Sprint Interval
Training: A Randomized Crossover Study
Jacob T. Bonafiglia1, Mario P. Rotundo1, Jonathan P. Whittall1, Trisha D. Scribbans1, Ryan
B. Graham2, Brendon J. Gurd1*
1 School of Kinesiology and Health Studies, Queen’s University, Kingston, Ontario, Canada, 2 School of
Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada
* gurdb@queensu.ca
Abstract
The current study examined the adaptive response to both endurance (END) and sprint
interval training (SIT) in a group of twenty-one recreationally active adults. All participants
completed three weeks (four days/ week) of both END (30 minutes at ~65% VO2peak work
rate (WR) and SIT (eight, 20-second intervals at ~170% VO2peak WR separated by 10 sec-
onds of active rest) following a randomized crossover study design with a three-month
washout period between training interventions. While a main effect of training was observed
for VO2peak, lactate threshold, and submaximal heart rate (HR), considerable variability
was observed in the individual responses to both END and SIT. No significant positive rela-
tionships were observed between END and SIT for individual changes in any variable. Non-
responses were determined using two times the typical error (TE) of measurement for
VO2peak (0.107 L/min), lactate threshold (15.7 W), and submaximal HR (10.7bpm). Non-
responders in VO2peak, lactate threshold, and submaximal HR were observed following
both END and SIT, however, the individual patterns of response differed following END and
SIT. Interestingly, all individuals responded in at least one variable when exposed to both
END and SIT. These results suggest that the individual response to exercise training is
highly variable following different training protocols and that the incidence of non-response
to exercise training may be reduced by changing the training stimulus for non-responders to
three weeks of END or SIT.
Introduction
Considerable heterogeneity exists in the individual response in peak oxygen uptake (VO2peak)
following exercise training [1–3]. Specifically, VO2peak can increase [2,4], decrease [5], or
remain unchanged [6,7] following structured endurance training (END). Similarly, inter-indi-
vidual variability in training responses have also been observed following supra-maximal
sprint interval training (SIT) [8,9]. While variability in training responses has been demon-
strated following both END and SIT, it is currently unknown whether individuals who fail to
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December 9, 2016
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a11111
OPEN ACCESS
Citation: Bonafiglia JT, Rotundo MP, Whittall JP,
Scribbans TD, Graham RB, Gurd BJ (2016) Inter-
Individual Variability in the Adaptive Responses to
Endurance and Sprint Interval Training: A
Randomized Crossover Study. PLoS ONE 11(12):
e0167790. doi:10.1371/journal.pone.0167790
Editor: Jose A. L. Calbet, Universidad de las
Palmas de Gran Canaria, SPAIN
Received: June 6, 2016
Accepted: November 20, 2016
Published: December 9, 2016
Copyright: © 2016 Bonafiglia et al. This is an open
access article distributed under the terms of the
Creative Commons Attribution License, which
permits unrestricted use, distribution, and
reproduction in any medium, provided the original
author and source are credited.
Data Availability Statement: All relevant data are
within the paper and its supporting information
files.
Funding: Funding was provided by the Natural
Sciences and Engineering Council of Canada (grant
number: 402635; http://www.nserc-crsng.gc.ca/
index_eng.asp) and the Canadian Foundation for
Innovation (grant number: 25476;https://www.
innovation.ca/). The funders had no role in study
design, data collection and analysis, decision to
publish, or preparation of the manuscript.
respond following one type of exercise training might respond to a different training stimulus
(i.e. different exercise volume, intensity and metabolic demand).
While END and SIT differ substantially in exercise volume, intensity, and metabolic
demand, at the group level they induce strikingly similar adaptations in VO2peak [10,11], lac-
tate threshold [12,13], and muscle oxidative potential [14–16]. Interestingly, limited evidence
demonstrating that central adaptations following training may differ between END and SIT
[17,18], supports the potential that the mechanisms underlying similar adaptations in
VO2peak may differ following END and SIT. Further, individual variability in both peripheral
[19,20] and central [17] adaptations following training have been observed. Together these
results suggest that both central and peripheral adaptations may vary in an individual follow-
ing END or SIT, supporting the hypothesis that an individual who fails to respond following
END may respond following SIT (and vis versa).
Therefore, in order to determine if individuals respond differently to END and SIT, the
present study compared individual responses following three weeks of both END and SIT uti-
lizing a randomized crossover study design with a three-month washout period between train-
ing interventions. Individual changes in VO2peak, lactate threshold, and submaximal heart
rate (HR) were compared and the incidence of response and non-response for all variables
were classified using typical error (TE), an index of measurement error that considers both
biological and technical variability [21]. We hypothesized that individual responses to END
would not necessarily reflect responses to SIT (and vis versa), potentially due to differences in
central and peripheral adaptations.
Methods
Twenty-one healthy recreationally active (self-reported < three hours of physical activity per
week) men (n = 9) and women (n = 12) volunteered to participate in the study. Each partici-
pant attended a preliminary screening session where they were briefed on the study, provided
informed consent, and had their height and weight recorded. Participants were not previously
trained in cycling and were not involved in a training program at the start of the study. Partici-
pants were informed to maintain their regular physical activity and nutritional habits through-
out the duration of the study. All experimental procedures performed on human participants
were approved by the Health Sciences Human Research Ethics board at Queen’s University.
Verbal and written explanation of the experimental protocol and associated risks was provided
to all participants prior to obtaining written informed consent.
Experimental Design
The current study utilized a randomized crossover design (Fig 1) where participants com-
pleted two, three-week training interventions separated by a three-month wash-out period
during which participants were instructed to return to their pre-study levels of physical activ-
ity. Physiological testing occurred in the week preceding, and the week following each three-
week training intervention. All physiological testing and training for both experiments was
performed on a Monark Ergomedic 874 E stationary ergometer (Vansbro, Sweden). Eight
additional participants completed a supplemental experiment to determine typical error for all
variables. All participants were asked to refrain from alcohol and caffeine 12 hours before, and
nutritional supplements and exercise 24 hours before all physiological testing.
Physiological Testing
In the week preceding (pre) and the week following (post) training, participants reported to
the lab on three separate occasions, separated by 24–48 hours. During each visit participants
Individual Responses to Endurance and Sprint Interval Training
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Competing Interests: The authors have declared
that no competing interests exist.
completed a VO2peak incremental ramp test to volitional exhaustion as described previously
[22]. Briefly, following a 20 minute warm-up of four alternating five minute periods of load-
less and 80W pedalling at 80 RPM, work rate was increased by 25W per minute until volitional
exhaustion. Gas exchange and heart rate (HR) were collected throughout each ramp test using
a metabolic cart (Moxus AEI Technologies, Pittsburgh, PA) and Polar HR monitors (Polar
Team2 Pro, Kempele, Finland). VO2peak was calculated for each test as the highest 30 second
average VO2 value, whereas submaximal HR was calculated for each test as the 30 second aver-
age HR value during the third stage of the ramp protocol (~156 W). Final pre- and post-train-
ing VO2peak and submaximal HR were determined by averaging the three values obtained
during each testing period. RPM was collected continuously throughout each test and peak
aerobic power (WRpeak) was calculated using the average WR from the last 30 seconds of the
test, whereas the WR at VO2peak was calculated using the average WR during the same 30 sec-
onds used to calculate VO2peak.
Lactate Threshold
Fingertip capillary blood (~20 uL) was sampled at rest (baseline) and within the last 10 s of
each successive one-minute stage during the first VO2peak ramp test of pre- and post-testing
test using a Lactate Scout + (EFK Diagnostics, Magdeberg, Germany) as done previously [13].
Lactate threshold was determined as the first recorded work rate (WR) where lactate was >4
mmol/L [23,24], often referred to as the onset of blood lactate accumulation at 4 mmol/L
[25–27].
Training Interventions
Training consisted of two, three week training periods separated by ~three months. During
each training period participants were instructed to either cycle for 30 minutes at ~65% of WR
at VO2peak (END) or perform eight, 20-second intervals at ~170% of WR at VO2peak, sepa-
rated by 10 seconds of rest (SIT). Both training interventions required participants to train
four times per week and the order of training was counterbalanced such that 12 (six males; six
females) participants completed END first. All training sessions were preceded by a one-min-
ute loadless warm-up. Participants were instructed to maintain a cadence of 80RPM and
received verbal encouragement throughout all training sessions. HR was collected during
Fig 1. Overview of experimental protocol.
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training, at three minute intervals (END) and at the end of each interval (SIT), using Polar HR
monitors (Polar Team2 Pro, Kempele, Finland). Ratings of perceived exertion (RPE) were col-
lected immediately following each training session using a 6–20 Borg Scale [28]. HR and RPE
were averaged over all training sessions to determine training HR and RPE for END and SIT.
Determination of Typical Error
In order to determine typical error (TE) for VO2peak, lactate threshold and submaximal HR, a
supplemental experiment involving eight recreationally active participants (four males; four
females, age, 21±1 yrs; BMI, 21±2 kg/m2; VO2peak, 44±6 mL/kg/min) reported to the lab on
two separate occasions separated by at least a week as described previously [9]. On each visit to
the lab participants performed identical incremental ramp tests to volitional fatigue as
described above. VO2peak, lactate threshold and submaximal HR were determined for each
test as described above and the resulting values were utilized to calculate TE.
Typical error (TE) of measurement was calculated for VO2peak, lactate threshold, and sub-
maximal HR as described previously [21] utilizing the following equation:
TE ¼ SDdiff=
ﬃﬃﬃ
2
p
Where SDdiff is the variance (standard deviation) of the difference scores observed between
the 2 repeats of each test. A non-responder for VO2peak, lactate threshold, or submaximal HR
was defined as an individual who failed to demonstrate an increase or decrease that was greater
than two times the TE away from zero. A change beyond two times the TE means there is high
probability (i.e. 12 to 1 odds) that this response is a true physiological adaptation beyond what
might be expected to result from technical and/or biological variability [21].
Statistical Analysis
Data are expressed as means and standard deviation. To ensure efficacy of the washout period
baseline and response measures of VO2peak, lactate threshold, and submaximal HR between
training period one and two were compared using unpaired t-tests as described previously
[29]. Effects of training protocol (END vs. SIT) and time (Pre vs. Post) for all variables were
examined using a two-way, repeated measures ANOVA. Any significant main effects or inter-
actions were subsequently analyzed using a Bonferroni post hoc test where appropriate.
Unpaired t-tests were also used to assess differences in the training response for all variables
between males and females following END and SIT separately, and to determine if responses
following END or SIT differed between training periods. A simple linear regression was used
to determine the relationship between baseline variables between training period one and two
and between the magnitude of response between END and SIT. Differences in training HR
and RPE between END and SIT were assessed using paired t-tests and simple linear regres-
sions were used to determine if these variables were related to the magnitude of physiological
responses following training. A McNemar’s test was used to determine whether END and SIT
elicited similar rates of response for VO2peak, lactate threshold, and submaximal HR. Statisti-
cal significance was accepted at p < 0.05.
Results
Attendance at training sessions was 100% and all data reported are solely from those partici-
pants that completed the full study protocol. Three participants dropped out of the study
following pre-training testing in the first training period and were not included in final analy-
sis. Average HR during and RPE immediately following SIT (HR: 172.8 ± 7.8 bpm; RPE:
Individual Responses to Endurance and Sprint Interval Training
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17.9 ± 0.9, mean ± SD) was significantly higher (p < 0.05) than END (HR: 166.2 ± 13.7 bpm;
RPE: 15.5 ± 1.4, mean ± SD). Interestingly, RPE reported immediately following each SIT
session was significantly related with the magnitude of change in VO2peak induced by SIT
(r = 0.5, p < 0.05). Baseline measures, and the magnitude of response for all variables for train-
ing periods one and two are presented in Table 1. Unpaired t-tests revealed no differences
between baseline measures for VO2peak (p = 0.62), lactate threshold (p = 0.12), and submaxi-
mal HR (p = 0.86) between training periods one and two. No differences were observed in the
magnitude of response between training periods one and two for VO2peak (p = 0.20), lactate
threshold (p = 0.55), or submaximal HR (p = 0.62). Additionally, there was no difference in
the mean END or SIT response for any variable between training periods. Further, baseline
measures for training periods one and two were significantly related for VO2peak (r = 0.94,
p < 0.05), lactate threshold (r = 0.82, p < 0.05), and submaximal HR (r = 0.82, p < 0.05).
Participant characteristics and pre- and post-training values for END and SIT are presented
in Table 2. A main effect of training (p < 0.05) was observed for VO2peak (Fig 2A), lactate
threshold (Fig 2B), submaximal HR (Fig 2C), and WRpeak (Fig 2D). No condition (END vs.
SIT) or interaction (condition x time) effects were observed for any variable examined. While
males had higher baseline VO2peak, lactate threshold, submaximal HR, and WRpeak than
females (p < 0.05), there were no statistical differences in the magnitude of training responses
between sexes (Table 2). No significant relationships were observed between END and SIT for
individual changes in VO2peak (r = 0.14, p = 0.57; Fig 3A), lactate threshold (r = 0.10, p = 0.70;
Fig 3B), or submaximal HR (r = 0.17, p = 0.46). Baseline VO2peak did not predict changes in
VO2peak following END (r = 0.28, p = 0.22) but was negatively related with the change in
VO2peak induced by SIT (r = -0.59, p < 0.01). Baseline lactate threshold, and submaximal
HR were not related with training-induced changes following either END (lactate threshold:
r = 0.0, p = 1.0; HR: r = 0.37, p = 0.10) or SIT (lactate threshold: r = 0.29, p = 0.23; HR: r = 0.11,
p = 0.63).
Unpaired t-tests revealed that the baseline characteristics of the participants used in the
ancillary TE study did not statistically differ from the participants in the present study for all
variables in Table 2. Two times TE was 0.107 L/min for VO2peak, 157 W for lactate threshold,
and 10.0 bpm for submaximal HR. Individual patterns of response and rates of non-response
for VO2peak, lactate threshold, and submaximal HR following both END and SIT are pre-
sented in Fig 4. Following training six non-responders were observed where an individual par-
ticipant failed to improve in one measured variable following either END or SIT; however, in
all cases these non-responders improved at least one variable following training utilizing the
other exercise protocol. McNemar’s tests did not reveal significant differences in the incidence
of response for VO2peak (p = 0.6), lactate threshold (p = 0.1), and submaximal HR (p = 0.6)
between END and SIT.
Table 1. Pre-training and magnitude of response for training periods 1 and 2 for all participants.
Training Period One
Training Period Two
Pre-training
Response
Pre-training
Response
VO2peak (L/min)
3.0 ± 0.9
+0.05 ± 0.2
2.9 ± 0.9
+0.15 ± 0.3
VO2peak (mL/kg/min)
42.7 ± 6.4
+0.7 ± 3.2
41.2 ± 6.9
+2.2 ± 3.2
Lactate Threshold (W)
165.9 ± 43.2
+20.2 ± 18.3
190.7 ± 51.4
+14.7 ± 34.9
HRsubmax (bpm)
153.9 ± 24.7
-5.8 ± 7.8
152.6 ± 21.5
-4.1 ± 12.8
Values are means ± standard deviation.
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Discussion
The current study examined individual responses in VO2peak, lactate threshold and submaxi-
mal exercise heart rate (HR) following three weeks of both END and SIT. Carryover effects
from training period one to two were absent and the magnitude of responses between training
periods was not different for any variable. These data highlight the effective implementation of
our randomized cross-over study design [29]. In summary, the current study demonstrates
inter-individual variability in the training responses to END and SIT and suggests that individ-
ual patterns of response are dependent on the training protocol utilized.
The major novel findings of the current study are that: 1) while END and SIT increased
VO2peak, lactate threshold and submaximal HR at the group level with no differences
observed between protocols, improvements within a given individual following END did not
predict the improvement observed following SIT (and vice versa), 2) individual patterns of
response were observed following both END and SIT, however these patterns varied within
individuals between END and SIT, and 3) while our analysis revealed non-responses for one
or more variables within most participants, we failed to observe a global non-response to END
and SIT in any individual.
Similar Group Responses in the Initial Adaptations to END and SIT
At the group level, END protocols are effective at increasing VO2peak and lactate threshold
[30], while SIT protocols at supra-maximal intensities also improve VO2peak [31] and lactate
Table 2. Participant characteristics and group responses to END and SIT.
END
Pre
Post
Males (n = 9)
Females (n = 12)
Total (n = 21)
Males (n = 9)
Females (n = 12)
Total (n = 21)
Age (yrs)
20.4 ± 1.2
19.9 ± 1.2
20.3 ± 0.9
-
-
-
Height (cm) †
181 ± 6
165 ± 7
172 ± 12
-
-
-
Body mass (kg) †
81.9 ± 10.3
62.0 ± 11.6
70.0 ± 14.7
82.0 ± 10.9
61.2 ± 11.5
69.5 ± 15.6
VO2peak (L/min) †
3.7 ± 0.5
2.4 ± 0.5
3.0 ± 0.9
3.8 ± 0.5
2.5 ± 0.5
3.1 ± 0.9*
VO2peak (mL/kg/min) †
46.0 ± 3.9
39.3 ± 6.7
42.2 ± 6.4
47.3 ± 5.4
41.4 ± 6.2
43.9 ± 6.4*
Lactate Threshold (W) †
209 ± 38
149 ± 40
175 ± 47
233 ± 40
171 ± 46
199 ± 51*
WRpeak (W) †
296 ± 42
196 ± 39
238 ± 64
309 ± 58
210 ± 32
252 ± 66*
HRsubmax (bpm) †
135 ± 11
166 ± 19
152 ± 22.
129 ± 8
159 ± 18
146 ± 21*
SIT
Pre
Post
Males (n = 9)
Females (n = 12)
Total (n = 21)
Males (n = 9)
Females (n = 12)
Total (n = 21)
Age (yrs)
20.4 ± 1.2
19.9 ± 1.2
20.3 ± 0.9
-
-
-
Height (cm)
181 ± 6
165 ± 7
172 ± 12
-
-
-
Body mass (kg) †
82.8 ± 11.6
62.2 ± 12.4
70.4 ± 15.6
83.1 ± 11.2
61.7 ± 11.5
70.3 ± 15.6
VO2peak (L/min) †
3.7 ± 0.6
2.4 ± 0.5
3.0 ± 0.9
3.7 ± 0.5
2.6 ± 0.4
3.1 ± 0.9*
VO2peak (mL/kg/min) †
45.0 ± 9.3
39.2 ± 5.5
41.7 ± 6.9
44.7 ± 5.5
41.6 ± 5.4
42.9 ± 5.5*
Lactate Threshold (W) †
215 ± 36
154 ± 40
180 ± 47
230 ± 33.3
165 ± 41
192 ± 47*
WRpeak (W) †
292 ± 45
202 ± 30
241 ± 57
314 ± 46
210 ± 32
255 ± 63*
HRsubmax (bpm) †
133 ± 13
169 ± 19
155 ± 24
129 ± 9
167 ± 20
151 ± 25*
Values are means ± standard deviation. WRpeak, peak aerobic power; HRsubmax, submaximal heart rate.
†Signiﬁcant baseline difference between males and females, p < 0.05.
*Main effect of training, p < 0.05.
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threshold [12,13]. Consistent with these results and previous work form our lab utilizing the
same protocols [16], a main effect of training was observed in the current study for VO2peak,
lactate threshold, and submaximal HR. Also consistent with previous studies comparing END
and SIT [14–16] no differences were observed between protocols for the magnitude of
response at the group level. While the primary purpose of present study was not to determine
if the group responses to END and SIT differ, the observation of similar group responses to
END and SIT may suggest that a larger sample size is required to attain statistical power in
order to detect potential interaction effects between training protocols.
Individual Variability in Responsiveness to END and SIT
While variability in the individual responses to END is established [2,6,7,19,32,33], we recently
demonstrated similar variability in response to the SIT protocol utilized in the present study
[9]. The major novel finding of the current study is our demonstration of variability in the indi-
vidual responses following different training protocols (END and SIT). Specifically, our results
demonstrated that exercise protocols which differ in intensity, time, and metabolic demand,
like END and SIT, can induce different adaptive responses in VO2peak, lactate threshold and
submaximal HR within a given individual. These findings confirm the hypothesis that individu-
als who are not sensitive to a given exercise protocol may experience adaptation if exposed to a
Fig 2. Group responses following 3 weeks of END and SIT. Group responses for VO2peak (A), lactate threshold (B), submaximal HR (C), and WRpeak (D).
*Significant main effect of training, p < 0.05.
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Individual Responses to Endurance and Sprint Interval Training
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different protocol [5], potentially due to different sensitivities to training volume [7] and/or
intensity [32]. While the mechanisms determining individual variability in sensitivities to differ-
ing training protocols are unknown, genetic predispositions [34] may be responsible for vari-
ance in the capacity of central [17] and peripheral [14,35] adaptations to training. A similar
disassociation between individual changes in VO2peak has previously been observed following
END and resistance training [33], but to our knowledge we are the first to demonstrate inter-
individual variability in the response to two protocols known to induce equivalent improve-
ments in aerobic capacity at the group level. Importantly, while the current data suggests that
individuals may respond favorably to a change in training stimulus, we cannot rule out the pos-
sibility that the different individual responses observed between END and SIT were a result of
simply training twice at two different times (i.e. it is possible that an individual completing
END twice may not demonstrate identical responses), differences in external physical activity
between training periods and/or changes in nutritional habits caused by different training pro-
tocols (i.e. END vs. SIT), or training at different times of the year (i.e. fall vs. winter). Addition-
ally, the present study only examined individual variability in the initial response to training
(i.e. the response to three weeks of training), and it remains possible that individual differences
Fig 3. Correlations of individual responses following 3 weeks of END and SIT. Relationship between individual
responses in VO2peak (A) and lactate threshold (B). Dashed lines represent the typical error cut-offs. Individuals falling
within the shaded area failed to improve either VO2peak or lactate threshold following both END and SIT, while the
hashed area represents an adverse response following both training protocols.
doi:10.1371/journal.pone.0167790.g003
Fig 4. Individual patterns of response following three weeks of training. Positive responses (white boxes), non-responses (grey boxes) and adverse
responses (black boxes) are shown for all participants across all variables following END (A) and SIT (B). A dashed box indicates that data was unavailable
for a given variable. Individuals who failed to improve any variables for either END or SIT, “Overall non-responders” are indicated by diamond filled boxes.
The percentage of participants demonstrating a non-response (NR; including both non- and adverse responses) for each variable, and overall, is also
provided.
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observed following three weeks of END and SIT may not persist following longer training peri-
ods. Thus, while our results support the consideration of multiple training protocols when
attempting to optimize individual exercise prescription [36], there remains very little data, and
much future work still needed, before we fully understand inter-individual responsiveness to
different training protocols.
Consistent with previous observations of heterogeneity in the individual response to END
[7,32,33,37] and SIT [8,9] we have also observed significant rates of non-response following
both END and SIT in the current study (Fig 4). The present finding that END and SIT elicited
similar rates of non-response for VO2peak, lactate threshold, and submaximal HR agrees with
previous observations that END and SIT Importantly, while inter-individual variability in the
response to training has been repeatedly demonstrated [7,33,37], attempts to quantify individ-
uals as responders or non-responders are relatively recent [5–9,32,38]. In the current study,
the use of two times the typical error (TE) to identify responders and non-responders [21]
may have led to higher incidences of non-responses than previously reported [6–8,32]. How-
ever, despite the use of this conservative method of identifying responders, we have observed a
subset of adverse responders to VO2peak, lactate threshold, and submaximal HR following
both END and SIT that is consistent with previous observations of adverse responses to exer-
cise for a variety of cardiovascular risk factors [5]. Interestingly, a non- or adverse response to
VO2peak, lactate threshold, or submaximal HR following one training protocol did not pre-
clude a positive response following the other training protocol. Recently, several reports have
recommended that before individuals are classified as responders or non-responders, it is
important to determine if variability in the individual responses within the experimental con-
dition are greater than within-subject variation [39–41]. While we were unable to conduct this
analysis due to our current study lacking a time-matched control group, it is important that
future studies examining rates of response/non-response to exercise training consider the
recently recommended approach to performing these analyses [39–41]. This the limitation
aside, the current study adds to a growing body of literature that identifies a portion of the
population that either does not respond, or responds adversely to exercise training and sug-
gests that these non-/adverse-responders may respond more positively to different training
protocols.
Mechanisms Underlying Individual Variability to END and SIT
Despite marked differences in the physiological stress they impose, a single bout of END or
SIT elicits analogous molecular responses in skeletal muscle [16], leading to similar peripheral
adaptations including changes in fibre-type distribution [16], increased skeletal muscle oxida-
tive capacity [14–16,42] and resting muscle glycogen content [14–16]. Interestingly, the central
adaptations elicited by END or SIT are inconsistent [17,18], however, only central adaptations
associated with six weeks of END prevails as independent predictors of the VO2peak responses
[43]. Few studies have compared both central and peripheral adaptations to multiple training
protocols and significant differences in training duration, frequency, and volume limits the
ability to compare and interpret findings from different studies [43,44]. While recent research
has elucidated mechanisms that primarily explain the adaptive responses to training [43],
future research is needed to determine if variability in the mechanisms that underlie changes
in exercise capacity/performance explain individual response variability following training.
At the individual level, heterogeneity in both central [17] and peripheral adaptations are
present following END [19,20] and SIT [14], which suggests that variability in individual
responses to END and SIT may be due in part to individual variance in the magnitude of
peripheral and central adaptations. Why variance in central and/or peripheral adaptations
Individual Responses to Endurance and Sprint Interval Training
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may exist within an individual following different training protocols is currently unknown,
however, evidence from the HERITAGE study suggests that much of this variability may
results from a genetic predisposition to a specific type of training stimulus [2]. Interestingly,
recent evidence has found associations between several genetic markers and individual train-
ing responses [34,45,46], however, while these findings are a step towards optimizing individ-
ual exercise prescriptions [34] whether genetic signatures exist that may predict which type of
training an individual is most likely to respond to is unknown. This remains an interesting
and important area for future investigation.
Individual Patterns of Response
Following END and SIT we observed individual patterns of response, where improvements in
VO2peak were not necessarily associated with improvements in lactate threshold or submaxi-
mal HR (Fig 4). The existence of individual patterns of response is consistent with previous
studies demonstrating that non-responders in VO2peak can be responders to other variables
associated with END [6,19] and SIT [8,9]. An additional novel finding of the present study is
that individual patterns of response were different following END and SIT. This variability in
individual patterns of response meant that even though several individuals failed to improve
any variable following either END or SIT, no “global non-responders” (i.e. individuals that
failed to improve following either protocol) were observed. These results further support the
consideration of multiple training protocols when prescribing exercise, and raise the possibil-
ity that an individual who does not appear to be responding to an initial exercise prescription
may respond more favourably if an alternative mode of training is prescribed. As continuing
the training stimulus beyond initial exposure (four weeks) reduces the incidence of non-
response in VO2peak [32], whether switching training protocols after initial exposure or
extending the amount of training prescription is equally effective at diminishing non-
responses remains an area for future research.
Conclusion
The current study assessed individual responses in VO2peak, lactate threshold, and submaxi-
mal exercise heart rate (HR) following three weeks of both END and SIT. While training elic-
ited significant improvements in all variables at the group level, considerable heterogeneity
was observed in the individual responses including a number of non-/adverse-responders.
Further, individual patterns of response were not related across END and SIT and appear to be
training protocol dependent. All participants demonstrated a positive response in at least one
variable following the completion of both END and SIT suggesting that the existence of true
non-responders to exercise training is unlikely and that different training protocols should be
considered when optimizing individual exercise prescription.
Supporting Information
S1 Table. Raw data used for all tables and figures.
(XLSX)
Acknowledgments
The authors would like to thank Elizabeth Mathew and Wendy Fu for their help with HR data
analysis and a dedicated group of volunteers for their help in conducting training sessions.
Individual Responses to Endurance and Sprint Interval Training
PLOS ONE | DOI:10.1371/journal.pone.0167790
December 9, 2016
11 / 14
Author Contributions
Conceptualization: JB MR JW TS RG BG.
Data curation: JB MR JW TS RG BG.
Formal analysis: JB MR JW TS RG BG.
Funding acquisition: BG.
Methodology: JB MR JW TS RG BG.
Writing – original draft: JB MR JW TS RG BG.
Writing – review & editing: JB MR JW TS RG BG.
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Inter-Individual Variability in the Adaptive Responses to Endurance and Sprint Interval Training: A Randomized Crossover Study.
Bonafiglia, Jacob T,Rotundo, Mario P,Whittall, Jonathan P,Scribbans, Trisha D,Graham, Ryan B,Gurd, Brendon J