RPE Association with Lactate and Heart Rate

during High-Intensity Interval Cycling

JAMES M. GREEN1, JOHN R. MCLESTER2, THAD R. CREWS3, PHILLIP J. WICKWIRE1,
ROBERT C. PRITCHETT1, and RICHARD G. LOMAX1
1
Department of Kinesiology, University of Alabama, Tuscaloosa, AL; 2Department of Health, Physical Education and
Sport Science, Kennesaw State University, Kennesaw, GA; and 3Department of Physical Education and Recreation,
Western Kentucky University, Bowling Green, KY

ABSTRACT
GREEN, J. M., J. R. MCLESTER, T. R. CREWS, P. J. WICKWIRE, R. C. PRITCHETT, and R. G. LOMAX. RPE Association with
Lactate and Heart Rate during High-Intensity Interval Cycling. Med. Sci. Sports Exerc., Vol. 38, No. 1, pp. 167–172, 2006. Purpose:
Physiological and perceptual measures during interval exercise are not well understood. The current study therefore examined the
correspondence between RPE, HR, and blood lactate concentration ([La]) during interval cycling. Methods: V̇O2peak and the 4.0
mmol·L⫺1 lactate threshold were determined. In session 2, subjects (N ⫽ 12) warmed up (10 min, 0 W) and completed five 2-min
intervals (INT) at ⬎4 mmol·L⫺1 workload, each separated by 3 min of recovery (REC) (60 rpm, 0 W). HR, RPE, and [La] were
recorded at 10 min, at the conclusion of each INT, and each REC and 5- and 10-min recovery. Results: Repeated-measures ANOVA
showed [La], HR, and RPE increased significantly across time (INT and REC). At each time point, repeated-measures ANOVA was
used to compare standardized data (␣ ⫽ 0.05). RPE (at INT) intensified concurrently with HR and [La] at INT. Correlations were
significant for INT (P ⱕ 0.05) (HR–RPE: r ⫽ 0.63, [La]–RPE: r ⫽ 0.43). Similarly, RPE and HR for REC systematically increased
with [La]. Correlations for REC were also significant (HR–RPE: r ⫽ 0.44, [La]–RPE: r ⫽ 0.34). Correlations were also significant for
INT and REC combined (HR–RPE: r ⫽ 0.70, [La]–RPE: r ⫽ 0.22). Conclusions: INT and REC independently showed moderate
correspondence for RPE–[La] and RPE–HR. However, tighter overall coupling of HR with RPE (vs [La] with RPE) and a dissociation
between RPE–[La] suggest RPE during intervals of intense cycling were more sensitive to acute metabolic demand (evidenced by HR)
versus [La]. Key Words: LACTIC ACID, PERCEIVED EXERTION, TRAINING, PERFORMANCE

A
lternating brief, higher and lower intensity bouts in
a given session is known as interval training. Inter-
val training is purported to elicit improvements in
endurance performance capacity beyond the point at which
improvements result from submaximal steady intensity ex-
ercise (16). A potential benefit from high-intensity interval
or sprint-type training is improved buffering capacity (18)
and a positively altered respiratory compensation threshold
(10). RPE, a viable adjunct to oxygen consumption (V̇O2),
HR, and other objective measures of intensity (1) remain
very stable (13–15) at the lactate threshold regardless of
training status (5,13,24). Further, RPE is sensitive to train-
ing-induced threshold changes (14). Although lactate may
be a more meaningful marker of intensity (26), hygiene
issues and the impracticality of taking multiple blood sam-
ples make indirectly regulating lactate via RPE an attractive
option. In this regard, previous research supports the effec-
tiveness of this paradigm (4,25).
Address for correspondence: J. M. Green, Department of Kinesiology, Box
870312, Moore Hall, University of Alabama, Tuscaloosa, AL 35487;
E-mail: mgreen@bamaed.ua.edu.
Submitted for publication January 2005.
Accepted for publication June 2005.
0195-9131/06/3801-0167/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE®
Copyright © 2006 by the American College of Sports Medicine
DOI: 10.1249/01.mss.0000180359.98241.a2
167
Previous investigations demonstrate an association of
RPE with blood lactate concentration [La] during graded
exercise testing (3,5,13), across exercise modes (13), and
steady-state exercise (4,5) suggesting [La] serves as a
perceptual mediator. Others studies have produced dis-
sonant results. Green et al. (9) evaluated [La], RPE, and
HR during 60 min of constant-workload cycling showing
a clear RPE–[La] divergence beginning at 30 min. Welt-
man et al. (27) also demonstrated an uncoupling of RPE
and blood [La] with discordance observed across three
repeated 30-min bouts within a single day. These studies
indicate the RPE–[La] association may be disrupted un-
der certain circumstances such as longer duration, steady
workload (9), and repeated independent exercise bouts
(27). It is also plausible that other factors potentially
altering fatigue (hydration status, blood glucose) may
alter the RPE–[La] association.
The RPE–[La] response during interval exercise is not
well understood. Seiler and Sjursen (23) compared the ef-
fects of varying work duration (from 1 to 6 min) during
running bouts on RPE and physiological responses. With the
knowledge of the prescribed duration, interval running ve-
locity (self-paced) declined as interval duration increased.
RPE increased 2– 4 units (6- to 20-point scale) from initia-
tion to cessation of an interval session with a slight increase
in [La] from midpoint to endpoint of each session. Only
intervals of 1-min duration resulted in a significant increase
in [La]. Authors concluded RPE increases were not associ-
ated with increased lactate. Examining the potential associ-
FIGURE 1—Flowchart of interval cycling
protocol including timeline of INT and REC
periods and time points for HR, RPE, and
[La] assessment. Shaded bars, interval (2
min); open bars, recovery (3 min); black tri-
angles, HR, RPE, [La] measured.
ation between RPE and [La] and determining the strength of
[La] as a mediator of exertional perceptions would be en-
hanced by evaluating the correspondence of these variables
at multiple time points during exercise and recovery. Con-
sidering the popularity and potential performance benefits
of interval exercise (16) and the convenience of using RPE
to quantify intensity, research investigating the correspon-
dence of [La] and RPE during interval exercise is warranted.
This study examined RPE, [La], and HR responses during
repeated, high-intensity interval cycling.
MATERIALS AND METHODS
Subjects. Twelve physically active male volunteers
served as participants. Based on an alpha level of 0.05, an
effect size of 1.5 (RPE units), an SD of 2 units for RPE, and
a power of 0.80, a power analysis indicated 12 subjects
would be required for this study, which suggests that the
sample size for the current investigation was adequate. Be-
fore data collection, subjects completed a written informed
consent outlining requirements. All procedures were ap-
proved by the local review board for protection of human
subjects. Each participant arrived at the lab with previous
instructions to have consumed adequate fluids in the pre-
ceding 24-h period. Subjects also reported 3 h postprandial
with instructions to have abstained from caffeine and alco-
hol for a minimum of 24 h. Age (yr), height (cm), and mass
(kg) were recorded. Height and mass were measured using
a Detecto balance-type scale (Detecto, Brooklyn, NY).
Body fat percentage was estimated using Lange skinfold
calipers (Cambridge, MD) and a three-site method (chest,
abdomen, thigh) (20).
V̇O2peak trial. Following descriptive data collection,
participants completed a maximal exertion cycling trial for
V̇O2peak determination. Seat height was appropriately set on
a Monark cycle Ergometer (Varberg, Sweden) with handle-
bars preferentially adjusted. Subjects maintained 60 rpm by
using a Franz XB 700 metronome (Franz, New Haven, CT).
Subjects were fitted with an appropriately sized air-cush-
ioned face mask (Vacu-med, Ventura, CA) that was checked
upon mounting for appropriate seal and to ensure there were
no leaks. At this point, subjects also donned a Polar HR
monitor (Stamford, CT). Participants completed a warm-up
(4 min, 60 rpm, 0 W). Following the warm-up, power output
was increased 60 W every 2 min. All stages following the
warm-up were 2 min. Cadence was constant (60 rpm).
Power output was increased in this manner until subjects
achieved volitional exhaustion or could not maintain the
required cadence. Metabolic data (V̇O2, V̇CO2, respiratory
exchange ratio, ventilation) were collected using a Vacu-
168 Official Journal of the American College of Sports Medicine
med Vista mini-cpx (silver) metabolic measurement system
(Vacu-med). Turbofit software (Vacu-med), designed for
use with the metabolic system, was set to report mean
metabolic data over 15-s periods. The system was calibrated
before each test with a gas of known composition. A 3-L
syringe (Hans Rudolph, Kansas City, MO) was used to
calibrate the system for ventilation. HR was recorded using
a receiver interfaced with the computer. RPE relative to
overall feelings were collected during the last 15 s of each
stage using the Borg category (6 –20) scale. Instructions for
anchoring RPE were that “6” corresponds to seated rest, and
“19 –20” corresponds to maximal exertion. This verbal an-
choring procedure was completed just before initiating ex-
ercise. Criteria for achievement of V̇O2peak were a) RPE
ⱖ18, b) RER ⱖ1.1, c) plateau of V̇O2 with increased
workload, and d) ⬎85% of age-predicted maximum HR
(17). Each participant met at least two of these four criteria.
The highest recorded value across a 15-s period was ac-
cepted as V̇O2peak . During the V̇O2peak trial, capillary blood
samples were collected at the fingertip during the final 10 s
of each stage. During the warm-up, a sample was taken at 2
and 4 min. Blood samples were immediately analyzed for
[La] using a YSI 1500 Sport Lactate analyzer (Yellow
Springs Instruments, Yellow Springs, OH). Before each test,
the YSI was calibrated using 5 mmol·L⫺1 standard and
checked for linearity with 15 mmol·L⫺1 standard.
Interval cycling. Within 14 d of the V̇O2peak trial,
subjects returned to the lab with instructions to be well
rested, well hydrated, and 3 h postprandial, and to have
abstained from caffeine and alcohol for 24 h. Participants
donned a Polar HR monitor, made appropriate adjustments
to the Monark Ergometer and then completed a 10-min
warm-up (60 rpm, 0 W). Interval bouts were started at 10
min. Five 2-min bouts of high-intensity cycling (INT) were
completed with a 3-min recovery cycling (REC) (60 rpm, 0
W) between each INT. At the conclusion of the final 3-min
recovery bout, an additional 10 min of recovery cycling was
completed. Figure 1 provides a flowchart regarding the
interval cycling protocol including timing of measurements.
Resistance for INT was individualized. From the V̇O2peak
trial, the 4-mmol·L⫺1 [La] threshold was identified using a
graphic plot with power output on the x-axis and [La] on the
y-axis. INT resistance was set at 20 W greater than power
associated with the 4-mmol·L⫺1 [La]. This resulted in a
power output for INT of 286 ⫾ 41 W. This procedure was
meant to mimic an intensity at which interval training might
be completed.
During testing, capillary blood samples were collected
at the end of the 10-min warm-up, at the completion of
each INT, at the conclusion of each REC, and at 5- and
http://www.acsm-msse.org
TABLE 1. Descriptive characteristics of subjects (N ⫽ 12) and RPE responses at
4 mmol䡠L⫺1.
Variable Mean
Age (yr) 22.8
Height (cm) 181.9
Mass (kg) 79.2
Body fat (%) 7.5
V̇O2peak (mL䡠kg⫺1䡠min⫺1) 53.2
4 mmol䡠L⫺1 (% V̇O2peak) 78.1
RPE (at 4 mmol䡠L⫺1) 14.8
10-min REC. Samples were analyzed for [La] using the
YSI 1500 Sport lactate analyzer (Yellow Springs Instru-
ments), which was calibrated before each trial using 5
mmol·L⫺1 standard with linearity checks using 15
mmol·L⫺1 standard. HR and RPE were also recorded at
the same time intervals as [La].
Statistics. To compare values across time, a repeat-
ed-measures ANOVA was used for each variable ([La],
HR, RPE) with separate analyses for INT and REC.
Simple contrasts were used with INT5 and REC5 as the
reference categories when analyzing INT and REC, re-
spectively. Comparisons at each time point were also of
primary importance. Therefore, RPE, [La], and HR data
were standardized with each data point transformed to a
z score [z ⫽ (raw score – mean)/SD] using the variable-
specific grand mean and SD. Means for standardized
values were then compared at each time point using
repeated-measures ANOVA with simple contrasts. Re-
sults were considered significant at P ⱕ 0.05. Addition-
ally, to more thoroughly evaluate INT and REC re-
sponses, correlations were computed for [La]–RPE and
HR–RPE solely at peaks (conclusion of each INT) and for
values obtained at the conclusion of REC and for INT and
REC values combined. For correlations, raw scores were
used as opposed to standardized values.
RESULTS
Descriptive characteristics are presented in Table 1.
INT responses. Results for INT are presented in
Table 2. [La] at INT5 was significantly greater than all
other INT points. HR at INT5 was significantly greater
than HR at all other INT points. RPE at INT5 was sig-
nificantly greater (P ⬍ 0.05) than RPE at INT1, INT2, and
INT3 with the difference between INT4 approaching sig-
nificance (P ⫽ 0.08).
REC responses. Results for REC are presented in
Table 3. [La] was significantly greater at REC5 than at
warm-up, at each REC, and at 5- and 10-min recovery.
HR at REC5 was significantly greater than at warm-up,
REC1, REC2, REC3, and at 5- and 10-min recovery. RPE
TABLE 2. Responses at each INT for [La], HR, and RPE.
Variable INT1 INT2 INT3
[La] (mmol䡠L⫺1) 3.0 ⫾ 0.8* 5.0 ⫾ 0.9* 5.8 ⫾ 1.5* 6.2 ⫾ 1.5*
HR (bpm) 151 ⫾ 9* 160 ⫾ 12* 166 ⫾ 13* 172 ⫾ 7*
RPE (Borg) 12.4 ⫾ 2.9* 13.3 ⫾ 2.7* 14.3 ⫾ 2.6* 15.3 ⫾ 2.3** 15.8 ⫾ 2.0
Values are means and SD.
* P ⫽ 0.05 vs INT5. ** P ⫽ 0.08 vs INT5.
RPE, LACTATE, HEART RATE DURING INTERVALS
was significantly greater at REC5 than at warm-up, REC1,
REC2, and at 10-min recovery. The difference between
SD REC5 and the 5-min recovery approached significance
3.4 (P ⫽ 0.06).
5.6
12.3 Time point comparisons. Standardized values for
2.5 HR, [La], and RPE for INT and REC are presented in Figure
8.6
8.6 2. HR was significantly greater than [La] at each INT and
2.5 significantly less than [La] at each REC and at 5-min re-
covery. There were no significant differences between RPE
and HR at any point. RPE and [La] were not significantly
different at REC1, REC2, REC3, REC4, or at the 5- and
10-min recovery points. RPE was significantly less than
[La] at REC5. RPE was significantly greater than [La] at
INT1 with a marginal difference at INT4 (P ⫽ 0.06) and
INT5 (P ⫽ 0.07). [La] was significantly less than RPE at
10-min warm-up; however, there were no significant differ-
ences for values at 10-min recovery.
Correlations. Significant (P ⱕ 0.05) correlations were
found for HR–RPE and [La]–RPE responses for INT, for
REC and INT and REC combined. These data are presented
in Table 4.
DISCUSSION
Evidence suggests the RPE–[La] association is disrupted
during longer duration (9) and repeated independent exer-
cise bouts (23,27). Research has not definitively determined
responses between RPE and associated physiological vari-
ables during interval training or the potential RPE mediators
during such training. This study examined HR, blood [La],
and RPE during interval cycling.
[La] increased systematically upon initiating interval
bouts (Fig. 2), with significantly greater sequential values
for [La] within INT and REC. Visual observations also
show each REC value greater than the preceding INT.
Increasing concentration suggests lactate production ex-
ceeded removal. Further, with insufficient duration for [La]
to decline, it can also be concluded that, through recovery,
lactate continued to empty to blood faster than tissue uptake.
The time lag in lactate kinetics presents at least a partial
explanation for the observed RPE–[La] divergence. First,
the delay between lactate production and appearance in
blood creates difficulty in interpreting this measure. Higher
[La] at the end of recovery (vs previous interval) discredits
the concept that [La] at the immediate conclusion of an
interval accurately reflects intramuscular metabolism. An
alternative would be to use peak [La] following an interval
as an indicator. However, this is also problematic. First,
multiple measures would be required at tight time intervals
to obtain a true peak. For example, if samples were taken at
1, 3, and 5 min post, it is possible a higher [La] occurred
between these time points (i.e., 2 min, 2 min 30 s) (2).
Additionally, an intention of interval training is to achieve
INT4 INT5 an overload by repeating higher intensity bouts without
6.6 ⫾ 1.8 permitting excessive recovery. Therefore, delaying subse-
174 ⫾ 8
quent intervals for measurements would compromise ses-
sion quality. Maintaining a typical sequence of intervals
consequently results in residual lactate from previous inter-
Medicine & Science in Sports & Exercise姞 169
TABLE 3. Responses at each REC for [La], HR, and RPE.
Variable Warm-up REC1 REC2
[La] (mmol䡠L⫺1) 1.4 ⫾ 0.3* 4.6 ⫾ 0.9* 5.7 ⫾ 1.5*
HR (bpm) 102 ⫾ 17* 117 ⫾ 10 120 ⫾ 11*
RPE (Borg) 7.1 ⫾ 0.9* 9.3 ⫾ 2.1* 10.3 ⫾ 2.8*
Values are means and SD.
* P ⫽ 0.05 vs REC5.
vals contaminating serial samples, again interfering with
interpretation. Finally, independent of these difficulties, lac-
tate uptake during recovery would be unknown, also mag-
nifying complications. Unlike [La], RPE in the current study
demonstrated a quicker response to alternating workloads
(Fig. 2). Consequently, it can be concluded that dissimilar
response times or acute sensitivity of the different measures
to changing workloads accounted for the weak correspon-
dence between RPE and [La]. The current design used
3-min recovery periods. There was a considerable decrease
in [La] at 5-min recovery following the final interval bout,
and it is conceivable that extending recovery periods would
have enhanced RPE–[La] correspondence. Previous work
by Seiler and Sjursen (23) does not support this contention
when comparing shorter and longer work–rest durations.
However, in that study, [La] was only assessed at the mid-
point and end of the interval session. In Weltman et al. (27)
1.5- or 3-h recovery occurred between successive 30-min
steady-state (70% V̇O2max) bouts. Although this hardly clas-
sifies as interval training, there were significant main effects
for time, showing a drift upward in RPE and a decline in
[La]. The potential association with varying recovery dura-
tions warrants further investigation.
Unlike the [La]–RPE dissociation, perceived exertion
was tightly coupled with HR throughout the session (Fig. 2).
Analogous with the above rationale for the independence of
[La] and RPE, HR responded more rapidly to workload
alterations during intervals and therefore demonstrated a
pattern similar to RPE. HR represents a primary mechanism
by which acute cardiovascular demand is met. Although not
a dead-end product of metabolism, lactate conceptually
characterizes a sequestered source of stored energy while in
FIGURE 2—Means for standardized values (z-scores) for HR, [La],
and RPE at 10-min warm-up, INT1–INT5, REC1–REC5, and 5- and
10-min recovery. * HR vs [La], P < 0.05. § RPE < [La], P < 0.05.
‡ RPE > [La], P < 0.05. ‡‡ RPE > [La], P ⴝ 0.06. ‡‡‡ RPE > [La],
P ⴝ 0.07; RPE vs HR, NSD.
170 Official Journal of the American College of Sports Medicine
REC3 REC4 REC5 5 min 10 min
6.2 ⫾ 1.7* 6.4 ⫾ 1.8* 6.8 ⫾ 2.0 5.5 ⫾ 1.9* 3.8 ⫾ 1.6*
124 ⫾ 9* 130 ⫾ 13 128 ⫾ 13 119 ⫾ 11* 116 ⫾ 11*
11.2 ⫾ 3.0 11.6 ⫾ 2.9 11.1 ⫾ 2.4 10.4 ⫾ 1.9 9.4 ⫾ 1.6*
the blood. Because adenosine triphosphate turnover is not
dependent on lactate supply, lactate removal from blood for
energy purposes is not critical owing to the relatively slug-
gish response to workload change for [La] compared with
HR. Conversely, HR must be quicker to respond because
metabolic demand changes rapidly and is partially de-
pendent on cardiac output (and therefore indirectly reliant
on HR). Whereas the correspondence between RPE and
HR should be viewed as coincidental and not causal,
there was clearly a closer association of RPE with HR
compared with [La]. Because HR is more sensitive to
acute changes in workload (as encountered during inter-
val training), current results suggest RPE also is more
sensitive to acute metabolic demand with the mediating
influence of [La] being auxiliary.
Although lactate may not be a primary RPE mediator
during interval training, current results do not discredit it
entirely in this construct. Closer evaluation of RPE, HR, and
[La] reveals significant increases across time when evalu-
ating INT and REC bouts exclusively (Tables 2 and 3,
respectively). These RPE results mirror those of Seiler and
Sjursen (23) who found an upward drift for RPE during
running intervals. The current study also found a drift for
RPE during recovery. Conclusions from concurrent incre-
mental changes would be consistent with previous studies
identifying [La] as an RPE mediator (3,5,13,24). Whereas
this is a reasonable hypothesis, an alternate explanation
would be that successive intervals amplified fatigue (possi-
bly due to a variety of factors such as acidosis, neuromus-
cular factors, substrate depletion), and this increase was
reflected in RPE. Literature consistently indicates RPE may
be attributed to a variety of factors with no single variable
being exclusively dominant (19,21). It should also be em-
phasized that concurrent increases in [La], HR, and RPE
occurred even though workloads for REC and INT were
consistent throughout. This could imply that increased [La]
could have influenced RPE. Alternatively, cumulative fa-
tigue or other physiological changes resulting from multiple
bouts could have played a significant role in elevating RPE.
Seiler and Sjursen (23) found a 2- to 4-unit RPE drift
(Borg’s 15-point scale) throughout a given interval session.
Measures were taken only at a mid- and endpoint during
testing. Current results are comparable, showing a 3.4-unit
drift from INT1 to INT5 (Table 2). Interestingly, the present
TABLE 4. Correlations for HR, [La], and RPE.
HR-RPE [La]-RPE HR-[La]
INT (60 observations) 0.63* 0.43* 0.41*
REC (60 observations) 0.44* 0.34* 0.41*
INT ⫹ REC (120 observations) 0.70* 0.22* 0.05
* Significant (P ⫽ 0.05) correlation.
http://www.acsm-msse.org
investigation also shows a similar RPE drift (4 units) from
REC1 to REC5 (Table 3). Whereas concurrent [La] increases
offer one explanation for RPE drift, it should also be noted
that HR at REC increased significantly across time (Table
3), indicating the effect of [La] was likely not isolated.
Weltman et al. (27) showed repeated exercise in a day
(1.5–3 h apart) dissociates [La] and RPE. Although not
mentioned by authors, it is plausible that participants in-
curred a level of cumulative fatigue from multiple bouts,
consequently intensifying RPE. As with other variables, it is
difficult to segregate independent influences of certain vari-
ables on RPE. However, within certain limitations, current
results suggest [La] may play an auxiliary role in RPE
during interval exercise.
Studies showing [La] as an RPE mediator have often
employed incremental exercise tests (3,5,13). The tight re-
lationships of RPE with numerous physiological measures
are predictable in this paradigm. Physiological and bio-
chemical responses to graded testing are well founded, and
concomitant increases in RPE with elevated workload/
power should be expected. Unfortunately, graded exercise
testing does not mimic typical daily training regimens of
recreational or elite athletes who practice various types of
training including steady-state and interval sessions. RPE
has major advantages including its convenience as a viable
measure in nonlaboratory settings where objective physio-
logical variables such as oxygen consumption (V̇O2), blood
lactate, and even HR are more difficult or impossible to
obtain. Research tends to support use of RPE as an adjunct
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