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Copyright © 2017 American College of Sports Medicine
Sex Differences in Cardiac Baroreflex Sensitivity following
Isometric Handgrip Exercise
André L. Teixeira
1, Raphael Ritti-Dias
2, Diego Antonino
1, Martim Bottaro
1,
Philip J. Millar3, and Lauro C. Vianna
1
1NeuroVASQ – Integrative Physiology Laboratory, Faculty of Physical Education, University of
Brasília, Brasília, DF, Brazil; 2Department of Physical Education, Hospital Israelita Albert
Einstein, São Paulo, SP, Brazil; 3
Department of Human Health and Nutritional Sciences,
University of Guelph, Guelph, Ontario, Canada
Accepted for Publication: 6 November 2017
Sex Differences in Cardiac Baroreflex Sensitivity following Isometric
Handgrip Exercise
André L. Teixeira1, Raphael Ritti-Dias
2, Diego Antonino
1, Martim Bottaro
1,
Philip J. Millar3, and Lauro C. Vianna
1
1NeuroVASQ – Integrative Physiology Laboratory, Faculty of Physical Education, University of
Brasília, Brasília, DF, Brazil; 2
Department of Physical Education, Hospital Israelita Albert
Einstein, São Paulo, SP, Brazil; 3
Department of Human Health and Nutritional Sciences,
University of Guelph, Guelph, Ontario, Canada
Correspondence:
Lauro C. Vianna, PhD
NeuroVASQ - Integrative Physiology Laboratory
Faculty of Physical Education University of Brasília
Darcy Ribeiro Campus, Brasília, Brazil
tel: +55 (61) 31072531
fax: +55 (61) 31072512
email: [email protected]
This study was in part funded by CAPES, CNPq, and FAPDF. The results of this study are
presented clearly, honestly, and without fabrication, falsification or inappropriate data
manipulation and the results of the present study do not constitute endorsement by ACSM. The
authors declare that they have no conflict of interest.
Medicine & Science in Sports & Exercise, Publish Ahead of Print DOI: 10.1249/MSS.0000000000001487
Copyright © 2017 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
ABSTRACT
Purpose: To investigate potential sex-related differences on spontaneous cardiac baroreflex
sensitivity (cBRS) following acute isometric handgrip (IHG) exercise. Methods: Twenty men
(23±3 years) and 20 women (24±4 years) randomly performed four sets of 2-min IHG exercise
(two sets for each limb) at 30% maximum voluntary contraction (MVC – experimental) or 3%
MVC (sham). Beat-to-beat heart rate (HR) and arterial blood pressure (BP) were monitored
using finger photoplethysmography before and 10-, 20-, and 30-min following IHG.
Spontaneous cBRS was assessed via the sequence technique and cardiac autonomic modulation
via time- and frequency-domain HR variability. Results: Following IHG, spontaneous cBRS
increased during 10-min of recovery in men (∆13±5%, P=0.03 vs. rest) and increased further in
women (∆23±4%, P<0.01 vs. rest; P=0.04 vs. men). During 20 and 30-min of recovery, cBRS
returned to baseline in men, but remained elevated in women. HR decreased 10-min following
IHG in men (10-min: ∆-2±1 beats.min-1
, P<0.01 vs. rest; 20-min: ∆-1±1 beats.min-1
, P=0.39 vs.
rest; 30-min: ∆1±1 beats.min-1
, P=0.31 vs. rest) and throughout recovery in women (10-min: ∆-
5±1 beats.min-1
, P<0.01 vs. rest; 20-min: ∆-3±1 beats.min-1
, P<0.01 vs. rest; 30-min: ∆-2±1
beats.min-1
, P<0.01 vs. rest). Systolic BP increased 10-min after IHG and remained elevated
during 20-min and 30-min in men (P<0.05). In women, systolic BP increased during 10-min
(P<0.01) and returned to baseline during 20-min and 30-min of recovery. Time domain HR
variability (root mean square of successive differences) was increased during recovery in men
and women (P<0.05). Sham had no effect on any variables. Conclusion: Acute IHG exercise
increases cBRS and cardiac vagal activity in healthy young subjects, but the magnitude and the
time course of changes in cBRS differ between men and women.
Key Words: static exercise, autonomic nervous system, heart rate, blood pressure.
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INTRODUCTION
Isometric handgrip (IHG) training (>4 weeks) has been shown to reduce resting arterial
blood pressure (BP) in both normotensive and hypertensive populations with a magnitude of
effect larger than that reported previously with dynamic aerobic or resistance training (1-5).
Given this accumulating body of evidence, the American Heart Association indicates that IHG
training may be used as a potential alternative strategy to lower resting BP (Class IIB, Level of
Evidence C) (6). However, the mechanisms underlying these chronic adaptations remain largely
unknown, although improvements in cardiac autonomic modulation have been reported (7, 8).
Despite the potential benefits of IHG for BP management, relatively few studies have
assessed the acute effects of IHG on BP control (9-12). This area of study could yield important
mechanistic information given that chronic adaptations may result from temporal summation of
acute responses (13). A single bout of IHG exercise, consisting of four 2-minute isometric
contractions at 30% of maximal voluntary effort, decreased systolic BP and improved cardiac
parasympathetic modulation in older (primarily male) normotensive subjects (10, 11). The latter
observation suggests involvement of the autonomic nervous system but provides little insight
into potential mechanisms. More recently, an acute bout of bilateral isometric leg exercise was
reported similarly to lower BP and increase cardiac parasympathetic modulating in concert with
increased sensitivity of arterial baroreflex control of heart rate (HR) in pre-hypertensive men
(12).
The arterial baroreflex represents an important closed-loop, negative feedback control
system involved in regulating BP (14). Mechanically-sensitive receptors located in the carotid
body and aortic arch relay information to the brainstem regarding beat-to-beat changes in blood
pressure (14). The resultant neural feedback provides critical information to modulate HR
(cardiac baroreflex) or peripheral vasoconstrictor outflow (sympathetic baroreflex) in order to
maintain pressure homeostasis at rest and in response to pertubations (e.g. standing) (15).
Importantly, it is now well established that the mechanisms regulating BP differ between men
Copyright © 2017 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
and women (16, 17). In particular, women present commonly with reduced cardiac baroreflex
sensitivity (cBRS), a measure of reflexive vagal modulation (18-20). Such sex-based differences
in BP control may contribute to a recent meta-analytic observation that men experience larger
reductions in BP following IHG training compared to women (4). However, recent trials not
included in this analysis suggests that potential sex differences are unclear, Badrov et al. (21) and
Somani et al. (22) demonstrated that IHG training lowered similarly arterial BP in healthy men
and women. Unfortunately, prior studies examining the acute cardiovascular effects of IHG have
recruited predominantly (or solely) men and were not designed to investigate potential sex-
related differences in the BP control.
Therefore, the present study was undertaken to test the hypothesis that a single bout of
IHG exercise would improve BP control by increasing cBRS and cardiac parasympathetic
modulation in young healthy subjects, and to characterize the potential sex differences in these
responses.
METHODS
Participants
Twenty men (mean ± standard deviation, 23 ± 3 years) and 20 women (24 ± 4 years)
participated in the study. All subjects were healthy, normotensive, non-smokers, and were
recreationally active (self-reported habitual physical activity for at least 6 consecutive months
with a minimum frequency of 3 days per week in ≥ 30-min sessions). Subjects had no history or
symptoms of cardiovascular, pulmonary, metabolic, or neurological disease as determined from a
detailed medical health history questionnaire. No subjects were using prescribed or over-the-
counter medications. To avoid potential influence of female sex hormones on BP control, all
women were non-users of oral contraceptive pills for at least six consecutive months and were
studied during the early follicular phase of their menstrual cycle (i.e. first five days after
menstruation onset). Participants were recruited through posters placed at the University of
Copyright © 2017 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
Brasília, Brazil. Informed written consent was obtained from all subjects and all procedures were
approved by the University of Brasília institutional research committee in accordance with the
Declaration of Helsinki (CAAE: 38922414.7.0000.0030).
Experimental protocol
The study involved a prospective randomized, sham-controlled, cross-over design,
whereby each subject completed both experimental and sham interventions separated by 48–72
h. All subjects were asked to refrain from consuming caffeine/alcohol and from engaging in
physical exercise for 6 and 24 h, respectively, prior to the tests. Subjects were 2-h postprandial
upon arrival to the laboratory. To avoid potential diurnal variations, subjects were always tested
at the same time of day for each subject and in the same quiet, temperature-controlled room (22–
24°C).
Upon entering the laboratory, weight and height were determined via standard methods,
and body mass index (BMI) calculated. Following instrumentation, the subjects were asked to be
seated (90° of hip and knee flexion) and rest for 20 min. The initial 10-min rest period was used
for stabilization of cardiovascular variables, while the final 10-min period was used to collect
baseline measurements. A handgrip dynamometer was interfaced with a personal computer so
that real-time force output feedback could be displayed visually to the subjects (Powerlab 16/35,
AD instruments, Australia). Subjects completed three maximum isometric voluntary contractions
(MVC), each separated by >1 min of rest, in each limb. The highest of three maximal efforts was
designated MVC. Subjects next performed four sets of unilateral IHG (two for each limb). The
protocol consisted of 2-min static contractions at 30% (experimental) or 3% (sham) MVC
separated by 1-min rest periods (11). Following completion of IHG, seated recovery was
monitored for 30 min.
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Continuous beat-to-beat HR and arterial BP were measured using finger
photoplethysmography (Human NIBP Controller, AD instruments, NSW, Australia). Brachial
arterial BP was also measured with an automated digital sphygmomanometer (Dixtal, DX2022,
Brazil) for absolute measures of BP and to confirm finger measurement accuracy. Respiratory
movements were monitored using a strain-gauge pneumograph placed in a stable position around
the abdomen (Pneumotrace; UFI, Morro Bay, CA) in order to avoid the potential confounding
influence of large respiratory excursions on cardiovascular measurements and to ensure subjects
did not perform any Valsalva maneuvers during IHG. Measurements were performed during
baseline (10-min) and thrice following IHG (5th
to 10th
min, 15th
to 20th
min and 25th
to 30th
min
of recovery). Rating of perceived exertion (RPE) was obtained at the end of exercise using the
OMNI-RES scale (0–10) (23).
Spontaneous cBRS
Spontaneous cBRS was assessed using the sequence technique as previously reported
(24, 25). The sequence technique is based on the identification of consecutive beats in which
progressive increases (or decreases) in systolic BP (input variable) are followed by a progressive
lengthening (or shortening) in RR interval (output variable). Briefly, sequences of three or more
consecutive and concurrent beats with corresponding increases or decreases in systolic BP and
RR interval were identified as arterial baroreflex sequences (CardioSeries v2.4, Brazil).
Sequences of ≥ 3 consecutive cardiac cycles were detected only when the variations in systolic
BP and RR interval were ≥ 1 mmHg and ≥ 1.0 ms, respectively. A linear regression was applied
to each individual sequence and only those sequences in which r was >0.85 were accepted. The
slopes of the systolic BP and RR interval relationships for up and down sequences were then
calculated and averaged for a measure of spontaneous cBRS. Overall results were similar when
HR was used as the dependent variable for these cBRS measures and therefore only RR interval
measures are presented.
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HR variability
HR variability was determined in accordance with the guidelines of the Task Force of
the European Society of Cardiology and the North American Society of Pacing and
Electrophysiology (26). Variables were sampled at 1000 Hz and stored for offline analysis
(CardioSeries v2.4, Brazil). Only segments without signal noise were analyzed. All ectopic beats
on the ECG trace were identified both automatically and manually before exclusion from the
analysis. Time domain HR variability was performed using the square root of the mean of the
sum of successive differences in RR interval (RMSSD) as recommended for the estimation of
short-term high-frequency variability of HR that is primarily mediated by parasympathetic nerve
activity (26). A fast Fourier transformation (512 points) was used for spectral analysis of HRV.
The power spectra were quantified by measuring the area under the following frequency bands:
very low frequency power (VLF) (<0.04Hz), low-frequency power (LF) (0.04–0.15 Hz) and
high-frequency power (HF) (0.15–0.4 Hz). Normalized units were calculated by dividing each
spectral band by the total power minus the VLF power and were multiplied by 100. The ratio of
LF to HF power (LF/HF) was also calculated as a measure of cardiac autonomic balance (26).
Statistical analyses
An a priori sample size calculation was completed for the primary variable, cBRS gain
(G*Power 3.1 Dusseldorf University, Germany), based on a mean difference of 33 ± 1% in
cBRS gain between men and women (18, 19) with an α = 0.05 and power of 0.80. The resultant
calculation yielded an estimated sample size of 10 subjects in each group. Comparisons of
physiological variables were made using three-way analyses of variance (ANOVA) with
repeated measures, in which sex (men, women), time [baseline, recovery (10-min, 20-min, 30-
min)], and trial (experimental, sham) were the main factors. Comparisons of changes (∆) during
experimental protocol were made using a 2 x 3 (sex x time) ANOVA. In addition, an ANCOVA
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(with baseline score as a covariate) analysis were performed to compare relative changes from
rest in physiological variables throughout recovery between men and women. Post hoc analysis
was employed using LSD test to investigate main effects and interactions. Baseline
characteristics were compared using an independent sample t test. Statistical significance was set
at P < 0.05 and values are presented as means ± S.E.M. Analyses were conducted using
Statistical Package for the Social Sciences (SPSS, version 22, USA) for windows.
RESULTS
Subject baseline characteristics are displayed in Table 1. Men and women were matched
for age, however, women had lower body weight, height, and BMI compared with men (All P <
0.01). In addition, measures of right and left handgrip MVC (absolute and relative to body
weight) were lower in women (All P < 0.01). Importantly, RPE was not different between groups
during both sham (men: 1.0 ± 0.3 vs. women: 1.5 ± 0.3; P = 0.16) and experimental (men: 8.5 ±
0.3 vs. women: 8.9 ± 0.2; P = 0.23) sessions.
Hemodynamics variables are shown in Table 2. At rest, HR was higher (P < 0.01)
whereas arterial BP was lower (P < 0.01) in women than men. In men, HR decreased slightly
from rest during 10-min of recovery in the experimental protocol (∆-2 ± 1 beats.min-1
; P < 0.01
vs. rest) and returned to baseline during 20-min (∆-1 ± 1 beats.min-1
; P = 0.39 vs. rest) and 30-
min (∆1 ± 1 beats.min-1
; P = 0.31 vs. rest) of recovery. In women, HR remained lower from rest
during the recovery period (10-min: ∆-5 ± 1 beats.min-1
, P < 0.01 vs. rest; 20-min: ∆-3 ± 1
beats.min-1
, P < 0.01 vs. rest; 30-min: ∆-2 ± 1 beats.min-1
, P < 0.01 vs. rest). Systolic BP
increased from rest following 10-min of IHG (∆6 ± 1 mm Hg, P < 0.01 vs. rest) and remained
slightly elevated during 20-min (∆2 ± 1 mm Hg, P = 0.02 vs. rest) and 30-min (∆2 ± 1 mm Hg, P
= 0.02 vs. rest) in men. In women, systolic BP increased from rest during 10-min (∆3 ± 1 mm
Hg, P < 0.01 vs. rest) and returned to baseline during 20-min (∆1 ± 1 mm Hg, P = 0.15 vs. rest)
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and 30-min (∆1 ± 1 mm Hg, P = 0.22 vs. rest) of recovery. No interaction effects were found for
diastolic or mean BP, though both had sex and time effects (Table 2). During the sham protocol,
all hemodynamics variables remained unchanged from rest in both men and women. Similarly,
respiratory rate were not different between men and women during both experimental and sham
protocols (P > 0.05; data not shown).
No interaction effects were found for any measure of HR variability (All P > 0.05), but
all presented significant time effects (Table 2). Following IHG, total power and RMSSD
increased from rest in the experimental protocol in both men and women (Table 2).
Figure 1 shows cBRS gain at rest and following IHG at 30% MVC (experimental) and
3% MVC (sham) in both men (panel A) and women (panel B). As expected, resting cBRS gain
was higher in men compared with women (P = 0.01). During 10-min of recovery in the
experimental protocol, cBRS increased from rest in both men and women. However, during 20-
min cBRS returned to baseline in men and remained elevated in women. cBRS was unchanged in
both men and women throughout the sham protocol (P > 0.05). The percent change (∆) in cBRS
from rest to recovery intervals are presented in Figure 2. Following 10-min of IHG in the
experimental protocol, cBRS increased in men (∆13 ± 5%, P = 0.03 vs. rest) and further
increased in women (∆23 ± 4%, P < 0.01 vs. rest; P = 0.04 vs. men). During 20-min and 30-min
of recovery, cBRS returned to baseline in men (∆-4 ± 4%, P = 0.22 vs. rest and ∆-7 ± 4%, P <
0.12 vs. rest, respectively), but remained elevated in women during 20-min (∆14 ± 4%, P < 0.01
vs. rest; P < 0.01 vs. men) and slightly, but not significantly elevated during 30-min (∆7 ± 6%, P
= 0.17 vs. rest; P < 0.01 vs. men). Adjustment for baseline differences in HR did not alter the
interpretation of cBRS results.
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DISCUSSION
The novel main finding of the present study is that a single bout of IHG increases
acutely spontaneous cBRS gain in young healthy subjects; however, the magnitude and time
course of these responses differed between men and women. In men, cBRS increased during 10-
min of recovery and returned to baseline after 20-min of IHG, but in women, cBRS markedly
increased from rest during 10-min and remained elevated until 30-min of recovery. In addition,
acute IHG exercise was able to reduce HR and increase RMSSD, a non-invasive marker of
cardiac parasympathetic activity, in both men and women. Collectively, these findings suggest
that one session of IHG exercise can acutely increase the sensitivity of arterial baroreflex control
of HR, a measure of reflexive vagal modulations, though sex dependent differences in responses
are present.
Historically, fatiguing isometric efforts have been associated with exaggerated
hypertensive responses and contraindicated for special populations (27). However, low-to-
moderate intensity, submaximal, isometric contractions produce cardiovascular responses similar
to dynamic aerobic (12) and resistance exercise (28). Wiley et al. (29) first reported the
hypotensive effects of submaximal IHG exercise training, after which, a number of randomized
controlled and uncontrolled trials have investigated a role for isometric exercise training to
reduce BP. Recent meta-analyses have confirmed reductions in BP, which may also be greater
following isometric training when compared with traditional aerobic and/or dynamic resistance
training (1-5). Interesting, it is worthy to note that total power of HRV increased following IHG
exercise in both men and women, which is different to others modalities of exercise. As a result,
IHG is an intervention that can acutely improve cardiac autonomic regulation, which adds weight
to supporting IHG as a promising non-pharmacological therapy for the management of
hypertension (6).
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Despite the mounting evidence regarding the beneficial effects of isometric exercise
training on BP management, a recent review of the literature reinforced that the underlying
mechanisms responsible for these adaptations remain largely unknown, though, preliminary data
suggest that changes in cardiac autonomic modulation, sympathetic vasomotor tone, endothelial
dilator function, and oxidative stress may be involved (30). With respect to changes in cardiac
autonomic modulation, a recent study in pre-hypertensive men reported the first evidence of
increased cBRS following acute leg isometric exercise (12). The results of our study extend this
neural response to a single bout of IHG, a much smaller contracting muscle mass, and to a
population of young healthy men and women. Taken together, these findings support the concept
that modulations in the sensitivity of the arterial baroreflex may be one of the mechanisms
involved in the reported reductions in resting BP following IHG training. In contrast, with prior
works (10-12), increases in cBRS occurred independent of acute reductions in arterial BP during
recovery. This could be explained, in part, due the fact that the subjects in our sample were
normotensive and had lower resting BP values. Indeed, previous studies showing acute
reductions in BP following isometric exercise were performed in older adults (10, 11) or pre-
hypertensive subjects (12).
A novel observation of the present investigation is that the time-course and magnitude
of increases in cBRS following acute IHG exercise in healthy normotensive subjects were sex
dependent. Specifically, during the recovery period, cBRS rapidly returned to baseline in men
but remained elevated in women. This sex-related difference in cBRS responses to IHG is not
fully understood. It has been reported that men present higher resting cBRS than women (18-20),
a finding reinforced with the present results. Given this, we can speculate that women may
possess a higher range for increases in cBRS following IHG exercise due to their lower baseline
values compared with men. The present results also suggest that in response to acute IHG, a
stimulus which raises BP, young women may buffer these pressor responses primarily through
changes in cardiac chronotropy (31). This is supported by the persistent reduction in HR
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throughout recovery in women but not men. In contrast, men may buffer increases in BP
primarily through changes in peripheral vasoconstrictor outflow (31). Importantly, the increased
cBRS gain in women is unlikely to be mediated by female sex hormones (i.e., estrogen and
progesterone) as cyclical fluctuations across the menstrual cycle do not appear to influence cBRS
gain (32) or autonomic modulation (33, 34). Future studies are needed to confirm the role of
female sex hormones on cBRS gain following IHG exercise. Furthermore, it is an interesting
observation that the LF/HF ratio is below baseline at 10 and 30-min post IHG in females
compared with a sustained elevation post IHG in males. These differential autonomic responses
may, in part, be a mechanism for the differences reported in cBRS following IHG exercise and
warrant further investigation. Although men and women presented similar relative effort during
IHG contractions, as confirmed by no significant differences in RPE, we cannot exclude the
possibility that men experienced larger pressor responses during IHG than women (35, 36).
Whether differences in cardiovascular responses during acute IHG impact the sex-differences in
cBRS gain warrants future study.
The present results add to a growing body of literature revealing sex differences in
cardiovascular control during and following a bout of exercise. For example, Wong et al. (37)
demonstrated that during the onset of IHG, women had smaller increases in HR and BP than men
which seemed to be mediated by differential neural activation in several forebrain sites
associated with autonomic regulation. Further, a recent study showed that women exhibit faster
cardiac vagal reactivation following maximum aerobic exercise than age-matched men (38). The
results of these studies demonstrate clearly that cardiovascular responses during and following
exercise can differ between men and women. The present investigation extends this body of
work, demonstrating that acute IHG exercise can increase cBRS, a measure of reflexive vagal
modulations, but that these responses are more pronounced in women.
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Clinical implications
The measurement of cBRS is considered to have strong prognostic value for risk
stratification and cardioprotection (39). Several cardiovascular and metabolic disease states are
accompanied by autonomic dysfunction and blunted cBRS (e.g. hypertension, diabetes, heart
failure, coronary artery disease and obesity). Although aerobic exercise training has been shown
to reduce BP and increase cBRS in patients with hypertension (40), the effects of an acute bout
of aerobic exercise on cBRS are less clear. For example, 30 minutes of upright cycling at 65% of
peak oxygen consumption decreased cBRS during recovery in young healthy men (24). In
contrast, our results demonstrate that eight minutes of low intensity IHG can increase
spontaneous cBRS and cardiac parasympathetic activity without altering resting arterial BP.
These transient autonomic responses may be involved in mediating the chronic hypotensive
benefits of IHG training by reducing BP reactivity to stress. Sensitivity of the cardiac baroreflex
has been reported to be inversely related to BP responses to mental stress (41), a predictor of
future BP levels (42). The clinical implications of chronic IHG training warrant further study.
Limitations
The present study has some limitations. First, we studied only young healthy, physically
active, subjects limiting extrapolation of our results to other populations most likely to benefit
from IHG exercise such as older, sedentary and/or diseased patients. Future studies are necessary
to examine the acute effects of IHG on BP control in these populations. Second, cBRS was
calculated based on spontaneous data which assesses a limited range of pressure for the stimulus-
response baroreflex relationship. Perturbational methods, such as the infusion of vasoactive
drugs (i.e. modified Oxford) allow for a more comprehensive examination of the prevailing
range of pressure inputs. However, sequence method has been shown to correlate with the
Oxford technique (43) and studies employing the sequence technique have reported high
reproducibility of spontaneous cBRS at rest and during perturbations (44-46). Third, we
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evaluated a limited range of time following IHG (i.e., 30-min post-exercise). Future studies
should be conducted with more time points to assess the prolonged effect of IHG on BP control,
for example 24-h post-exercise. Fourth, the IHG protocol used was based on prior studies which
showed reductions in arterial BP with training (7-9, 11, 47), but whether it is the most efficacious
for lowering BP, or differs between men and women is unknown.
Conclusion
In summary, we found that IHG exercise acutely improves spontaneous cBRS and
cardiac vagal activity in healthy, young subjects and that these improvements are more
pronounced in women compared with men. These results allow us to suggest that an
enhancement in cBRS may be one of the underlying mechanisms involved in the previously
reported improvements in resting BP control following IHG.
Acknowledgments
The time and effort expended by all the volunteer subjects is greatly appreciated. We thank Luiza
M. Mascarenhas for their excellent support with data collection. This study was in part funded by
CAPES, CNPq and FAPDF. The results of this study are presented clearly, honestly, and without
fabrication, falsification or inappropriate data manipulation and the results of the present study
do not constitute endorsement by ACSM.
Conflict of interest
The authors declare that they have no conflict of interest.
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FIGURE LEGENDS
Figure 1. Cardiac baroreflex sensitivity (cBRS) gain at rest and following one session of
isometric handgrip exercise at 30% (experimental) and 3% MVC (sham) in men (panel A) and
women (panel B). ∗P < 0.05 vs. rest, †P < 0.05 vs. sham protocol.
Figure 2. Percent change from rest (∆) in cardiac baroreflex sensitivity (cBRS) gain following
isometric handgrip exercise at 30% MVC in men (black squares) and women (white squares). ∗P
< 0.05 vs. men.
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Copyright © 2017 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
Copyright © 2017 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
Table 1. Baseline characteristics.
Men (n=20) Women (n=20) P value
Age (years) 23 ± 1 24 ± 1 0.46
Weight (kg) 77.9 ± 2.8 58.4 ± 1.5 <0.01
Height (m) 1.78 ± 0.01 1.64 ± 0.01 <0.01
BMI (kg/m2) 24.4 ± 0.8 21.8 ± 0.4 <0.01
MVCabsolute (kg.f)
Right 47.1 ± 1.5 29.6 ± 1.2 <0.01
Left 46.4 ± 1.6 27.9 ± 1.1 <0.01
MVCrelative (kg.f/kg)
Right 0.62 ± 0.01 0.51 ± 0.02 <0.01
Left 0.62 ± 0.02 0.48 ± 0.02 <0.01
Values represents means ± S.E.M. BMI, body mass index; kgf, kilogram-force; MVC, maximum
voluntary contraction (absolute and relative to the body weight). P values are derived from
independent sample t test.
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Table 2. Hemodynamics variables at rest and following 10-, 20- and 30-minutes of isometric handgrip exercise at 30% (experimental)
and 3% (sham) maximum voluntary contraction in men and women.
Men Women P value
Rest 10-min 20-min 30-min Rest 10-min 20-min 30-min Sex Time Conditi
on
Interacti
on
Hemodynamics
HR
(beats.min-1
)
Experimen
tal 66 ± 2 64 ± 2*† 66 ± 2 67 ± 2 75 ± 2‡ 70 ± 2*†‡ 73 ± 2*‡ 73 ± 2*‡ 0.01
<0.00
1 0.12 0.001
Sham 67 ± 1 67 ± 1 67 ± 2 67 ± 1 75 ± 2‡ 74 ± 2‡ 75 ± 2‡ 75 ± 2‡
Systolic BP
(mm Hg)
Experimen
tal 113 ± 2 119 ± 2*† 115 ± 2*† 115 ± 2*† 100 ± 1‡ 103 ± 2*†‡ 101 ± 2†‡ 101 ± 2†‡
<0.00
1
<0.00
1 <0.001 0.04
Sham 112 ± 2 113 ± 2 112 ± 2 113 ± 2 99 ± 2‡ 100 ± 1‡ 98 ± 2‡ 99 ± 1‡
Diastolic BP
(mm Hg)
Experimen
tal 61 ± 1 63 ± 1 62 ± 1 62 ± 1 57 ± 1 59 ± 1 59 ± 1 59 ± 1 0.01 0.01 0.17 0.36
Sham 62 ± 1 62 ± 1 62 ± 1 62 ± 1 56 ± 1 57 ± 1 57 ± 1 59 ± 1
Mean BP
(mm Hg)
Experimen
tal 78 ± 1 81 ± 1 79 ± 1 80 ± 1 71 ± 1 73 ± 1 73 ± 1 73 ± 1
<0.00
1 0.001 0.01 0.22
Sham 79 ± 1 79 ± 1 79 ± 1 79 ± 1 70 ± 1 71 ± 1 70 ± 1 72 ± 1
HR variability
RMSSD (ms)
Experimen
tal 54.7 ± 4.7 62.3 ± 6.5 59.3 ± 5.8 59.5 ± 7.2 40.5 ± 3.1 52.5 ± 4.7 46.5 ± 3.6 46.0 ± 3.3 0.07 0.001 0.06 0.92
Sham 52.0 ± 5.2 51.5 ± 4.5 53.0 ± 5.4 54.8 ± 6.5 42.0 ± 3.2 43.6 ± 3.0 44.2 ± 2.9 42.7 ± 2.9
LF (ms2)
Experimen
tal
1424.7 ±
372.1
2132.2 ±
520.1
2700.8 ±
761.5
2839.4 ±
894.5
996.4 ±
119.0
1325.3 ±
178.1
1390.2 ±
184.9
1323.3 ±
228.4 0.11 <0.01 0.06 0.31
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Sham 1438.1 ±
387.5
1485.5 ±
217.7
1768.8 ±
261.9
2291.0 ±
637.6
929.2 ±
105.9
1075.3 ±
132.4
1290.3 ±
194.8
1285.7 ±
154.2
HF (ms2)
Experimen
tal
1389.3 ±
381.4
1748.6 ±
422.1
1459.0 ±
295.1
1635.5 ±
409.9
860.6 ±
177.6
1391.5 ±
297.2
1087.6 ±
209.6
1037.6 ±
166.0 0.22 0.03 0.15 0.78
Sham 1288.3 ±
423.6
1153.0 ±
315.2
1354.9 ±
281.4
1650.1 ±
452.1
825.1 ±
105.4
874.5 ±
103.3
952.1 ±
132.6
917.5 ±
139.2
Total power
(ms2)
Experimen
tal
3674.1 ±
841.7
4992.9 ±
1071.7
5645.1 ±
1244.4
6262.9 ±
1529.0
2488.2 ±
301.8
3670.8 ±
492.4
3371.0 ±
417.7
3245.4 ±
457.0 0,12 <0.01 0,03 0,08
Sham 3644.7 ±
938.6
3604.7 ±
599.6
4258.6 ±
617.5
5338.0 ±
1237.1
2329.9 ±
233.4
2562.3 ±
236.1
3214.9 ±
379.8
3081.1 ±
324.5
LF/HF
Experimen
tal 1.31 ± 0.18 1.47 ± 0.18 1.94 ± 0.25 2.25 ± 0.36 1.65 ± 0.22 1.31 ± 0.12 1.71 ± 0.20 1.48 ± 0.17 0.46 <0.01 0.30 0.07
Sham 1.69 ± 0.25 2.10 ± 0.40 1.75 ± 0.28 2.07 ± 0.35 1.57 ± 0.29 1.60 ± 0.29 1.70 ± 0.17 1.83 ± 0.24
Values represents means ± S.E.M. HR, heart rate; BP, blood pressure; RMSSD, square root of the mean of the sum of successive
differences in R-R interval of HR variability; LF, low-frequency; HF, high-frequency; LF/HF, ratio between low- and high-
frequency components of HR variability. P values are derived from ANOVA examining main effects of sex, time, condition and
interaction (sex × time × condition). ∗P < 0.05 vs. rest, †P < 0.05 vs. sham protocol, ‡P < 0.05 vs. men.
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