Comparing Parasympathetic Reactivation in Different Exercise Types, Essays (university) of Abnormal Psychology

A study comparing the parasympathetic reactivation after repeated sprinting (rs), high-intensity intermittent exercise (hi), and moderate-intensity continuous exercise (mc). The study aimed to quantify the time course of parasympathetic reactivation after rs exercise and observe the effects of muscular power engagement, anaerobic participation, aerobic power level, and energy expenditure on postexercise autonomic control. The results of the study, which showed that hrr60s, t30, sdnn5–10min, pnn505–10min, rmssd5–10min, lnhf5–10min, and hfnu5–10min were comparable across the rs and hi trials but were significantly lower than those shown in the mc trial. Hrr was shorter after the mc exercise than after the rs trial, and both were shorter than that shown after the hi trial.

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Parasympathetic reactivation after repeated sprint exercise
Martin Buchheit,
1
Paul B. Laursen,
2
and Saı¨d Ahmaidi
1
1
Laboratoire de Recherche EA 3300 (APS et Conduites Motrices: Adaptations Re´adaptations), Faculte´ des
Sciences du Sport d’Amiens, Universite´ de Picardie Jules Verne, France; and
2
School of Exercise,
Biomedical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia
Submitted 16 January 2007; accepted in final form 26 February 2007
Buchheit M, Laursen PB, Ahmaidi S. Parasympathetic reac-
tivation after repeated sprint exercise. Am J Physiol Heart Circ
Physiol 293: H133–H141, 2007. First published March 2, 2007;
doi:10.1152/ajpheart.00062.2007.—The purpose of this study was to
examine the effects of muscular power engagement, anaerobic par-
ticipation, aerobic power level, and energy expenditure on postexer-
cise parasympathetic reactivation. We compared the response of heart
rate (HR) after repeated sprinting with that of exercise sessions of
comparable net energy expenditure and anaerobic energy contribu-
tion. Fifteen moderately trained athletes performed 1) 18 maximal
all-out 15-m sprints interspersed with 17 s of passive recovery (RS),
2) a moderate isocaloric continuous exercise session (MC) at a level
of mean oxygen uptake similar to that of the RS trial, and 3)a
high-intensity intermittent exercise session (HI) conducted at a level
of anaerobic energy expenditure similar to that of the RS trial.
Subjects were immediately seated after the exercise trials, and beat-
to-beat HR was recorded for 10 min. Parasympathetic reactivation
was evaluated through 1) immediate postexercise HR recovery, 2) the
time course of the root mean square for the successive R-R interval
difference between successive 30-s segments (RMSSD
30s
) and 3)HR
variability vagal-related indexes calculated for the last 5-min station-
ary period of recovery. RMSSD
30s
increased during the 10-min period
after the MC trial, whereas RMSSD
30s
remained depressed after both
the RS and HI trials. Parasympathetic reactivation indexes were
similar for the RS and HI trials but lower than for the MC trial (P
0.001). When data of the three exercise trials were considered to-
gether, only anaerobic contribution was related to HR trial-derived
indexes. Parasympathetic reactivation is highly impaired after RS
exercise and appears to be mainly related to anaerobic process
participation.
heart rate recovery; vagal-related indexes; autonomic activity; sprint
interval training
REPEATED SPRINT (RS) training, characterized by recurring ses-
sions of brief repeated bouts of supramaximal exercise, may be
a time-efficient strategy for inducing metabolic adaptations in
human skeletal muscle (15). Adaptations shown after a short
time course of RS training include increased resting glycogen
content (20), increased maximal activities of various enzymes
involved in glycolytic (31) and oxidative energy provision (10,
20), an increased H
buffer capacity (17, 20), and decreased
cycling time-trial performance (10, 15, 20). As a result, RS
training has been proposed as a viable alternative to classically
prescribed submaximal endurance training (10, 17, 20).
Today, there are growing social and psychological reasons
to encourage RS training within clinical populations. First, RS
training is remarkably time efficient and more compatible with
the Western world’s time-poor modern lifestyle. Second, the
concept of RS training may also be more attractive than
continuous exercise for sedentary individuals who have diffi-
culty handling exercise sessions that are perceived to be of a
long duration and of a monotonous nature. Third, the high level
of muscular power needed to perform RS training stresses
more type II muscle fibers, which comprise approximately
one-half of the fibers within the thigh (vastus) and calf (gas-
trocnemius) muscles of most people and of which are not
recruited during low-intensity exercise. Not surprisingly, RS
training has been shown to result in maintenance of and even
an improvement in muscular strength (17).
Although the effectiveness of RS training for maintaining
and improving muscular performance is established (47), its
influence on postexercise autonomic function is unknown.
Knowledge of this effect, however, is critical for clinicians
dealing with patients with certain disease states that may leave
them more prone to adverse cardiovascular events. Indeed,
sympathetic hyperactivity (4) or reduced cardiac vagal tone (3)
after exercise may confer a poor cardioprotective background
and underlie ischemic heart disease and the pathogenesis of
malignant ventricular arrhythmias and sudden cardiac death.
To quantify parasympathetic reactivation after exercise, the
time course of HR recovery (HRR) and HR variability (HRV)
indexes have been used (7, 13, 22, 42, 45). The validity of
these markers has been examined with the use of drugs that
cause a parasympathetic blockade (i.e., atropine) (22, 45). The
simplest and most used HRR index is the number of heart beats
recovered within 60 s after the cessation of exercise (13).
Fitting postexercise HRR to a first-order exponential decay
curve has also been used (7, 42). Regarding HRV, it is the
vagal-related indexes, such as the root mean square of succes-
sive differences of R-R intervals (RMSSD) or the power
density in the high-frequency (HF) range obtained by spectral
analysis, that are the most widely used methods (50). Finally,
a new and simple temporal time-varying parasympathetic in-
dex has recently been proposed by Goldberger et al. (22). This
index is derived from the time course of the RMSSD measured
on successive 30-s segments (RMSSD
30s
) over the recovery
period.
The acute effects of a single exercise bout on HRV have
been placed into long- and short-term categories. From 24 to
48 h after exercise, a rebound of parasympathetic activity,
which seems independent of the exercise type undertaken (38),
has often been described (18, 26). Concerning the short-term
evolution of autonomic activity, an initial decrease in HRV and
vagal-related indexes has been observed within minutes to
hours after exercise (38, 39, 51). Moreover, vagal restoration
Address for reprint requests and other correspondence: M. Buchheit, Labora-
toire de Recherche Adaptations Re´adaptations (APS et conduites motrices), Fac-
ulte´ des Sciences du Sport, Univ. de Picardie Jules Verne. Alle´ e P. Grousset,
80025 Amiens Cedex 1, France (e-mail: [email protected]).
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked advertisement
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Am J Physiol Heart Circ Physiol 293: H133–H141, 2007.
First published March 2, 2007; doi:10.1152/ajpheart.00062.2007.
0363-6135/07 $8.00 Copyright ©2007 the American Physiological Societyhttp://www.ajpheart.org H133
pf3
pf4
pf5
pf8
pf9

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Parasympathetic reactivation after repeated sprint exercise

Martin Buchheit,^1 Paul B. Laursen,^2 and Saı¨d Ahmaidi^1

1 Laboratoire de Recherche EA 3300 (APS et Conduites Motrices: Adaptations Re´adaptations), Faculte´ des

Sciences du Sport d’Amiens, Universite´ de Picardie Jules Verne, France; and^2 School of Exercise,

Biomedical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia

Submitted 16 January 2007; accepted in final form 26 February 2007

Buchheit M, Laursen PB, Ahmaidi S. Parasympathetic reac-

tivation after repeated sprint exercise. Am J Physiol Heart Circ

Physiol 293: H133–H141, 2007. First published March 2, 2007;

doi:10.1152/ajpheart.00062.2007.—The purpose of this study was to

examine the effects of muscular power engagement, anaerobic par-

ticipation, aerobic power level, and energy expenditure on postexer-

cise parasympathetic reactivation. We compared the response of heart

rate (HR) after repeated sprinting with that of exercise sessions of

comparable net energy expenditure and anaerobic energy contribu-

tion. Fifteen moderately trained athletes performed 1 ) 18 maximal

all-out 15-m sprints interspersed with 17 s of passive recovery (RS),

2 ) a moderate isocaloric continuous exercise session (MC) at a level

of mean oxygen uptake similar to that of the RS trial, and 3 ) a

high-intensity intermittent exercise session (HI) conducted at a level

of anaerobic energy expenditure similar to that of the RS trial.

Subjects were immediately seated after the exercise trials, and beat-

to-beat HR was recorded for 10 min. Parasympathetic reactivation

was evaluated through 1 ) immediate postexercise HR recovery, 2 ) the

time course of the root mean square for the successive R-R interval

difference between successive 30-s segments (RMSSD30s ) and 3 ) HR

variability vagal-related indexes calculated for the last 5-min station-

ary period of recovery. RMSSD30s increased during the 10-min period

after the MC trial, whereas RMSSD30s remained depressed after both

the RS and HI trials. Parasympathetic reactivation indexes were

similar for the RS and HI trials but lower than for the MC trial ( P 

0.001). When data of the three exercise trials were considered to-

gether, only anaerobic contribution was related to HR trial-derived

indexes. Parasympathetic reactivation is highly impaired after RS

exercise and appears to be mainly related to anaerobic process

participation.

heart rate recovery; vagal-related indexes; autonomic activity; sprint

interval training

REPEATED SPRINT (RS) training, characterized by recurring ses-

sions of brief repeated bouts of supramaximal exercise, may be

a time-efficient strategy for inducing metabolic adaptations in

human skeletal muscle (15). Adaptations shown after a short

time course of RS training include increased resting glycogen

content (20), increased maximal activities of various enzymes

involved in glycolytic (31) and oxidative energy provision (10,

20), an increased H^ buffer capacity (17, 20), and decreased

cycling time-trial performance (10, 15, 20). As a result, RS

training has been proposed as a viable alternative to classically

prescribed submaximal endurance training (10, 17, 20).

Today, there are growing social and psychological reasons

to encourage RS training within clinical populations. First, RS

training is remarkably time efficient and more compatible with

the Western world’s time-poor modern lifestyle. Second, the

concept of RS training may also be more attractive than

continuous exercise for sedentary individuals who have diffi-

culty handling exercise sessions that are perceived to be of a

long duration and of a monotonous nature. Third, the high level

of muscular power needed to perform RS training stresses

more type II muscle fibers, which comprise approximately

one-half of the fibers within the thigh (vastus) and calf (gas-

trocnemius) muscles of most people and of which are not

recruited during low-intensity exercise. Not surprisingly, RS

training has been shown to result in maintenance of and even

an improvement in muscular strength (17).

Although the effectiveness of RS training for maintaining

and improving muscular performance is established (47), its

influence on postexercise autonomic function is unknown.

Knowledge of this effect, however, is critical for clinicians

dealing with patients with certain disease states that may leave

them more prone to adverse cardiovascular events. Indeed,

sympathetic hyperactivity (4) or reduced cardiac vagal tone (3)

after exercise may confer a poor cardioprotective background

and underlie ischemic heart disease and the pathogenesis of

malignant ventricular arrhythmias and sudden cardiac death.

To quantify parasympathetic reactivation after exercise, the

time course of HR recovery (HRR) and HR variability (HRV)

indexes have been used (7, 13, 22, 42, 45). The validity of

these markers has been examined with the use of drugs that

cause a parasympathetic blockade (i.e., atropine) (22, 45). The

simplest and most used HRR index is the number of heart beats

recovered within 60 s after the cessation of exercise (13).

Fitting postexercise HRR to a first-order exponential decay

curve has also been used (7, 42). Regarding HRV, it is the

vagal-related indexes, such as the root mean square of succes-

sive differences of R-R intervals (RMSSD) or the power

density in the high-frequency (HF) range obtained by spectral

analysis, that are the most widely used methods (50). Finally,

a new and simple temporal time-varying parasympathetic in-

dex has recently been proposed by Goldberger et al. (22). This

index is derived from the time course of the RMSSD measured

on successive 30-s segments (RMSSD30s) over the recovery

period.

The acute effects of a single exercise bout on HRV have

been placed into long- and short-term categories. From 24 to

48 h after exercise, a rebound of parasympathetic activity,

which seems independent of the exercise type undertaken (38),

has often been described (18, 26). Concerning the short-term

evolution of autonomic activity, an initial decrease in HRV and

vagal-related indexes has been observed within minutes to

hours after exercise (38, 39, 51). Moreover, vagal restoration

Address for reprint requests and other correspondence: M. Buchheit, Labora- toire de Recherche Adaptations Re´adaptations (APS et conduites motrices), Fac- ulte´ des Sciences du Sport, Univ. de Picardie Jules Verne. Alle´e P. Grousset, 80025 Amiens Cedex 1, France (e-mail: [email protected]).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Am J Physiol Heart Circ Physiol 293: H133–H141, 2007. First published March 2, 2007; doi:10.1152/ajpheart.00062.2007.

http://www.ajpheart.org 0363-6135/07 $8.00 Copyright © 2007 the American Physiological Society H

has been shown to be more delayed after intense [80% peak

oxygen uptake (V˙^ O 2 peak)] than after moderate-intensity exer-

cise (50% V˙^ O 2 peak) (38, 39). Parasympathetic activity has also

been shown to be more impaired after resistance exercises than

with a moderate cycling effort (27). Nevertheless, in all of

these previous studies, the absence of anaerobic metabolite

measurements has made less clear the influences that muscular

power engagement, anaerobic participation, and aerobic power

level have on postexercise parasympathetic reactivation. For

RS exercise, although V˙^ O 2 peak is sometimes reached (16), this

is not always the case (21, 47); therefore, from a metabolic

point of view, the aerobic exercise intensity could be consid-

ered to be “submaximal.” Nevertheless, sprinting requires the

development of very high muscular power, so that the exercise

might also be considered to be “supramaximal” from a mus-

cular and anaerobic point of view. As a result, the effects of RS

on parasympathetic reactivation are difficult to predict.

The primary purpose of the present study was to quantify the

time course of the parasympathetic reactivation after RS exer-

cise and to observe the respective effects of muscular power

engagement, anaerobic participation, aerobic power level, and

energy expenditure on postexercise autonomic control. We

used multiple HR-derived parasympathetic indexes measured

after RS exercise and compared these with indexes obtained

after exercises of 1 ) comparable levels of net energy expendi-

ture to distinguish the specific effect of anaerobic process

participation and muscular power engagement and 2 ) compa-

rable anaerobic contribution to observe the explicit incidence

of net energy expenditure. Finally, we used multiple linear

regressions to show the respective consequence of each meta-

bolic and mechanical exercise characteristic on postexercise

autonomic regulation.

METHODS

Participants

Based on the assumption that a 8  5 beat/min difference in HRR 60

is meaningful (7, 13), we used Minitab 14.1 software (Minitab, Paris,

France) to determine that a sample size of nine subjects was needed to

provide a power of 80% with an alpha of 0.05. Although the evalu-

ation of the incidence of RS exercise on autonomic function is

especially crucial in sedentary individuals and patients, we preferred

here to recruit moderately trained subjects because we expected that

they would be more able to cope with this innovative experimentation

( n  15; age  21.3  3.1 yr, height  178.1  7.5 cm, body mass 

73.8  10.4 kg, muscle mass  30.7  0.3 kg, body surface area 

1.91  0.05 m^2 ). All participants were routinely involved (6.6  2.

h/wk) in various intermittent activities (soccer, handball, basketball,

or tennis) and had no history or clinical sign of cardiovascular or

pulmonary diseases. Muscle mass was estimated based on forearm

and thigh calf girths and skinfolds (33), whereas body surface area

was calculated according to the formula provided by Mosteller (37).

Subjects were not taking prescribed medications and presented with

normal levels of blood pressure and ECG patterns. The study con-

formed to the recommendations of the Declaration of Helsinki, and

participants gave voluntary written consent to participate in this

experiment, which was approved by the local ethics committee.

Experimental Design

Subjects performed, at the same time of day (1 h) over a 2-wk

period, one graded aerobic test and three sessions of short exercise

bouts. Each test was separated by at least 48 h. All tests were

performed on an indoor synthetic track where ambient temperature

ranged from 18 to 22°C. The graded maximal aerobic test was

performed first, followed by the three other tests in a random and

balanced order for each subject. The exercise bouts consisted of a

repeated sprinting bout (RS trial), a submaximal and continuous bout

completed at comparable net energy expenditure to that of the RS bout

(MC trial), and a high-intensity intermittent bout completed at a level

of anaerobic energy expenditure comparable to that of the RS bout (HI

trial). Subjects were familiarized with the exercise procedure before

commencement of each test. Subjects were asked not to perform

exercise on the day before a test and were asked to consume their

usual last meal at least 3 h before the scheduled test time. All three of

the experimental exercise bouts were preceded by a supervised and

standardized warm-up consisting of 5 min of running at 45% of V IFT

(where IFT is intermittent fitness test, corresponding to a “maximal

intermittent aerobic reference velocity,” see below) along with a few

athletic drills (i.e., skipping) and short bursts of progressive acceler-

ations on the track. Exercise bouts began 2 min after this warm-up

period.

Maximal graded aerobic test. Maximal aerobic performance of

each subject was assessed with a 30 –15 intermittent fitness test. This

intermittent shuttle field test elicits V˙^ O 2 peak and has been shown to be

accurate for individualizing intermittent shuttle running exercise (6).

Moreover, this test has been shown to be reliable (intraclass correla-

tion coefficient  0.96) for the final running speed ( V IFT ). The 30 –

intermittent fitness test consists of 30-s shuttle runs interspersed with

15-s passive recovery periods. For this test, velocity was set at 8 km/h

for the first 30-s run, and speed was increased by 0.5 km/h for every

30-s stage thereafter. Subjects were required to run back and forth

between two lines set 40 m apart at a pace that was governed by a

prerecorded beep. The prerecorded beep allowed the subject to adjust

their running speed within a 3-m zone placed in the middle and at each

extremity of the field. During the 15-s recovery period, subjects

walked in the forward direction toward the closest line (at either the

middle or end of the running area, depending on where their previous

run had stopped); this line determined where they would start the next

run stage. Subjects were instructed to complete as many stages as

possible, and the test ended when the subject could no longer maintain

the required running speed or when subjects were unable to reach a

3-m zone in time with the audio signal on three consecutive occasions.

The velocity attained during the last completed stage was determined

as the subject’s V IFT. Respiratory gas exchanges were measured with

an automated portable metabolic system (VO2000; Medgraphics,

St. Paul, MN) (34). Before each test, the O 2 and CO 2 analysis systems

were calibrated. V˙^ O 2 peak was defined as the highest oxygen uptake

(V˙^ O 2 ) attained in a 20-s period. Subjects were considered to have

reached V˙^ O 2 peak if at least two of the following criteria were met:

1 ) respiratory exchange ratio was 1.1, 2 ) a maximal HR (HRmax )

was attained within 10 beats/min of the age-predicted maximum, and

3 ) volitional fatigue occurred (28).

RS exercise. RS exercise consisted of repeated 15-m sprints with

17 s of passive recovery (52). Subjects ran in the opposite direction

after the 17-s rest. Total duration of the test was 6 min. Respiratory

gas exchanges were measured during the test as previously described.

Equivalent RS net energy expenditure exercise. This trial was used

to evaluate the influence of the muscular power engagement and/or

anaerobic participation on postexercise parasympathetic reactivation.

The “aerobic” intensity (%V˙^ O 2 peak ) of MC (moderate and continuous)

exercise was similar to that measured during RS and corresponded to

65% of V IFT (6). The exercise duration was determined a priori to

achieve similar levels of net energy expenditure compared with the

RS trial. Total calculated MC trial duration ranged from 368 to 501 s.

As for other exercises, respiratory gas exchanges were measured

during the test.

Equivalent RS anaerobic energy exercise. To examine the influence

of net energy expenditure on parasympathetic reactivation, we at-

tempted to compare the RS trial to that which occurred during a

12-min high-intensity intermittent exercise trial (HI trial). Our choice

H134 PARASYMPATHETIC REACTIVATION AFTER SPRINTING

Wilk normality tests. Because absolute HF power values were

skewed, HF power density was transformed by taking its natural

logarithm to allow parametric statistical comparisons that assume a

normal distribution. A one-way ANOVA with Tukey’s post hoc test

was used to compare the variables of HRR60s , T30, HRR, HRamp ,

SDNN5–10min , pNN505–10min , RMSSD5–10min , lnHF5–10min , and

HFnu5–10min , as well as the HR5–10min distributions between the three

exercise bouts. For time-varying RMSSD30s , a 3 (exercise trial) 20

(time) repeated-measures ANOVA was used to examine for main

effects and/or interactions of intensity and time. When statistical

significance was identified, a Tukey’s post hoc test was used to further

delineate differences between exercise trial or time. Multiple linear

regressions were used to establish the respective relationships be-

tween parasympathetic indexes and exercise characteristics. Other

polynomial regressions were rejected on the basis of importantly

higher residuals. Adjusting calculations based on age and body mass

index did not significantly change the outcomes. Moreover, because

data were homogenous, we did not need to make adjustments to avoid

overfitting. All statistical analyses were carried out with Minitab 14.

software (Minitab, Paris, France) with the level of significance set at

P  0.05.

RESULTS

Maximal Aerobic Test

Mean V˙^ O 2 peak, HRmax, and [La]b were 51.6  1.4 ml

O 2 min 1 kg 1 , 200  2 beats/min, and 10.9  0.9 mmol/l.

Mean VIFT was 18.9  1.1 km/h.

Cardiorespiratory Measures During the Three

Exercise Trials

All subjects successfully completed the 360-s RS and the

720-s HI exercise trials. The mean duration of the MC trial was

422  21 s. As expected, mean V˙^ O 2 was similar between RS

and MC trials (78.4  8.3 vs. 76.0  9.5% V˙^ O2 peak ; P  0.18)

and significantly higher during the HI trial (91.1  5.2%

V˙^ O 2 peak; P  0.001). Mean HR for the RS trial (87  2%

HRmax) was higher than for the MC trial (80  3% HRmax ; P 

0.01), whereas mean HR for the HI trial (93  4% HRmax ) was

greater than that for both RS and MC trials ( P  0.001).

Energy System Contribution and Energy Expenditure During

the Three Exercise Trials

Mean (SE) values of cumulated net V˙^ O 2 during exercise,

estimated total oxygen stores, measured [La]b, [La]b O 2 equiv-

alent, PCr O 2 equivalent, percent aerobic energy contribution,

and percent anaerobic energy contribution to exercise during

the trials are presented in Table 1. Mean (SE) values for the

net energy expenditure and total aerobic and anaerobic contri-

bution to the RS, MC, and HI trials are summarized in Fig. 1.

The net O 2 cost was marginally higher for the MC trial than for

the RS trial ( P  0.04) but more than twice as high during the

HI trial than during the RS and MC trials ( P  0.001). The

difference in net exercise O 2 cost between the RS and MC

trials was compensated for by the higher anaerobic energy

contribution observed during the RS trial. As a result, the net

energy expenditure was equivalent. Mean anaerobic energy

contribution was comparable between the RS and HI trials and

was significantly higher than the MC trial ( P  0.001). In

addition, the net energy expenditure for the HI trial was more

than double that of the RS and MC trials.

Mechanical Power During the Three Exercise Trials

Figure 1, top right , illustrates the estimated mean power

developed during RS, MC, and HI trials. Mean estimated

power during RS was almost four times higher than the power

developed during the MC trial and nearly three times higher

than the power developed during the HI trial (11.4  0.2 vs.

3.1  0.1 and 4.6  0.1 W/kg; P  0.001). Power during the

HI trial was also higher than during the MC trial ( P 

Parasympathetic Reactivation After the Three

Exercise Trials

The time course of the R-R intervals after each exercise trial

is illustrated in Fig. 2, and the HRR and HRV indexes are pre-

sented in Table 2. HRR60s, T30, SDNN5–10min, pNN505–10min,

RMSSD5–10min, lnHF5–10min, HFnu5–10min, and HR5–10min were

comparable across the RS and HI trials but were significantly

lower than those shown in the MC trial ( P  0.001); no

difference was observed across trials for HRamp. HRR was

shorter after the MC exercise than after the RS trial ( P 

0.001), and both were shorter than that shown after the HI trial

( P  0.001). Correlation coefficients of the regression line for

T30 were 0.99  0.01 for the three exercise trials. A significant

time-by-exercise trial interaction was observed for RMSSD30s

during the 10-min period after MC; however, post hoc analysis

revealed that RMSSD30s remained constant and similar for the

RS and HI trials (Fig. 3). Concerning HRR indexes, simple

linear regression analyses demonstrated that the relationship

was stronger between HRR60s and T30 ( r  0.84, P  0.001)

than between HRR60s and HRR ( r  0.68, P  0.001) or

between T30 and HRR ( r  0.66, P  0.001). Relationships

between HRR indexes and resting HRV indexes were all

significant and moderate to strong (0.53  r  0.81). However,

correlation coefficient values were higher for short-term than

for long-term indexes (T30 vs. lnHF5–10min: r  0.81, P 

0.001; T30 vs. lnHF5–10min : r  0.75, P  0.001; whereas

HRR vs. lnHF5–10min : r  0.53, P  0.001).

Relationship Between Parasympathetic Reactivation Indexes

and Exercise Characteristics

Results from multiple linear regressions between HR-

derived parasympathetic indexes and exercises characteristics

are presented in Table 3. Only anaerobic process contribution

Table 1. Energy system contributions of the

three exercise trials

RS MC HI

Cumulated O 2 uptake, ml/kg 254.78.8 276.79.1* 563.814.8† O 2 stores, ml/kg 2.30.0 2.30.0 2.30. [La]b , mmol/l 10.90.6 3.50.2 11.60.5† [La]b O 2 equivalent, ml/kg 29.61.7 7.40.7* 31.91.6† PCr O 2 equivalent, ml/kg 15.20.2 15.20.2 15.20. %Aerobic energy contribution 85.20.7 92.40.3* 97.30.4† %Anaerobic energy contribution 14.80.7 7.60.3 2.70.4*†

Values are means  SE. Estimated oxygen stores indicate myoglobin content. [La]b , blood lactate concentration; PCr, phosphocreatine; RS, repeated sprint exercise trial; MC, moderate continuous exercise trial; HI, high-intensity exercise running trial. *Significant difference vs. RS ( P  0.001). †Significant difference between HI and MC ( P  0.001).

H136 PARASYMPATHETIC REACTIVATION AFTER SPRINTING

was significantly related to vagal-restoration indexes. Figure 4

presents the simple linear relationships between the T30 and

O 2 equivalent for the anaerobic energy contribution ( r  0.83,

P  0.001).

DISCUSSION

The aims of this study were to examine the time course of

the parasympathetic reactivation using indexes of HRV after

repeated sprint running and to quantify the postexercise auto-

nomic regulation response in relation to exercise bouts of equal

net energy expenditure, mean (aerobic) exercise intensity, mus-

cular power, and anaerobic process participation. Results revealed

that, compared with the MC trial of a similar energy expenditure,

parasympathetic reactivation during the first 10 min of recovery

was significantly more delayed after the RS exercise. Second,

most of the vagal HR-derived indexes were similar after RS

running than with the HI running bout of similar anaerobic energy

release and double the energy expenditure. Thus we present novel

data to suggest that anaerobic contribution and other factors

associated with a high level of fast-twitch fiber recruitment (i.e.,

central stress command, catecholamine and sympathetic cotrans-

mitter release, and lactate and H^ accumulation), rather than

mean aerobic power or net energy expenditure, are of primary

importance in determining the level of parasympathetic reactiva-

tion after repeated sprint running.

Postexercise Parasympathetic Reactivation After RS Exercise

Parasympathetic reactivation, i.e., the time course of

RMSSD30s, was highly impaired after the RS trial, so that the

Fig. 1. Mean  SE net exercise energy ex- penditure (NEE), mean power, net O 2 cost, O 2 equivalent of net anaerobic energy cost, and parasympathetic reactivation indexes [number of heart beats recovered in 60 s after exercise cessation (HRR60s ) and high fre- quency (HF) power or R-R intervals] for each of the 3 exercise trials: repeated sprinting (RS), moderate continuous running (MC), and high-intensity running (HI) exercise. bpm, Beats/min. *Significant difference vs. RS ( P  0.001). †Significant difference be- tween HI and MC ( P  0.001).

Fig. 2. Mean  SE R-R intervals during recovery from 3 different exercise trials: RS, MC, and HI exercise (HI). The R-R interval was calculated as the mean R-R intervals over the 5-s segment of interest. For the sake of clarity, symbols indicating significant differences vs. RS have not been added.

PARASYMPATHETIC REACTIVATION AFTER SPRINTING H

levels (35) but not by cardiac postganglionic sympathetic nerve

stimulation (36). In contrast, elevated cardiac sympathetic

nerve activity can augment the dynamic HR response to vagal

nerve stimulation via activation of the postjunctional -adren-

ergic cascade (30, 32). Unfortunately, in the present study, we

did not measure any objective indexes of muscular power

engagement (i.e., EMG measurement) or system stress (i.e.,

sympathetic muscle nerve activity, hormones, and muscle me-

tabolite sampling) to assess objectively the level of contribu-

tion this may have had on HRV markers. Nevertheless, because

high plasma norepinephrine levels have been repeatedly ob-

served after high-intensity or sprint exercise (5, 40, 41), we put

forth that the poor parasympathetic reactivation level observed

after RS and HI exercise in the present study might be partly

attributed to high sympathetic activity and associated metabo-

lite persistence. Additionally, the potential presence of postex-

ercise hypotension after acute exercise could have stimulated

the arterial baroreflex, elevating sympathetic outflow and de-

laying the restoration of vagal tone. Changes in plasma volume

have been reported to alter cardiac autonomic balance (48), and

the occurrence of a plasma volume shift during the exercise

trials in the present study could have altered the parasympa-

thetic reactivation indexes.

Effect of Net Energy Expenditure on

Parasympathetic Reactivation

All HR vagal-related indexes were different between the RS

and MC trials, whereas these two exercises were equivalent

with respect to their net energy expenditure. Moreover, a

doubling of the net energy expenditure while a similar level of

anaerobic energy contribution was maintained (RS vs. HI) was

not associated with any further lowering of most indexes of

parasympathetic reactivation (9 of the 10 indexes considered;

Table 2). We also cannot exclude the possibility that our

10-min postexercise recording duration may have been too

short to reveal differences between RS and HI in stationary

HRV indexes. Nevertheless, these findings conform with the

studies of Parekh and Lee (39) and Mourot et al. (38), which

have shown that the total work or energy expenditure is not the

main factor influencing parasympathetic reactivation after ex-

ercise. It should be noted, however, that HRR was signifi-

cantly different between the RS and the HI trials, whereas

HRR60s and T30 were not significantly different. These differ-

ences, together with the moderate correlation coefficients that

we found between short-term recovery indexes (HRR60s and

T30) and HRR, confirm previous investigations that have

shown that HRR, in contrast to T30 or HRR60s, is influenced

by additional factor(s) and not only vagal modulation (29,

When the effects of parasympathetic vs. complete auto-

nomic blockade on T30 and HRR were compared, Imai et al.

(29) found that T30 was primary mediated by vagal activity,

whereas HRR explained not only the prompt parasympathetic

reactivation (rapid initial decrease in HR) but also the level of

sympathetic activity (slow second decrease). Perini et al. (41)

found that, in the absence of autonomic control in heart-

transplanted recipients, the HR decrease began only after 50 s

(which corresponds to the slow second phase) and was related

to plasma norepinephrine clearance. Thus the present differ-

ences shown between our RS and HI trials suggest that HI

exercise might be associated with a higher persistence of

postexercise sympathetic activity compared with that shown

with RS exercise, despite a similar time course of vagal activity

restoration (similar HRR60s and T30). This possible higher

norepinephrine plasma concentration after the HI vs. the RS

trial could in part be attributed to differences in exercise bout

duration between the two exercises, as sprint times during the

RS trial were almost 10-fold shorter than the intermittent runs

during the HI trial. Exercise bout duration has been shown to

Fig. 4. Relationship between time constant of short-time heart rate recovery (T30; see MATERIALS AND METHODS ) and oxygen equivalent of the net anaerobic energy cost of each of 3 exercise trials. Dotted lines represent 95% confidence intervals.

Table 3. Relationships between postexercise parasympathetic reactivation indexes and mechanical

and metabolic exercise characteristics

Constant Aerobic Contribution Anaerobic Contribution NEE Muscular Power

Overall Relationship

P P P P P r^2 P

HHR60s 74.454.92 0.001 0.010.01 0.97 0.430.22 0.05 0.080.07 0.27 0.830.61 0.19 0.60 0. T30 22.4831.16 0.48 0.030.15 0.86 2.991.33 0.03 0.620.44 0.17 9.123.78 0.02 0.73 0. HRR 8.5911.97 0.48 0.080.06 0.19 1.160.52 0.03 0.10.17 0.96 0.851.47 0.57 0.57 0. HR5–10min 68.436.87 0.001 0.040.03 0.26 0.630.29 0.03 0.010.09 0.89 0.580.83 0.49 0.55 0. RMSSD5–10min 29.644.21 0.001 0.010.02 0.73 0.120.18 0.49 0.060.06 0.2 0.890.50 0.09 0.47 0. InHF5–10min 7.880.74 0.001 0.010.01 0.49 0.040.03 0.24 0.010.01 0.22 0.230.09 0.06 0.65 0.

-Coefficient values are means  SE. NEE, net exercise energy expenditure. P values were from multiple linear regressions.

PARASYMPATHETIC REACTIVATION AFTER SPRINTING H

be essential in determining the level of muscle deoxygenation

and consequently the level of anaerobic participation and

plasma catecholamine accumulation (12).

Implications for the Clinical Use of RS Training

Although evaluation of the influence that RS exercise has on

autonomic function is crucial in sedentary individuals and

patients, we intentionally recruited moderately trained subjects

for the present study because we expected that they would

likely be able to cope better with this innovative experimenta-

tion. Trained subjects often display high HRR indexes (7), so

the present results should be viewed with caution when infer-

ence is made as to what might occur in a sedentary subject.

Whether individuals with low-activity levels show a similar

response to RS exercise needs to be confirmed.

In summary, the present study has shown that short-term

parasympathetic reactivation is impaired after repeated sprint

running and that anaerobic contribution rather than muscular

engagement and net (aerobic) energy expenditure appears to be

of primary importance in determining the level of parasympa-

thetic reactivation. This finding may be of particular impor-

tance for clinicians wishing to prescribe sprint training to

clinical populations. Longitudinal studies that examine the

effect of long-term repeated sprint training on autonomic

control of the heart, parasympathetic reactivation, and cardio-

vascular risk prognostic are warranted.

ACKNOWLEDGMENTS

The authors thank the subjects for participation in the study, as well as Daniel Mercier and Irmant Cadjjiov for helpful comments during the prepa- ration of this manuscript.

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