Journal of Strength and Conditioning Research Publish Ahead of Print

DOI: 10.1519/JSC.0000000000002372

TITLE PAGE

Acute effect of aerobic and strength exercise on heart rate variability and baroreflex

sensitivity in men with autonomic dysfunction

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Running title: Post-exercise recovery and autonomic dysfunction

Tainah de Paula1,2, Mario Fritsch Neves1,3, Alex da Silva Itaborahy1, Walace Monteiro2,4, Paulo

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Farinatti2,4,5, and Felipe A. Cunha2,5,6

1) Post-Graduate Program in Medical Sciences, Faculty of Medical Sciences, University of Rio de Janeiro

State, Rio de Janeiro, Brazil

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2) Laboratory of Physical Activity and Health Promotion, University of Rio de Janeiro State, Rio de

Janeiro, Brazil.

3) Department of Clinical Medicine, University of Rio de Janeiro State, Rio de Janeiro, Brazil.
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4) Post-Graduate Program in Physical Activity Sciences, Salgado de Oliveira University, Niterói, Rio de

Janeiro, Brazil.
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5) Post-Graduate Program in Exercise Science and Sports, University of Rio de Janeiro State, Rio de
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Janeiro, Brazil.

6) Post-Graduate Program in Rehabilitation Sciences, Augusto Motta University Center (UNISUAM),

Rio de Janeiro, Brazil.

Address for correspondence: Felipe Amorim da Cunha, PhD. Institute of Physical Education and

Sports, Laboratory of Physical Activity and Health Promotion, University of Rio de Janeiro State. Rua

São Francisco Xavier 524 / sala 8121F - Maracanã, Rio de Janeiro, RJ, Brazil. CEP: 20550-013; Phone:

(21) 2334-0775. E-mail: felipeac@globo.com

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ABSTRACT

The extent to which post-exercise cardiac autonomic control depends on exercise modality remains

unclear, particularly among individuals with autonomic dysfunction (CAdysf). This study compared heart

rate variability (HRV) and baroreflex sensitivity (BRS) responses to acute aerobic (AE) and strength

exercise (SE) in men with CAdysf. Twenty men were assigned into control (n=10: 33.8±3.0 yr; 23.7±1.5

kg/m2) and CAdysf (n=10: 36.2±9.8 yr; 28.4±2.6 kg/m2) groups. CAdysf underwent AE, SE, and a non-

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exercise control day (CTL) in a randomized, counter-balanced order. HRV and BRS were assessed in a

supine position during 25-min of recovery after AE, SE, and CTL. Both HRV indices [P < 0.05; Effect

size (Cohen's d): > 1.4] and BRS at rest were significantly lower in CAdysf than controls [P < 0.01;

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Effect size (Cohen's d): ≥ 1.36]. In CAdysf, post-exercise increases in heart rate, sympathetic activity

(low-frequency band, LF), and sympathovagal balance (LF:HF ratio), as well as decreases in R-R

interval, parasympathetic activity (high-frequency band, HF), and BRS were observed in AE [P < 0.05;
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Effect size (Cohen's d): ≥ 1.31] and SE [P < 0.05; Effect size (Cohen's d): ≥ 0.79] vs. CTL, but changes

were larger after AE than SE [P < 0.05; Effect size (Cohen's d): ≥ 0.73]. In conclusion, both AE and SE

elicited post-exercise changes in HRV and BRS among CAdysf men, primarily reflected by lowered

vagal modulation, increased sympathovagal balance, and a delayed BRS recovery pattern. However,

those changes seem to be more likely to occur after AE than SE.

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Keywords: blood pressure; prehypertension; sympathovagal balance; physical activity; fitness; health.
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INTRODUCTION

The autonomic nervous system (ANS) plays a key role in maintaining homeostasis under normal and

pathological conditions. Cardiac autonomic imbalance and baroreflex dysfunction are implicated in blood

pressure (BP) increase and cardiovascular disease (1). Greater sympathetic drive is often observed before

diagnosis in prehypertensive individuals (2, 3), who are usually overweight and sedentary (4). On the

other hand, there is a growing body of empirical evidence supporting that exercise capacity (or

cardiorespiratory fitness) is strongly associated with indirect measures of cardiac vagal activity (5),

thereby having a positive effect on cardiac autonomic status (6). Taking into account that heart rate (HR)

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recovery after cessation of exhaustive exercise serves as a robust index of individual ability to recruit

vagal tone (5), the recovery pattern of cardiac autonomic control from acute aerobic exercise (AE) and

strength exercise (SE) may provide useful information of risks and benefits of those exercise modalities.

In this context, heart rate variability (HRV) has emerged as a noninvasive physiological marker for

evaluating the modulation of cardiac autonomic nervous system (ANS) activity, which reflects beat-to-

beat changes in HR, expressing the sympathovagal interaction obtained from the variation of both

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instantaneous HR and R-R intervals within the cardiac cycle (7). Lower variance in HRV might be

explained by either lower parasympathetic or higher sympathetic activity, and has been associated with

the development of hypertension (8). Like sympathetic-parasympathetic activity in HRV, baroreflex

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sensitivity (BRS) is another strategy employed to evaluate the cardiac autonomic influence during post-

exercise recovery, using a transfer function technique between beat-to-beat HR and systolic blood

pressure oscillation spectra (9). The baroreflex function is generally characterized by a dynamic gain,
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namely BRS. In brief, the recovery patterns of HRV and BRS indirectly reflect the return to homeostasis

or “overall recovery”. Moreover, changes in those indices seem to influence acute BP after exercise (10).

Previous research suggests an increase in sympathetic activity and delayed BRS recovery after AE and SE

compared to preexercise or a non-exercise control day (10-13), while others failed to detect changes in
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autonomic activity after AE or SE (14), or reported a reduction in sympathetic activity following AE (15).

The few studies investigating post-exercise HRV and BRS in AE vs. SE suggest that acute SE may elicit
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greater sympathetic activity and delayed BRS recovery pattern than AE, at least in physically active men

(11, 12). However, to the best of our knowledge none of those studies compared the isolated effects of AE
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vs. SE on HRV and BRS during post-exercise recovery in sedentary, overweight, and prehypertensive

men, which often exhibit autonomic dysfunction (CAdysf). Notwithstanding, it is worth noting that an

emerging area of research concerning “the physiology of recovery” may provide insights that could help

optimize exercise recommendations for health and performance (16). For example, some adaptations to

physical training appear to result from the summation of acute effects of exercise bouts (17). In terms of

chronic training, albeit available evidence indicates that AE, but not SE would improve vagal-cardiac

control or BRS in young healthy individuals (18, 19), there is lack of information in patients with

CADysf. A better understanding of acute changes in autonomic control following AE and SE in

individuals with CADysf would be important to outline expectations for chronic training in these patients.

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Thus, the extent to which post-exercise cardiac autonomic control (as measured by HRV and BRS)

depends on exercise modality (AE vs. SE) remains unclear and warrants further investigation. Therefore,

the purpose of the present study was to investigate the impact of acute AE and SE upon HRV and BRS,

compared with a control session (CTL) in sedentary, overweight, and prehypertensive men with CADysf.

We hypothesized the recovery pattern of HRV and BRS would differ across exercise modalities.

METHODS

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Experimental approach to the problem

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Participants with CAdysf visited the laboratory six times on separate days, while those assigned into the

control group did not complete the last four visits. Data from control group provided reference values to

ascertain the presence of CAdysf among sedentary, overweight, and prehypertensive individuals. On the

first visit, participants completed a pre-participation questionnaire for cardiovascular risk and were
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screened for BP (normotension vs. prehypertension), body mass (normal weight vs. overweight/obese)

and physical activity level (physically active vs. sedentary) to ensure they met the study inclusion criteria.

On the second visit, HRV and BRS were assessed to evaluate cardiac autonomic control. Subsequently,

maximal oxygen uptake (VO2max) and gas exchange threshold (GET) were determined through
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cardiopulmonary exercise testing (CPET). On the third visit, the load corresponding to participants’ 15-

repetition maximum (RM) of bilateral knee extension exercise was determined. On fourth, fifth and sixth

visits interspersed with 48- to 72 h intervals, participants performed either AE, SE or CTL in a
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randomized counter-balanced order. Before AE, SE, and CTL, baseline autonomic and BRS were

assessed. Within 5 sec of exercise (or control) session termination, participants were placed in the supine
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position, and recovery data collection was recorded after AE, SE or CTL during 25-min in a quiet room

kept at relatively constant temperature (21-23°C). All visits were scheduled at the same time of the day,

between 07:00 and 12:00.

Participants

Twenty men volunteered for the study and were assigned into CAdysf (n = 10) and control groups (n =

10). The following inclusion criteria were considered for CAdysf: a) systolic blood pressure (SBP)

between 120-139 mmHg and/or diastolic blood pressure (DBP) between 80-89 mmHg; b) body mass

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index (BMI) between 25.0-34.9 kg/m²; and c) did not meet the recommended minimum level of physical

activity required for the control group. Inclusion criteria for controls were: a) SBP < 120 mmHg and

DPB < 80 mmHg; BMI < 25.0 kg/m²; and c) regular engagement in physical activity (i.e. 3-5 times/wk,

20-60 min/session) for at least six months prior to the study.

Exclusion criteria for both groups were: a) smoking; b) use of drugs that could affect cardiovascular

function or any ergogenic substances; c) diabetes mellitus; d) angina pectoris, heart failure, or coronary

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artery disease; e) renal dysfunction; f) hepatic dysfunction; g) acute myocardial infarction or history of

stroke, peripheral vascular disease, peripheral neuropathy, chronic obstructive pulmonary disease, asthma,

acute inflammation or chronic thyroid dysfunction; and h) bone, joint, or muscle problems that could limit

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exercise performance.

During the study, participants were told to wear clothing and shoes consistent with sporting activities; to

avoid alcoholic beverages or stimulants (coffee, chocolate, teas, etc.) up to 24 h before tests; and to avoid
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intense physical activities such as running, long walks, or weight training up to 48 h before testing. The

study gained approval from the institutional ethics committee (process 3113/2011). Participants were

informed of characteristics and potential risks of the experiment and provided informed consent prior to

enrolling in the study.

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Procedures

Maximal cardiopulmonary exercise testing (CPET)

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A ramp-incremented maximal CPET was performed on cycle ergometer, as described elsewhere (20). In

brief, a nonexercise model developed to estimate VO2max (21) was applied to determine initial and final

work rates (corresponding to 50% and 100% estimated VO2max, respectively) using cycling equations

proposed by the American College of Sports Medicine (ACSM) (22). Work rate increments were

individualized to elicit each participant’s limit of exercise tolerance within 8–12 min. The test was

considered to have elicited peak capacity when at least three of the following criteria were observed (23):

a) maximum voluntary exhaustion defined by attaining a 10 on the Borg CR-10 scale; b) ≥ 90% predicted

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maximal heart rate (HRmax) [220 – age] or presence of a HR plateau (∆HR between two consecutive

power outputs ≤ 4 beats·min-1); c) presence of a VO2 plateau (∆VO2 between two consecutive power

outputs < 2.1 mL⋅kg-1⋅min-1); and d) respiratory exchange ratio > 1.10.

The gas exchange threshold (GET) was determined in accordance with the combined procedure described

by Gaskill et al. (24). This procedure includes the following three methods: a) ventilatory equivalent

method, with GET defined as the VO2 corresponding to the first sustained rise in the ventilatory

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equivalent of O2, without a concomitant rise in the ventilatory equivalent of CO2; b) excess carbon

dioxide method, with GET defined as the VO2 corresponding to the first sustained rise in excess CO2; and

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c) modified V-slope method, with GET defined as the VO2 value corresponding to the first point of

increase in the VO2-VCO2 slope. The final GET value for each participant was detected by

simultaneously evaluating full page graphs of data plotted for each of the three methods. Visual

inspection to determine GET was independently performed by two experienced investigators. If the
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difference between evaluators with regard to VO2 at GET was within 3%, the mean value was adopted as

the final result. When the difference exceeded 3%, a third investigator was asked to determine GET. The

combination of these three methods has been shown to improve the accuracy and reliability of GET

determination (24).
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Pulmonary gas exchange was determined using a VO2000 analyzer (Medical GraphicsTM, Saint Louis,

MO, USA) and a silicone face mask (Hans RudolphTM, Kansas, MO, USA). Gas exchange variables were
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30-sec stationary time-averaged, which provided a good compromise between removing noise in the data

while maintaining the underlying trend (25). Prior to testing, gas analyzers were calibrated according to
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manufacturer’s instructions, using a certified standard mixture of oxygen (17.01%) and carbon dioxide

(5.00%), balanced with nitrogen (AGATM, Rio de Janeiro, RJ, Brazil). Flows and volumes of the

pneumotacograph were calibrated with a syringe graduated for a 3 L capacity (Hans RudolphTM, Kansas,

MO, USA). Heart rate was measured continuously using a cardiotachometer (RS800cx, PolarTM,

Kempele, Finland) and beat-by-beat data were 30-s stationary time-averaged. All cycling tests were

performed on the same cycle ergometer (Cateye EC-1600, CateyeTM, Tokio, Japan).

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Assessment of 15 repetition-maximum (15-RM)

The load corresponding to 15-RM was determined for the bilateral knee extension exercise. To minimize

possible errors, the following strategies were adopted: a) Standard instructions on the general routine of

data assessment and exercise technique were given to participants before testing; b) Exercise technique

during testing sessions was continuously monitored and corrected; and c) Participants were given verbal

encouragement during the tests. The warm-up consisted of 15 repetitions with self-selected load. This

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load was used as a parameter to establish the initial load of the test, so that 40 to 50% of warm-up load

was added for the first attempt. Depending on the repetitions performed, the load was increased by 1 to 5

kg per attempt until the 15-RM was elicited. After obtaining the load for the bilateral knee extension

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exercise, a 30-min interval was used to check for reproducibility. All tests were performed at the same

period of the day (9:00 to 12:00).

Hemodynamic and cardiac autonomic control assessments

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Blood pressure screening followed standard procedures according to the European Society of

Hypertension recommendations (26). Participants remained seated in an upright position, with the right

arm resting on a table at heart level in a quiet and comfortable environment to stabilize blood pressure.
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After 15 min of seated rest, five assessments were performed with 3-min intervals between each

measurement by an oscillometric device (OMRONTM - HEM-433 INT, Bannockburn, Illinois, USA).

Blood pressure was calculated as the mean of three readings.

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HRV and BRS were derived by finger photoplethysmography with a height correction applied from a
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pressure recording from the left brachial artery (FinometerTM, FMS, Amsterdam, The Netherlands). A

cuff was placed on the left middle finger for a beat-by-beat BP assessment. A short-term HRV and BRS

assessment was performed for screening puposes (control vs. experimental groups), and to investigate the

recovery pattern of cardiac autonomic control following CTL, AE and SE. In all cases, 25-min HRV and

BRS recordings were obtained with participants in the supine position. In order to optimize the stability of

HRV and BRS signals, post-exercise data for the first 5-min of each exercise bout were omitted (7), and

all indices were calculated based on the last 10-min (i.e. screening and baseline assessments) and 20-min

(i.e. 2 × 10-min intervals of post-exercise period) of each recording.

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Participants were advised not to talk or move excessively, to maintain a spontaneous breathing rhythm,

and to avoid irregular respiration during the 25-min recording.

For spectral analysis of R–R interval time series, data were processed by Fast Fourier Transform (FFT)

with the Welch’s method, with a Hanning window with 50% overlap using a customized algorithm from

HeartScopeTM II software (version 1.4, A.M.P.S., LLC, New York, USA) (27). Beat-by-beat R–R interval

series were then converted into equally spaced time series with 256 ms intervals using cubic spline

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interpolation (7, 28). Spectral analysis was expressed in normalized units (n.u.) (7). The ratio between

low frequency and high frequency bands (LF:HF) was used as an index of sympathovagal balance, with

the LF band (0.04-0.15 Hz) being considered as a marker of sympathetic predominance, and the HF band

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(0.15-0.50 Hz) as a marker of parasympathetic predominance (29). The BRS was analyzed from the alpha

index from the low frequency band (α-LF) of the beat-by-beat SBP and pulse interval (30). Only detected

spectral gains with coherence > 0.5 (arbitrary threshold) were accepted.
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Exercise sessions

Detailed instructions were provided to participants before AE and SE. AE consisted of 40-min continuous

cycling on cycle ergometer (7-min warm-up; 30-min bout at a HR corresponding to GET; and 3-min cool
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down). SE consisted of 10 sets of 12- to 15 repetitions of bilateral knee extension exercise (70% of 15-

RM workload with 2-min intervals between sets), preceded by 5-min warm-up at 60-70 rpm on cycle

ergometer, followed by 2-min rest interval. Exercises were completed at volitional speeds and Valsalva
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maneuver was avoided (participants were instructed to expire during the concentric phase and to inspire

in the eccentric phase of the exercise).

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The present SE protocol must be justified, because it could be claimed that it is not consistent with

conventional lifting. The choice was based on common training programs, which are mostly designed

using submaximal loads and repetitions. As for the use of a single exercise, we notice that strength

training often applies multiple sets of two or more exercises performed by the same muscle group. In the

present study, instead of testing the effects of several exercises performed by a given muscle group, due

to logistic reasons the planned exercise volume was achieved through multiple sets of a single exercise

involving a large muscle mass.

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In order to ensure that an equivalent exercise volume was applied within AE and SE, as proposed in prior

studies (31) bouts were matched for the total duration (not including warm-up and cool down). During

CTL participants remained seated at rest for 30-min, and HRV and BRS were assessed in the supine

position by the same protocol used before and after exercise bouts.

Statistical Analyzes

Gaussian distribution of data was verified by the Shapiro-Wilk test, and natural logarithmic (ln)

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transformations were employed whenever necessary. Data were summarized using means and standard

deviations (SD). Cohen's d effect sizes for mean differences were calculated and defined as small (0.20),

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moderate (0.50), and large (0.80) (32). Baseline differences between groups were checked by Student t-

tests. The effect of Condition (i.e. CTL, AE and SE) and Time were compared using a 2-way analysis of

variance (ANOVA) for repeated measures followed by Fisher post-hoc verifications in the event of

significant F ratios. Percentage changes in HRV indices and BRS in each experimental session were
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calculated as ∆ values [i.e. difference between post- and pre-intervention values]. In all cases,

significance level was fixed at P ≤ 0.05. Calculations were made with Statistica 10.0 software (StatsoftTM,

Tulsa, OK, USA) and graphs were prepared using GraphPad Prism 5 (GraphPad Software, San Diego,

CA, USA).
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RESULTS
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Anthropometric, hemodynamic/cardiac autonomic control at rest, and cardiorespiratory fitness profiles of

CAdysf and control groups are summarized in Table 1. The two groups were similar only for age and
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height. As expected, participants assigned to CAdysf were overweight (e.g. higher BMI than controls; P <

0.001), prehypertensive (i.e. higher resting BP than controls; P < 0.001), had poor fitness (e.g. lower

VO2max than controls; P < 0.001), and lower HRV and BRS than controls (P < 0.05).

INSERT TABLE 1

Table 2 depicts differences between AE, SE, and CTL in regards to HR, R-R interval, lnLF, lnHF,

lnLF:HF ratio, and lnBRS. A significant main effect for condition was observed for HR (F = 11.52, P <

0.01), R-R interval (F = 9.64, P < 0.001), lnLF (F = 5.3, P < 0.05), lnHF (F = 11.82, P < 0.001), lnLF:HF

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ratio (F = 8.58, P < 0.01), and lnBRS (F = 7.10, P < 0.01). HR, lnLF and lnLF:HF ratio were significantly

higher during recovery from AE and SE vs. CTL (P < 0.001), and AE vs. SE (P ≤ 0.04). The opposite was

observed for R-R interval, lnHF and lnBRS, which were significantly lower following AE and SE vs.

CTL (P < 0.001), as well as after AE vs. SE (P < 0.05). A significant exercise x time interaction showed

that differences between CTL and exercise conditions decreased over time for HR (F = 17.85, P < 0.001),

R-R interval (F = 18.18, P < 0.001), lnLF interval (F = 7.2, P < 0.05), lnHF (F = 10.47, P < 0.001),

lnLF:HF ratio (F = 10.64, P < 0.001), and lnBRS (F = 14.08, P < 0.001).

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INSERT TABLE 2

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Figure 1 shows comparisons between CTL, AE and SE of autonomic variables expressed as percent

changes throughout recovery (∆%: difference between post- and pre-intervention values). The largest ∆%

differences were typically found between AE vs. CTL, SE vs. CTL, and AE vs. SE at 10-min of recovery.
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INSERT FIGURE 1

DISCUSSION

The present study aimed to compare acute HRV and BRS responses to AE and SE in men with and
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without CAdysf. The main findings were: (a) the group composed of sedentary, overweight, and

prehypertensive men was characterized by CAdysf; (b) AE and SE increased sympathetic activity,
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decreased parasympathetic activity, and blunted BRS responses throughout post-exercise recovery when

compared to CTL. However, HRV and BRS were more markedly reduced after acute AE than SE.
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To date, several studies have investigated the isolated cardiac autonomic control effects of AE (15, 33,

34) and SE (35-37), or even AE vs. SE in healthy men (11, 13, 38), but none of those studies compared

the isolated effects of AE vs. SE in CAdysf individuals. Niemela et al. (13), for example, investigated the

association between exercise mode and recovery pattern of BRS after AE (50% of maximal power output

on cycle ergometer), and SE (light-intensity: 30% of 1RM; and heavy-intensity: 80% of 1RM) in 12

healthy men. Compared to CTL, BRS was significantly blunted until 30-min after AE and both SE

intensities; however, BRS after heavy SE was significantly decreased for 60-min compared to CTL

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(∆%BRS: 62%). According to the authors, the delayed BRS recovery pattern after heavy SE was due to

withdrawal of vagal outflow and increased sympathetic tone.

Heffernan et al. (38) investigated the acute responses of cardiac autonomic control assessed by HRV after

AE (30-min of upright stationary cycling at 65%VO2peak) vs. SE (3 sets of 10-RM for 8 exercises for the

whole body) in 14 healthy and moderately active men (age: 25.3 ± 0.7 years; BMI: 24.6 ± 0.6 kg/m2;

VO2max: 41.7 ± 1.6 mL·kg-1·min-1). Cardiovascular control was not totally normalized within 30-min of

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recovery from either acute AE or SE, but the increase in HR was greater after SE than AE (∆%: ~13% vs.

~24%, respectively). The delayed HR recovery was concomitant to sympathetic predominance after AE

and SE (∆% LF:HF ratio: 64% vs. 81%, respectively), while the decrease in total power was greater in SE

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than AE (∆% total power: -18% vs. -3%, respectively). In practical terms, it has been suggested that

longer HR recovery after acute SE vs. AE would be due to slower vagal reactivation in healthy and

moderately active men. Later, the same group investigated the acute BRS response induced by AE vs. SE

in 13 healthy and moderately active men (age: 25 ± 0.7 years; BMI: ~24.4 kg.m-2; VO2max: 41.8 ± 1.7
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mL·kg-1·min-1) (11). Acute BRS lowered within 20-min after AE and SE vs. preexercise; however, this

reduction was greater following SE than AE (∆%BRS: -49% vs. -20%, respectively). The greater

reduction in BRS following acute SE was proposed to reflect alterations in both neural and mechanical

baroreflex gain, where stiffer central arteries may result in reduced vessel wall deformation and,
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therefore, attenuated baroreceptor activation in moderately active men.

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The present data in sedentary, overweight, and prehypertensive men with CAdysf concur, in part, with

those previous reports from Heffernan et al. (11, 38) using spectral analysis in healthy and moderately
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active men. The cardiac autonomic control evaluated by HRV and BRS remained significantly increased

(e.g. HR, lnLF and lnLF:HF ratio) or decreased (e.g. R-R interval, lnHF and lnBRS) following AE and

SE compared to CTL. In other words, both AE and SE induced significant acute HRV and BRS changes,

characterized by increased sympathetic and reduced parasympathetic activity. The attenuated BRS also

suggests a persistent sympathetic rather than vagal activation after exercise, which in turn, should be

taken into account throughout exercise prescription routines. However, unlike the findings from

Heffernan et al. (11, 38), our data support the notion that AE induces greater changes in HRV and BRS

than SE in CAdysf men (see Table 2 and Figure 1).

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The particular role of exercise intensity and volume to produce changes in post-exercise autonomic

control is uncertain. Michael et al. (34), for instance, examined the effect of three AE intensities (low: 40-

45%; moderate: 75-80%; vigorous: 90-95% of heart rate reserve – HRR) upon HRV indices during 10-

min post-exercise. Higher exercise intensities produced greater decreases in HRV. The role of SE

intensity is controversial (36, 39, 40). While some authors reported that higher SE intensity would result

in larger post-exercise increase in cardiac sympathovagal balance (39, 40), this possibility has been

questioned (36). Our data with CADysf men reinforce the premise that acute SE performed with

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moderate-to-high intensity may influence post-exercise autonomic control, increasing the sympathovagal

balance with concomitant attenuation of BRS.

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On the other hand, prior studies by our group (33) suggested that total exercise volume would be a major

determinant of post-exercise changes in autonomic control. Cunha et al. (33) compared HRV and BRS

after three different maximal CPETs (running, walking and cycling). Although CPETs were performed
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with equivalent relative intensity (i.e., maximum), increases in sympathovagal balance and reductions in

BRS within 60-min recovery were larger following the test performed with greater energy expenditure

(running > walking or cycling). Figueiredo et al. (35) also investigated the role of exercise volume on

HRV responses following SE performed with 1, 3, and 5 sets (8-10 repetitions at 70% 1-RM of bench

press, lat pull down, shoulder press, biceps curl, triceps extension, leg press, leg extension, and leg curl)
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in healthy weight-trained individuals. The increase in sympathetic and decrease in parasympathetic

activity during 60-min of recovery were greater after the protocol performed with 5 sets vs. 1 or 3 sets.
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It is feasible to think that differences in exercise volume across exercise modalities could at least in part
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explain our data indicating greater influence of AE vs. SE upon post-exercise changes in autonomic

control. The high number of sets performed at 70% of 15-RM workload does not allow considering SE as

light. However, even though AE and SE were matched for the total duration, it must be remembered that

SE is intermittent. Actually, more than 50% of SE corresponded to rest intervals (18 min in 10 sets). This

could be a potential reason for differences between our findings and those from Heffernan et al. (11, 36).

Additionally, the amount of exercised muscle mass is also a relevant aspect of exercise volume. While the

present study applied multiple sets of a single exercise for the lower limbs, in trials by Heffernan et al.

(11, 36) SE consisted of exercises for the entire body. Evidently, further research is needed to confirm

this hypothesis.

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Some limitations of this study must be acknowledged. Firstly, the total energy expenditure within AE and

SE bouts was not quantified, thus it is not possible to ensure that exercise volume was really the major

determinant of post-exercise changes in HRV and BRS. Secondly, differences between the present SE

protocol and more conventional resistance training limits to some extent the external validity of our

findings.

In conclusion, both AE and SE increased sympathetic and decreased vagal modulation post-exercise with

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concomitant attenuation in BRS, in sedentary, overweight, and prehypertensive men with CAdysf.

However, these changes were greater after AE than SE, probably due to differences in exercise volume.

Further studies comparing isolated or combined AE and SE could help to clarify potential determinants of

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autonomic and BRS responses during post-exercise recovery.

PRACTICAL APPLICATIONS
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The translation of our data into practical applications comprise clinical and training features. HRV

recovery provides insight into future disease risk, particularly among individuals with CAdysf, while

BRS is a mechanism of short-term BP regulation. In our sample of sedentary, overweigth and

prehypertensive individuals with CAdysf, AE induced greater autonomic imbalance post-exercise than
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SE. The window for the investigation of post-exercise autonomic recovery would be therefore greater

following AE than SE of similar duration, which should be contemplated in clinical and research sets.
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As for exercise prescription, individuals with CAdysf may be more vulnerable to negative outcomes

during recovery from exercise. For instance, the inability to normalize the autonomic control increases the
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risk of arrhythmias. In practical terms, our findings suggest that: 1) the risk of undesirable cardiovascular

events in individuals with CAdysf would be lower after SE than AE; 2) assuming that exercise volume

would be determinant of delayed HRV and BRS recovery, training routines designed for individuals with

CAdysf should rather focus on exercise intensity than volume.

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ACKNOWLEDGEMENTS

This study was partially funded by grants from the Brazilian Council for Technological and Research

Development (CNPq) and Carlos Chagas Foundation for the Research Support at the Rio de Janeiro State

(FAPERJ). The authors thank Professor Antonio Felipe Sanjuliani (in memoriam) for originally

conceiving this research project.

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Figure Legends
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Figure 1. Mean ± SD percentage change in HR, R-R interval, InLF, InHF, InLF:HF ratio, and InBRS

(∆%: difference between post- and pre-intervention values) at 10-min intervals within a 20-min recovery
A

after CTL, AE and SE. *: Significantly different from CTL [P = 0.044 to P < 0.001; Effect size (Cohen's

d): 0.73 to 3.63]. P values and effect sizes (Cohen's d) indicate significant differences between AE vs. SE.

CTL = control session (non-exercise day); AE = aerobic exercise; SE = strength exercise; HR = heart

rate; R-R interval = average of all normal R-R intervals; HF = high frequency band; LF = low frequency

band; LF:HF ratio = sympathovagal balance; BRS = spontaneous baroreflex sensitivity.

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Table 1. Baseline subjects’ characteristics.

Control group CAdysf group Effect size

Moment Variable Mean diff 95%CI t-test P-value
Mean ± SD Mean ± SD (Cohen's d)
Age (yr) 33.8 ± 3.0 36.2 ± 9.8 2.4 -5.1 to 9.9 0.7 0.489 0.35

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Height (cm) 172.5 ± 4.6 176.5 ± 6.2 3.94 -1.9 to 9.7 1.5 0.160 0.77
Anthropometric assessment
Body mass (kg) 70.6 ± 6.8 88.1 ± 6.4 17.5 10.2 to 24.7 5.5 < 0.001 3.31
2
BMI (kg/m ) 23.7 ± 1.5 28.4 ± 2.6 4.7 2.6 to 6.8 5.2 < 0.001 2.33

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SBP (mmHg)a 113.3 ± 4.0 130.9 ± 5.4 17.6 11.9 to 23.3 7.0 < 0.001 3.90
DBP (mmHg)a 64.9 ± 4.4 82.0 ± 7.4 17.1 10.0 to 24.1 5.5 < 0.001 2.96
-1
HR rest (beats·min ) 49.7 ± 6.1 60.9 ± 7.6 11.2 3.8 to 18.6 3.4 0.007 1.71
R-R interval (ms) 1212.2 ± 110.6 985.9 ± 89.6 226.3 53.0 to 267.5 3.4 0.008 2.37
Hemodynamic and cardiac autonomic 2
Total power (ms ) 13.954 ± 6960.0 5799.8 ± 3419.6 8154.5 3597.9 to 12711.1 4.1 0.002 1.57
control at rest

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LF power (n.u.) 34.6 ± 6.4 57.3 ± 7.2 22.8 15.3 to 30.2 6.9 < 0.001 3.51
HF power (n.u.) 47.7 ± 10.3 36.5 ± 6.7 10.9 0.8 to 21.1 2.4 0.037 1.36
LF:HF ratio 0.77 ± 0.29 1.65 ± 0.49 0.88 0.4 to 1.3 4.5 0.002 2.30
BRS (ms·mmHg-1) 18.7 ± 5.2 12.6 ± 1.9 6.1 2.1 to 11.4 3.3 0.009 1.64
-1 -1
VO2max (mL·kg ·min ) 43.8 ± 6.7 26.7 ± 4.7 17.1 13.3 to 21.3 10.0 < 0.001 3.11

Maximal cardiopulmonary exercise test

POmax (W)
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HRmax (beats·min-1)

VO2-GET (mL·kg-1·min-1)
188.4 ± 6.1
277.3 ± 36.1
22.2 ± 3.4
171.1 ± 12.1
182.1 ± 40.9
13.2 ± 4.2
17.3
95.2
9.0
6.9 to 27.7
57.1 to 133.3
4.8 to 13.1
3.8
5.8
5.1
0.005
< 0.001
0.001
1.86
2.60
2.48
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HR-GET (beats·min-1) 130.1 ± 6.8 117.7 ± 10.6 12.4 1.6 to 23.2 2.6 0.029 1.47
PO-GET (W) 131.3 ± 27.8 88.3 ± 20.6 43.1 21.2 to 64.9 4.6 0.002 1.85
a
= Average of three blood pressure screenings; BMI = body mass index; HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; HR = heart rate; R-R
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interval = average of all normal R-R intervals; HF = high frequency band; LF = low frequency band; LF:HF ratio = sympatho-vagal balance; BRS = spontaneous baroreflex

sensitivity; VO2 = oxygen uptake; PO = power output; GET = gas exchange threshold. CAdysf: cardiac autonomic dysfunction group.

Copyright ª 2017 National Strength and Conditioning Association

 Table 2. Mean ±SD values for HRV indexes and BRS for the CAdysf group (n = 10) at pre- and post- CTL, AE and SE, as well as two-way analysis of variance

and interactions.

ANOVA EFFECTS

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Post-exercise
Variables Condition Pre-exercise Effect size Effect size Effect size
Condition Time Interaction
(Cohen's d) (Cohen's d) (Cohen's d)
10 min 20 min

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CTL 62.1 ± 5.6 61.1 ± 5.1 60.9 ± 5.5
HR rest P = 0.002 P < 0.001 P < 0.001
AE 62.3 ± 5.1 79.5 ± 5.9* 74.2 ± 5.8* 1.60 3.35 1.99
(beats·min-1) (F = 11.52) (F = 50.53) (F = 17.85)
SE 62.3 ± 5.9 73.5 ± 7.7*a 69.0 ± 7.0* a,b
CTL 974.4 ± 91.2 989.5 ± 84.4 1008.9 ± 97.4
R-R interval 758.7 ± P < 0.001 P < 0.001 P < 0.001
AE 968.1 ± 82.1 812.8 ± 65.6* 1.46 3.34 2.01

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(ms) 57.1*± (F = 9.64) (F = 49.28) (F = 18.18)
SE 987.3 ± 96.7 823.7 876.8 ± 88.3* a
a
CTL 1.54 ± 0.19 85.1*
1.52 ± 0.16 1.52 ± 0.21
In LF power P = 0.011 P < 0.001 P = 0.011
AE 1.55 ± 0.15 1.80 ± 0.09* 1.75 ± 0.08* 1.08 1.99 1.26
(n.u.) (F = 5.3) (F = 17.9) (F = 7.2)
SE 1.55 ± 0.14 1.68 ± 0.07* 1.66 ±0.08 a
a
CTL 1.76 ± 0.09 1.75 ± 0.09 1.74 ± 0.13
In HF power
(n.u.)
AE
SE
1.75 ± 0.10
1.72 ± 0.07
1.42 ± 0.14*
1.55 ± 0.10*
a
C 1.54 ± 0.11*
1.61 ± 0.10* a
P < 0.001
(F = 11.82)
1.62
P < 0.001
(F = 34.9)
2.78
P < 0.001
(F = 10.47)
1.52
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CTL -0.22 ± 0.27 -0.23 ± 0.24 -0.22 ± 0.32
In LF:HF P = 0.001 P < 0.001 P < 0.001
AE -0.20 ± 0.25 0.38 ± 0.23* 0.21 ± 0.18* 1.38 2.63 1.54
ratio (n.u.) (F = 8.58) (F = 31.23) (F = 10.64)
SE -0.17 ± 0.19 0.13 ± 0.14* 0.05 ± 0.16 a,b
a
A
CTL 1.11 ± 0.10 1.11 ± 0.11 1.12 ± 0.13
In BRS P = 0.003 P < 0.001 P < 0.001
AE 1.09 ± 0.07 0.82 ± 0.10* 0.89 ± 0.12* 1.26 2.53 1.77
(ms·mmHg-1) (F = 7.10) (F = 28.86) (F = 14.08)
SE 1.07 ± 0.08 0.98 ± 0.14* 1.02 ± 0.15 a,b
a

*: Significantly different from CTL and pre-exercise (P < 0.05 to P < 0.001). Superscript letters indicate significant differences in relation to AE values throughout
recovery [i.e. a 10-min; b 20-min (P < 0.05 to P < 0.001)]. CTL = control session (non-exercise day); AE = aerobic exercise; SE = strength exercise; HR = heart rate;

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R-R interval = average of all normal R-R intervals; HF = high frequency band; LF = low frequency band; LF:HF ratio = sympatho-vagal balance; BRS =
spontaneous baroreflex sensitivity.

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