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Braz J Med Biol Res 35(6) 2002

Heart rate variability and cardiorespiratory responses in healthy menBrazilian Journal of Medical and Biological Research (2002) 35: 741-752ISSN 0100-879X

Effects of aerobic exercise trainingon heart rate variability duringwakefulness and sleep andcardiorespiratory responses ofyoung and middle-aged healthy men

1Laboratório de Fisioterapia Cardiovascular, Departamento de Fisioterapia, and2Departamento de Estatística, Universidade Federal de São Carlos,São Carlos, SP, Brasil3Departamento de Fisiologia e Biofísica, Instituto de Biologia,Universidade Estadual de Campinas, Campinas, SP, Brasil4Laboratório de Fisiologia do Exercício, Faculdade de Educação Física,Universidade Estadual de Campinas, Campinas, SP, Brasil5Divisão de Cardiologia, Departamento de Clínica Médica,Hospital das Clínicas, Faculdade de Medicina de Ribeirão Preto,Universidade de São Paulo, Ribeirão Preto, SP, Brasil

A.M. Catai1,3,M.P.T. Chacon-Mikahil3,4,

F.S. Martinelli3,4,V.A.M. Forti4, E. Silva1,

R. Golfetti4, L.E.B. Martins4,J.S. Szrajer4, J.S. Wanderley4,E.C. Lima-Filho4, L.A. Milan2,

J.A. Marin-Neto5,B.C. Maciel5

and L. Gallo-Junior5

Abstract

The purpose of the present study was to evaluate the effects of aerobicphysical training (APT) on heart rate variability (HRV) and cardiores-piratory responses at peak condition and ventilatory anaerobic thresh-old. Ten young (Y: median = 21 years) and seven middle-aged (MA =53 years) healthy sedentary men were studied. Dynamic exercise testswere performed on a cycloergometer using a continuous ramp proto-col (12 to 20 W/min) until exhaustion. A dynamic 24-h electrocardio-gram was analyzed by time (TD) (standard deviation of mean R-Rintervals) and frequency domain (FD) methods. The power spectralcomponents were expressed as absolute (a) and normalized units (nu)at low (LF) and high (HF) frequencies and as the LF/HF ratio. Control(C) condition: HRV in TD (Y: 108, MA: 96 ms; P<0.05) and FD - LFa,HFa - was significantly higher in young (1030; 2589 ms2/Hz) than inmiddle-aged men (357; 342 ms2/Hz) only during sleep (P<0.05); post-training effects: resting bradycardia (P<0.05) in the awake conditionin both groups; V

.O2 increased for both groups at anaerobic threshold

(P<0.05), and at peak condition only in young men; HRV in TD andFD (a and nu) was not significantly changed by training in eithergroups. The vagal predominance during sleep is reduced with aging.The resting bradycardia induced by short-term APT in both age groupssuggests that this adaptation is much more related to intrinsic alter-ations in sinus node than in efferent vagal-sympathetic modulation.Furthermore, the greater alterations in V

. O2 than in HRV may be related

to short-term APT.

CorrespondenceA.M. Catai

Laboratório de Fisioterapia

Cardiovascular - Núcleo de

Pesquisa em Exercício Físico,

Departamento de Fisioterapia,

UFSCar

Rodovia Washington Luís, km 235

13565-905 São Carlos, SP

Brasil

E-mail: mcatai@power.ufscar.br

Research supported by CAPES,

FAPESP (No. 91/4754-9), CNPq (No.

300528/85-0), and FAEP-UNICAMP.

Received July 17, 2001

Accepted April 1, 2002

Key words• Heart rate variability• Power spectral density

analysis• Anaerobic threshold• Aerobic exercise training• Autonomic nervous system

and aging processes in man

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Introduction

Heart rate variability (HRV) is mainlycaused by efferent autonomic modulation ofthe sinus node. For many years this variablehas been expressed only as mean values andstandard deviations, i.e., a measure in thetime domain representation. However, a non-invasive contribution by each division ofautonomic modulation to HRV is possiblewhen this variable is represented in its fre-quency domain, i.e., the power spectral den-sity analysis. Today, it is well accepted thatunder specific experimental conditions thepower spectrum is a tool of great value forassessing the neural mechanisms controllingheart rate (HR) (1).

Analysis of HRV in the frequency do-main obtained from mathematical process-ing of the R-R intervals in the electrocardio-gram recordings obtained under resting con-ditions can discriminate two main spectralcomponents: a high frequency one (rangingfrom 0.15 to 0.40 Hz) and a low frequencyone (ranging from 0.04 to 0.15 Hz), consid-ered to be markers of parasympathetic andsympathetic control, respectively (1,2). How-ever, Skyschally et al. (3) have suggestedthat low frequency is influenced by bothvagal and sympathetic activity.

Measurement of HRV may be useful as anoninvasive method to assess in man theautonomic nervous system modulation un-der several physiological conditions such asawake and sleeping situations, different bodypositions, physical training, and also in patho-logical conditions (1,4-6). Thus, the HRVexpressed both in the time and frequencydomains is reduced with age (4,7) due to thedominance of the sympathetic over the para-sympathetic balance in this particular condi-tion (4,7). This observation is relevant sincethe reduction of HRV with aging is related tohigher cardiovascular morbidity and mortal-ity rates (7,8).

There are conflicting reports in the litera-ture concerning the effects of aerobic train-

ing on HRV under resting conditions. Whilesome studies have reported an increase inthe magnitude of this variable in the timedomain (9), in the frequency domain othershave reported absence of modifications (10),and an increase (11) or decrease (12) ofsympathovagal balance in the sinus node.

The effect of age on physical workingcapacity has also been the subject of manystudies (13,14) that have shown that maxi-mal aerobic capacity, measured as V

. O2 max,

reaches a maximum value around the age of30 years and decreases progressively there-after. Concerning V

. O2 at the anaerobic thresh-

old, the literature has also shown a decline ofthis parameter with advancing age (13) andthere are studies indicating the occurrence ofsignificant changes in aerobic capacity andautonomic changes in HR after aerobic train-ing in middle-aged subjects (15,16).

On the basis of these considerations, thepurpose of the present study was to evaluatethe effects of 3-month aerobic physical train-ing on the efferent autonomic cardiac con-trol that modulates the HR response at rest inawake and sleeping conditions and on theoxygen uptake at ventilatory anaerobicthreshold and peak conditions during dy-namic exercise in young and middle-agedmen.

Material and Methods

Subjects

Seventeen men volunteered to take partin this study. All of them were in good healthbased on clinical and physical examination,and laboratory tests that included a standardelectrocardiogram (ECG), maximum exer-cise test (protocol I), chest X-rays, total bloodcount, urinalysis and clinical biochemicalscreen tests [glycose, uric acid, total choles-terol and fractions (LDL, HDL and VLDL),and triglycerides]. All subjects had seden-tary life-styles and most of them participatedonly eventually in weekend sport activities.

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Heart rate variability and cardiorespiratory responses in healthy men

None of the subjects studied was taking anytype of medication. Two different age groupswere compared: young group (N = 10), agerange of 19 to 29 years (median = 21), andmiddle-aged group (N = 7), age range of 50to 59 years (median = 53). The subjects wereinformed about the experimental proceduresand all signed an informed consent form toparticipate in the present study, which wasapproved by the Ethics Committee of theState University of Campinas. All individu-als were evaluated during the same time ofday at an experimental room temperature of23ºC and relative air humidity between 50and 60%. Before the day of the experimentthe subjects were taken to the experimentalroom for familiarization with the proceduresand the equipment to be used. Each subjecthad been oriented to avoid caffeinated andalcoholic beverages, to refrain from smok-ing and not to perform moderate or heavyexercise on the day before the application ofprotocols I and II or during the 24-h periodfor the Holter test. On each experimentalday, before conducting the programmed pro-tocols, the volunteers were interviewed andexamined to confirm the state of good health,the occurrence of a normal night sleep, andto confirm that the control conditions (HRand systemic blood pressure) were in thenormal range.

Protocols

Protocol I. All subjects were studied inthe resting condition (supine and seated) andduring two dynamic exercise tests in theseated position on a cycloergometer, using acontinuous protocol on different days sepa-rated by a 2-7-day interval, as follows:

a) Clinical and diagnostic evaluation. Themain purpose of this procedure was to in-clude in the study only healthy men, exclud-ing any subject with evidence of silent is-chemic heart disease or other pathologicabnormalities of the cardiovascular system.A 12-lead standard ECG recording was ob-

tained at rest in the supine position. Theexercise protocol consisted of 3-min steppower increments of 25 W, with a rotationfrequency of 60 rpm maintained throughoutthe test. The exercise tests ended when thesubjects presented one or more of the fol-lowing conditions: 1) clear evidence of physi-cal exhaustion, 2) reaching the age-predictedmaximal HR, and 3) inability to maintain astandard cycling frequency due to muscularfatigue. During the protocol the subjects weremonitored using the thoracic CM5 lead. AnECG tracing (CM5, aVF and V2) was ob-tained during the last 10 s of each powerlevel. Arterial pressure was measured by theauscultatory method using a mercury sphyg-momanometer during the last 15 s of eachpower level.

b) Functional capacity evaluation: oxy-gen uptake test. The subjects performed anoxygen uptake test using a progressive incre-mental exercise protocol. This protocol con-sisted of a 3-min warm-up at 4 W followedby a continuous power increase set at a valueof 12 to 20 W up to physical exhaustion. Thechoice of the power value increment foreach subject, i.e., 12, 15, 17 or 20 W/min,was based on the responses presented in theprevious clinical test described above (pro-tocol I-a). A braked electromagnetic cyclo-ergometer equipped with a microprocessor(model Corival 400, Quinton, Seattle, WA,USA) allowed the precise application of in-dividualized power ramp values. At the peakof effort each subject attributed a rating ofperceived exertion based on Borg’s scale(17), that varied from 0 to 10 units.

During the exercise test the subjectsbreathed through a low-resistance valve(Hans Rudolph 2900 device, Kansas City,MO, USA) with a small dead space, and themetabolic and ventilatory variables and pa-rameters were calculated using a specificmetabolic analyzer (MMC Horizon System,Sensormedics, Yorba Linda, CA, USA) thatprovided average values at 15-s intervals.The individual values of minute ventilation

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A.M. Catai et al.

(V. ), CO2 production (V

. CO2) and oxygen

uptake (V. O2) at each power were plotted

as a function of time; V. , V

.CO2 and V

. O2

peaks were selected as the highest valuesreached during the incremental exercise pro-tocol.

In all subjects, anaerobic threshold (inV. O2) was measured when the V

. and V

. CO2

began to increase non-linearly as comparedto V

. O2 (18). This was determined by visual

analysis of V., V

. O2 and V

. CO2 curve re-

sponses. Three different observers measuredthe anaerobic threshold values (in V

. O2) in

all exercise tests. Using this procedure,anaerobic threshold (in V

. O2) could be meas-

ured with a difference of about 2%. In thepresent study anaerobic threshold was ex-pressed as absolute (ml/min) and normalizedvalues, i.e., corrected for body weight (mlkg-1 min-1) and as percentage of peak V

. O2.

Absolute HR values at anaerobic thresh-olds and under peak conditions were ob-tained with an ECG recording system(Funbec, São Paulo, SP, Brazil). The signalswere recorded in real time after analog todigital conversion and the R-R intervals (pe-riods expressed in milliseconds betweenR-R peak waves of ECG signal) were calcu-lated on a beat-to-beat basis using a specificsoftware (19). The HR values are reported asaverages at 10-s intervals.

Protocol II: 24-h Holter electrocardio-gram. At least 48 h after the previous test (I-b), the subjects were submitted to a 24-hHolter recording. The main purpose of thistest was to assess the contribution of theautonomic nervous system to the control ofHR before and after physical training, bymeasuring HRV using time and frequencydomain methods. ECG signals (leads CM2and CM5) were recorded using a 24-h Holtertape recorder (Del Mar Avionics, Irvine,CA, USA).

At the beginning of the Holter recording,the volunteers were asked to rest in the su-pine position for 60 min. After this time, theywere instructed on how to proceed through-

out the recording period. After a 24-h re-cording, the volunteers returned to the labo-ratory to finish the procedure.

The reading and analysis of the ECGrecording were done using a Holter Manage-ment System (model 750 A Innovator, DelMar Avionics). A complete automated 24-hreport and a visual inspection by the re-searcher were performed to make sure thatthe cardiac rhythm was sinusal and that therewas no abnormality in atrioventricular elec-trical conduction. Then, the average HR andR-R interval, with the respective standarddeviations (time domain), were measuredunder awake (initial 60 min - 2:00-3:00 pm)and sleeping conditions (central 6 h - i.e.,without the first and last sleep hours - 0:00-6:00 am). Following the next step of analy-sis, the highest stationary sections of R-Rintervals on the monitor display were se-lected for analysis of HRV as a criterionrequired for correct application of frequencydomain analysis, i.e., fast Fourier transform(1).

The data of R-R intervals during a periodof resting in the supine position in the awake(2:00-3:00 pm) and sleeping states (0:00-6:00 am) were analyzed in short-term re-cordings which included four consecutivenonoverlapping windows of 256 s each. Thedata of R-R intervals during the sleep periodwere analyzed after an initial sleeping timeof approximately 160 min for the younggroup and 180 min for the middle-aged group.

The selected time domain parametersstudied were the mean R-R interval and thecorresponding standard deviation. For fre-quency domain analysis, the power spectralcomponents are reported at low (0.04 to 0.15Hz) and high (0.15 to 0.4 Hz) frequenciesobtained using the fast Fourier transform inabsolute and normalized units. The low/highfrequency ratio of absolute power was alsomeasured (5,20). The absolute low and highfrequencies are reported as ms2/Hz whilenormalized units were computed by dividingthe absolute power of a given low or high

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Heart rate variability and cardiorespiratory responses in healthy men

frequency component by the total power,after subtracting from it the power of thecomponent with a range frequency between0 and 0.03 Hz, i.e., very low frequency, andmultiplying this ratio by 100 (1,20).

Protocol III: aerobic exercise training.The program was conducted for 3 months ona field track and included stretching for 10min followed by walking and/or jogging for40 min, three times a week at a prescribedHR that corresponded to 70 to 85% of peakHR obtained during a continuous dynamicexercise test performed in a laboratory envi-ronment (protocol I-b: functional capacityevaluation). This intensity training rangewas also based on metabolic profile, since75% of peak HR in each volunteer corre-sponded or was very close to the HR at theanaerobic threshold obtained previously dur-ing the oxygen uptake test. Thus, in eachtraining session the subjects were submittedto progressive intensities of exercise (walk-ing and/or jogging) at HR values that werebelow, equal to and above those related toanaerobic threshold. During the exercise pro-gram the subjects used pulse monitors (mo-del Vantage XL, Polar, Port Washington,NY, USA) to ensure they were exercising atthe appropriate intensity. The aerobic train-ing intensity was adjusted during a 7-dayinterval based on rest and exercise HR meas-ured with the above specified pulse monitor,compared to the previous control period (pro-tocol I-b).

Statistical analysis

The data are reported as medians, quartiles(1st and 3rd) and minimum and maximumvalues using the Tukey box-plot. Due to non-Gaussian distribution and/or inhomogeneityof variance of variable values, nonparamet-ric tests were selected for statistical analysis.Thus, the Mann-Whitney and Wilcoxon non-parametric tests were used for intergroupand intragroup comparisons, respectively,with the level of significance set at 5%.

Results

The physical characteristics of the youngand middle-aged subjects are shown in Table1. Under control conditions, and after aero-bic training, median age, weight and bodymass index were higher in the middle-agedthan in the young group (P<0.05); only me-dian height was similar for the two groups.After aerobic training, the intragroup differ-ences in weight and body mass index werenot statistically significant.

Exercise conditions

Responses to dynamic exercise: anaero-bic threshold and peak oxygen uptake. Un-der control conditions, anaerobic thresholdand V

. O2 reported as absolute oxygen uptake

and normalized values for body weight werelower (P<0.05) in middle-aged than in youngmen (Table 2). Again, under control condi-tions the values of HR at anaerobic thresholdand peak effort, as well as power at anaero-bic threshold were significantly lower inmiddle-aged men than young men (Table 2).

After 3 months of aerobic physical train-ing the absolute and normalized values ofV. O2 at anaerobic threshold increased signifi-

cantly (P<0.05) for both groups; under peakconditions the same occurred for V

. O2 (abso-

lute) only for the young group and for thepower values for both groups. However, un-der peak conditions the inter- and intragroup

Table 1. Comparison of the anthropometric data for the subjects before (control) andafter three months of aerobic physical training (APT).

Variable Young group Middle-aged group

Age (years) 21* 52Height (cm) 174 168Weight (kg), control 67* 86Weight (kg), APT 67* 85Body mass index (kg/m2), control 22.9* 28.5Body mass index (kg/m2), APT 22.2* 28.2

Data are reported as medians. Young group, N = 10; middle-aged group, N = 7.*P<0.05 for intergroup comparisons (Mann-Whitney test).

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Holter ECG analysis: R-R interval and itsvariability in awake and sleeping conditions

Time domain index of HRV: before andafter exercise training. In the awake restingsupine position the mean R-R interval and itsstandard deviation did not differ betweengroups before or after training (Table 3). TheHR values were lower in the sleeping than inthe awake resting supine condition (the in-verse for R-R interval) for both groups(P<0.05). Aerobic physical training inducedsignificant (P<0.05) bradycardia (increasein average R-R interval) of comparable mag-nitude for both groups studied in the awakeresting supine position (Table 3).

Table 4 shows that the mean R-R intervaland standard deviation throughout the 6-hcentral sleep were significantly (P<0.05)higher in the young than in the middle-agedgroup under control conditions as well asafter physical training. The initial time ofsleep analysis for short-term time and fre-quency domains did not differ significantlybetween groups, being 159 min for the younggroup and 183 min for the middle-aged group.In relation to the effect of physical trainingon sleep, there were no statistically signifi-cant changes in average HR, average R-Rintervals or standard deviation of averageR-R intervals in either group studied.

Frequency domain index of HRV beforeand after exercise training. Tables 3 and 4show the HRV in the frequency domainexpressed as absolute values in the restingsupine position in the awake and sleepingcondition, respectively. In the awake controlcondition no statistical difference could befound in the low frequency, high frequencyor total power component between groups,as reported in absolute values. However,after aerobic physical training only the younggroup presented a significantly higher abso-lute low frequency power component com-pared to the control condition (P<0.05); in-tergroup analysis showed that in the post-training condition the young group presented

Table 2. Cardiorespiratory variables measured during dynamic exercise before (con-trol, C) and after three months of the aerobic physical training (APT).

Variable Young group Middle-aged group

C APT C APT

V. O2 AT (ml kg-1 min-1) 19*+ 22+ 13* 16

V. O2 peak (ml kg-1 min-1) 36+ 41+ 28 27

V. O2 AT (ml/min) 1292*+ 1466+ 1186* 1274

V. O2 peak (ml/min) 2630*+ 2800+ 2287 2410

HR (bpm) at AT 134+ 142+ 115 116HR (bpm) at peak 191+ 188+ 158 165Power (watts) at AT 106*+ 130+ 77 86Power (watts) at peak 213* 224 171* 183Borg’s scale 9 10 8 8.5

Data are reported as medians. Young group, N = 10; middle-aged group, N = 7. AT,anaerobic threshold; HR, heart rate.*P<0.05 for intragroup comparisons (Wilcoxon test).+P<0.05 for intergroup comparisons (Mann-Whitney test).

differences in effort perception (Borg’s scale)before and after training were not statisti-cally significant (Table 2).

Table 3. Comparison of heart rate variability during the resting supine awake condition(2:00-3:00 pm) before (control, C) and after three months of aerobic physical training(APT).

Variable Young group Middle-aged group

C APT C APT

Time span: 60 min wakeTime domain indexes

Average heart rate (bpm) 69* 60 72* 62Average R-R interval (ms) 880* 1003 845* 976Standard deviation average R-R interval (ms) 85 97 61 64

Time span: 17 min#

Time domain indexesAverage R-R interval (ms) 869* 1010 833* 1000Standard deviation average R-R interval (ms) 83 92 51 55

Frequency domain indexesLow frequency (ms2/Hz) 818* 1048+++++ 687 513High frequency (ms2/Hz) 277 429 265 253Total power (ms2/Hz) 1821 2870 2601 2942

Heart rate variability was determined using time and frequency domain methods. Dataare reported as medians. Young group, N = 10; middle-aged group, N = 7. #Fourconsecutive windows of 256 s each.*P<0.05 for intragroup comparisons (Wilcoxon test).+P<0.05 for intergroup comparisons (Mann-Whitney test).

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Heart rate variability and cardiorespiratory responses in healthy men

a significantly higher absolute low frequencypower component than the middle-aged one(P<0.05).

On the other hand, during the controlsleeping condition, the absolute high fre-quency component, an index of vagal tone,was 7.6 times higher (P<0.05) in the youngthan in the middle-aged group (median =2589 and 342 ms2/Hz, respectively). Thismagnitude decreased 2.8 times after training(P<0.05). The absolute low frequency com-ponent during sleep was significantly higher(P<0.05) in the young than in the middle-aged group only in the control condition(1030 and 357 ms2/Hz) and not in the aero-bic physical training condition (930 and 502ms2/Hz). Also, the total power was signifi-cantly greater (P<0.05) in the young than inthe middle-aged group in the control condi-tion (4862 and 1225 ms2/Hz, respectively)and in the post-training condition (3152 and1584 ms2/Hz, respectively).

The outstanding finding is that the aero-bic training did not change any frequencydomain component (absolute low and highfrequencies) when intragroup comparisonswere considered.

When the content of each frequency bandwas reported as normalized units (normal-ized high and low frequencies) and as a ratioof absolute values (low/high frequency) thedifferences were statistically significant onlyin the sleeping control condition, since nor-malized low frequency and the low/high fre-quency ratio were lower and normalized highfrequency was higher in the young than inthe middle-aged group. After aerobic train-ing the differences were also not statisticallysignificant for inter- or intragroup compari-sons (Figures 1 and 2).

Discussion

In the present study, aerobic exercisetraining caused an increase in aerobic capac-ity, i.e., oxygen uptake and transport, indi-cated by a significant increase in V

. O2-anaero-

Table 4. Comparison of heart rate variability during sleep (0:00-6:00 am), during controlconditions (C) and after three months of aerobic physical training (APT).

Variable Young group Middle-aged group

C APT C APT

Time span: 6 h sleepTime domain indexes

Average heart rate (bpm) 57* 52* 64 64Average R-R interval (ms) 1053* 1165* 940 942Standard deviation average 108* 124* 96 74R-R interval (ms)

Time span: 17 min+

Initial time of data analysis during sleep (min) 159 201 183 245Time domain indexes

Average R-R interval (ms) 1063* 1120* 930 1035Standard deviation average 70* 56* 38 47R-R interval (ms)

Frequency domain indexesLow frequency (ms2/Hz) 1030* 930 357 502High frequency (ms2/Hz) 2589* 1374* 342 488Total power (ms2/Hz) 4862* 3152* 1225 1584

Heart rate variability was measured using time and frequency domain methods. Dataare reported as medians. Young group, N = 10; middle-aged group, N = 7. +Fourconsecutive windows of 256 s each.*P<0.05 for intergroup comparisons (Mann-Whitney test).

Figure 1. Low and high frequency power spectral components in normalized units (nu),obtained during awake (A) and sleeping (B) conditions, in the young (Y) and middle-aged(MA) groups, during control (C) conditions and after aerobic physical training (APT). Data arereported as box-plots. P<0.05 obtained by the Mann-Whitney test.

Pow

er s

pect

rum

(nu

)

100

80

Y

C APTLow frequency

Y

C APTHigh frequency

C APTC APT

MA Y MA

Y MAMA

60

40

20

0

Pow

er s

pect

rum

(nu

)

100

80

60

40

20

0

B

A

C APTLow frequency

C APTHigh frequency

C APTC APT

MaximumMinimumMedian1st and 3rd quartiles

P<0.05

P<0.05

Outliers

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A.M. Catai et al.

bic threshold in both groups and in peak V. O2

for the young group only, as well as anincrease in power peak for both groups. Thisincrease in aerobic capacity has been docu-mented in other studies (10,15,16,21,22) forboth anaerobic threshold and peak V

. O2. The

reasons for the middle-aged group not toincrease the peak V

. O2 may not be due exclu-

sively to the experimental design used, i.e., alongitudinal study with short-time aerobictraining. Some possible explanations for thisdifference are: 1) anthropometric character-istics and the number of subjects studied; 2)type of experimental protocols used, i.e.,continuous exercise on a cycloergometer, inrelation to the type of exercise training, i.e.,walking and jogging on a field track. On theother hand, the perception of effort at peaklevel, evaluated with Borg’s scale (17), wasnot modified by exercise training despite theincrease in aerobic power, suggesting thatduring exercise the volunteers were pushedto their limits.

In addition, our data showed that theV.O2-anaerobic threshold when reported as

absolute and normalized (ml kg-1 min-1) val-ues proved to be more sensitive than peakV.O2 in detecting aerobic capacity changes

induced by short-term aerobic training inboth age groups. It should be emphasized

that anaerobic threshold has also the advan-tage of being a parameter measured directlyunder submaximal testing conditions inde-pendently of a required voluntary motiva-tion effort by the subjects, i.e., without theneed for vocal reinforcement by the re-searcher aiming to extend the exercise to thepower value needed to obtain the V

. O2 max

or peak V. O2 measurement (16,18).

The HR during the central 6 h of sleep inboth conditions was significantly lower inthe young than in the middle-aged group.These data agree with the study of Crasset etal. (23), which documented that the R-Rinterval did not differ between young andolder subjects during awake periods but washigher in the young than in the older subjectsduring both rapid eye movement (REM) andnon-REM sleep. Goldsmith et al. (24) havealso reported higher R-R interval values dur-ing the night in young men as an expressionof vagal predominance during sleep.

Under awake control conditions, the in-tergroup differences of HRV in both the timeand frequency domains found in our studywere not statistically significant. Neverthe-less, during the sleeping situation there weresignificant differences in parasympatheticmodulation between young and middle-agedmen. With respect to high frequency power,the higher values found in the young than inmiddle-aged group support the interpreta-tion that young men exhibit a higher para-sympathetic activity during sleep. Our re-sults were similar to those obtained by Jensen-Urstad et al. (25) who reported a higher highfrequency power value in younger than inolder subjects during sleep. Crasset et al.(23) also reported that R-R variability washigher in the young subjects than in oldervolunteers during the awake and sleeping con-ditions both in the REM and non-REM stages.

As a whole, the above findings of an age-dependent difference in R-R intervals and HRVduring the sleep condition indicate that theoccurrence of vagal predominance in this physi-ological condition is decreased by aging.

Figure 2. Ratio of the low versus high frequency power spectral components (LF/HF ratio),obtained during awake (A) and sleeping (B) conditions, in the young (Y) and middle-aged(MA) groups, during control (C) conditions and after aerobic physical training (APT). Data arereported as box-plots. P<0.05 obtained by the Mann-Whitney test.

MaximumMinimum

Median1st and 3rd quartiles

LF/H

F ra

tio

14

12

10

8

6

4

2

0

-2 C APTAwake

C APTSleeping

C APTC APTOutliers

P<0.05

Y YMA MA

BA

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Heart rate variability and cardiorespiratory responses in healthy men

It should be emphasized that the decreasein vagal tonus in the sinus node has also beenreported in pathological conditions such asmyocardial infarction, and is associated withan increased risk of new cardiac events andsudden death (8). However, it is not known ifthe age-dependent decrease in vagal tonushas the same risk effect on the heart ofhealthy middle-aged men, as documented inthe present study.

A limitation of our study was that the 24-h ECG recording was not accompanied bypolysomnographic sleep recording. Despitethis, the established criterion was to analyzeintervals with the highest stationary periodsof ECG recording during sleep since thiscondition most likely occurs in the non-REM stages - when there is a shift of cardiacsympathovagal balance, with a correspond-ing increase in parasympathetic over sympa-thetic stimulation in the sinus node (23,26,27).

However, it should be emphasized thatsleep is a peculiar physiological conditionand the mechanisms controlling the highfrequency component of R-R variability areunclear. The literature reports that the highfrequency component is mediated not onlyby direct modulation of vagal efferent activ-ity, resulting from baroreceptor responsesconveyed to respiratory and blood pressurecenters in the central nervous system (28),but also by mechanical effects on the sinusnode related to phasic changes in venousreturn caused by respiratory movement (29).

In spite of these considerations, the re-duction of HRV with age in man has beenwell documented in the literature (4,7,25).However, the mechanisms responsible forthis physiological response are unknown.Byrne et al. (4) suggested that age per se, andnot the reduction in aerobic capacity or theincrease in fat usually associated with theaging process, plays the major role in de-creasing HRV in older subjects. Also, it hasbeen shown that the decline in HRV withaging is mainly, but not exclusively, due to a

decline in parasympathetic tonus (23,30).Concerning the effects of aerobic train-

ing on HRV, several studies have foundHRV modifications in this physiological con-dition (7,15,24,31). Particularly important isthe investigation conducted by Goldsmith etal. (24) who studied and compared 24-hHRV in aerobically trained and untrainedhealthy young men and observed that para-sympathetic activity is substantially greaterin trained than in untrained men, during bothwaking and sleeping hours.

In the present study, although severalsignificant cardiorespiratory adaptations re-lated to oxygen uptake were induced bydynamic training in both groups, they werenot accompanied by significant changes inresting HR and HRV (time and frequencydomains) during the sleeping condition. How-ever, in the awake condition a resting brady-cardia was observed after training in bothgroups studied, without concomitant changesin time or frequency domain HRV. So, theresting bradycardia observed in this studywas not accompanied by an increase of thehigh frequency component, suggesting a non-significant participation of vagal modulationin this adaptive response. In this regard, ourresults are similar to those of Boutcher andStein (10) who reported significant increasesin both absolute and relative peak V

. O2 asso-

ciated with a corresponding decrease in rest-ing HR, without an increase in HRV (analy-sis in time and frequency domains in a middle-aged group (45 years) after aerobic training).In contrast, another study (31) on older awakesubjects (67 ± 5.1 years) observed an in-crease in HRV in both the time and fre-quency domain components (very low fre-quency and low frequency) after 6-monthaerobic training or even that exercise train-ing may increase parasympathetic activitythroughout the day (24). Moreover, Stein etal. (15), studying the effect of 12-monthsupervised aerobic training on cardiac auto-nomic modulation in healthy older adults(66 ± 4 years), found an increase in total

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HRV and a reduction in nocturnal HR. Also,the same investigators have shown that asustained increase in HRV lasted over a one-year period for those who maintained a steadytraining level.

Thus, the studies discussed above sup-port the fact that in short-term aerobic physi-cal training different mechanisms may beresponsible for the resting bradycardia in-duced by aerobic training. It should be men-tioned that this adaptation is a well-docu-mented response reported for both man(16,25,32) and other species (33).

The resting HR is modulated by a bal-ance between sympathetic and parasympa-thetic tone with a predominance of the latter(16,34). On this basis, some reports state thatan increased vagal tonus is the main mech-anism for the bradycardia induced by aero-bic physical training (35). Goldsmith et al.(24) reported that the bradycardia exhibitedby endurance-trained individuals is attrib-uted, at least in part, to greater parasympa-thetic activity. However, several other stud-ies have failed to demonstrate differences invagal tone between trained and untrainedsubjects (6,32,36,37). Yet, others have indi-cated a decrease in sympathetic activity inthe sinus node (38) or both an increase invagal activity and a decrease in sympatheticactivity (39). On the other hand, studies onanimals (33) and on humans (6,32,36,40)have suggested that this bradycardia is mainlydue to a reduction in intrinsic HR.

Within this context, our data suggest that,at least in men, resting bradycardia inducedby short-term aerobic training seems to bemediated by adaptations much more relatedto intrinsic alterations in the sinus node thanto changes in efferent vagal-sympatheticmodulation of the sinus node, because theresting bradycardia observed was not ac-companied by an increase of the high fre-quency component and/or a decrease of thelow frequency component that would ex-press a higher vagal modulation and/or a lowsympathetic modulation of this structure.

Our findings are consistent with previousstudies conducted on animals (33) and mainlyon humans (6,32,36,37,40) under carefullydesigned protocols using less invasive ornoninvasive procedures associated with bet-ter quantitative methods. Nevertheless,Negrão et al. (33) did not exclude the possi-bility of a decreased resting firing rate of thevagus after training when they observed im-pairment of vagal function evaluated by re-flex bradycardia and electrical vagal stimu-lation.

The absence of significant changes in HRVassociated with an increase in aerobic capacityinduced by aerobic training, documented inthe present study, may be related to the factthat the experimental design was directed toevaluate the cardiorespiratory adaptation inshort-term training. Our data support the re-sults of other studies that documented no HRVchange after aerobic exercise training in young(40) and middle-aged men (10).

The results of the present investigationindicate that the vagal predominance duringsleep in men is reduced with age. Again, theresting bradycardia induced by short-term aero-bic training in both young and middle-agedmen is much more related to intrinsic alter-ations in the sinus node than to changes inefferent vagal-sympathetic modulation. Fur-thermore, the greater alterations in aerobiccapacity than in HRV in both groups may berelated to the magnitude of different time-dependent responses of each cardiorespira-tory variable induced by the training stimulus.

Acknowledgments

The authors are grateful to Prof. Dr.Eduardo Arantes Nogueira, Disciplina deCardiologia and to the Departamento deClínica Médica, Faculdade de CiênciasMédicas, Universidade Estadual de Campi-nas (UNICAMP), where the clinical exami-nation and biochemical tests were performed.We are also indebted to Ricardo Vigatto forhelp with the preparation of the manuscript.

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Heart rate variability and cardiorespiratory responses in healthy men

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