ISMJ

International SportMed Journal

 

Original research article

Effect of caffeine intake on blood pressure and heart rate variability after a single bout of aerobic exercise

 

1Mr João Bruno Yoshinaga Costa, B Phys Ed, 1Mr Paulo Gomes Anunciação, MSc1 Mr Roberto José Ruiz, MSc, 2Mr Juliano Casonatto, MSc, *1Dr Marcos Doederlein Polito, PhD

1University of Londrina, Brazil

2North Paraná University, Paraná, Brazil

 

*Corresponding author. Address at the end of text.

 

Abstract

Background: The consumption of a dose of caffeine (CAF) may attenuate post-exercise hypotension. Research question: The purpose was to verify the effect of a dose of CAF on systolic (SBP) and diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR) and heart rate variability (HRV) after a session of aerobic exercise in normotensive individuals. Type of study: Randomized controlled study. Methods: Ten healthy, physically active men (24.4 ± 4.5yrs; 74.3 ± 11.8kg; 172.8 ± 8.6m; 36.8 ± 5.7ml.kg-1.min-1) were randomly submitted to two experimental protocols in distinct days, in a cross-over double-blind design, with the ingestion of 4mg.kg-1 of CAF or placebo and performance of an aerobic exercise in a cycle ergometer at 60% VO2peak. SBP, DBP, MAP, HR and HRV components were assessed at the pre-exercise rest period, 60min after substance ingestion and during 60-min post-exercise. Results: At the post-ingestion period, there were reductions on basal HR on both sessions and mean rises of 5 mmHg on SBP, of 7-8 mmHg on DBP and of 6-7 mmHg on MAP on the caffeine session. After exercise, there were reductions of 5-7mmHg on SBP, significant on the 30th and 40thmin, on the placebo session. During the caffeine session, maintenance of raised HR levels, no difference in relation to the pre-exercise period for SBP and MAP, and higher blood pressure compared to the placebo session. HRV was altered in each session; however there were no differences between the experimental sessions.  Conclusion: The ingestion of a 4 mg.kg-1 dose of CAF apparently does not significantly interfere on the cardiovascular behaviour after a session of aerobic exercise. Keywords: caffeine; post-exercise hypotension; aerobic exercise; blood pressure; heart rate

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Mr João Bruno Yoshinaga Costa, B Phys Ed

Mr Costa graduated in physical education from the University of Londrina, Brazil. His research interests include post-exercise hypotension.

Email: brunoycosta@yahoo.com.br

 

Mr Paulo Gomes Anunciação, MSc

Mr. Anunciação graduated in physical education from the University of Londrina, Brazil. His research interests include acute cardiovascular response and post-exercise hypotension.

Email: paulogomesuel@hotmail.com

 

Mr Roberto José Ruiz, MSc

Mr Ruiz graduated in physical education from the University of Londrina, Brazil. His research interests include cardiovascular physiology induced by caffeine intake.

Email: rjr_nh@hotmail.com

 

Mr Juliano Casonatto, MSc

Mr Casonatto taught in the Physical Education Department at the North Paraná University, Brazil. His research interests include physical activity for health and cardiovascular physiology.

Eailm: julianoc@sercomtel.com.br

 

*Dr Marcos Doederlein Polito, PhD

Dr Polito obtained his PhD in physical education at Gama Filho University, Brazil. He teaches at the Department of Physical Education at the University of Londrina, Brazil. His research interests include post-exercise hypotension and cardiovascular physiology.

Introduction

The high exposure of the world's population to caffeine, through its daily consumption from a variety of sources (coffee, teas, soft drinks, chocolate and medicines), may have an impact on cardiovascular risk 1. This fact is related to the evidence found in the scientific literature about the ability of caffeine (2-4 cups of coffee) to acutely rise resting blood pressure (BP) in adults 1,2. High levels of basal BP may be considered an independent risk factor to cardiovascular impairment 3.

 

Lifestyle changes have been recommended as a preventive and therapeutic strategy to aid in the control of resting BP levels. Among these modifications, the regular practice of physical activity is considered one of the main methods of intervention due to its capacity to provide beneficial effects to the cardiovascular system 4. In addition, evidence suggests that an isolated session of aerobic exercise can significantly reduce BP levels post-exercise 5, in comparison with the values observed pre-exercise, in the physiological response commonly referred to as post-exercise hypotension (PEH). PEH is clinically important because it enables a reduction in BP at rest regardless of medication, and may contribute to chronic cardiovascular changes even in normotensive individuals 4. 5. On the other hand, there is evidence that a single dose of caffeine (equivalent to the habitual daily consumption of adults, i.e. approximately 4mg.kg-1) 1,2 may attenuate PEH 6. This effect may be related to the antagonism of the vasodilator action of adenosine 6 and the inhibition of phosphodiesterases 2. However, the aforementioned study 6 followed the cardiovascular behaviour for only 10min after exercise, which is a short time for further inferences about the PEH. Accordingly, existing information regarding the cardiovascular effects of caffeine observed for many minutes after exercise are scarce. Considering that the PEH is clinically important and that caffeine may reduce the magnitude of this effect, it is appropriate to invest in studies that seek to evaluate the effects of caffeine ingestion on the post-exercise cardiovascular responses.

 

Besides the possible modification of BP, caffeine may interfere with heart rate variability (HRV) both before and after exercise 7. Thus even though some studies report little change in the PEH, the HRV can be altered 5. Therefore the autonomic activity in the heart may be different to the behaviour of BP. In this way, BP monitoring combined with HRV may provide additional information about post-exercise cardiovascular behaviour.

 

Therefore the aim of this present study was to verify the effects of a single dose of caffeine on BP and HR behaviour after an isolated bout of aerobic exercise in normotensive individuals. In addition, HRV analysis was used as an indicator of the autonomic function of the heart. The hypothesis of this study is that caffeine may attenuate post-exercise BP reductions for up to 60 minutes.

 

Methods

Subjects

The calculation of a sample size for the hypothesis testing of a mean, based on another experiment8 (standard deviation=10mmHg; difference to be detected=8mmHg; significance=5%; statistical power=80%), showed that 10 subjects were required. Accordingly, ten healthy, physically active, non-smoking, not on any medication, and normotensive (according to the criteria of the VII Joint National Committee3) subjects, were recruited for the study. All subjects voluntarily signed an informed consent form, complying with the rules of the Resolution 196/96 of the National Health Council on Research Involving Human Beings. The study was approved by the Research Ethics Committee of the Londrina State University (022/2008) in Brazil.

 

Experimental design

Initially, subjects were measured anthropometrically and were given diet recall forms accompanied by recommendations to avoid products containing caffeine during the experiment. In the same time, the subjects were evaluated during an ergospirometric test of their maximum effort on a cycle ergometer. Subsequently, all the subjects were randomly submitted to two experimental protocols:  an aerobic exercise session with caffeine (CAF) and an aerobic exercise session with a placebo (PLA), separated by a minimum time period of 72h, in a double-blind cross-over design, following the ingestion of 4mg.kg-1 of caffeine (CAF) or sucrose (PLA). Both substances were orally administered in identical gelatinous capsules, with 180ml of water at room temperature. The aerobic exercise session was performed on a cycle ergometer at 60% VO2peak over 50mins, including a 5min warm-up.

 

Before each experimental session, subjects remained comfortably seated for 10min in a calm location. After this period, resting BP and HR were recorded. Afterwards, the subjects ingested CAF or PLA and remained seated for 60min. In this period, BP and HR were monitored for 10min intervals (10th, 20th, 30th, 40th, 50th and 60th min).

 

Subsequently, the subjects performed the aerobic exercise session and, thereafter, the same rest position was adopted. On this occasion, the post-exercise measures (BP and HR) were recorded for 60 min, in cycles of 10 min (10th, 20th, 30th, 40th, 50th and 60th min). All the procedures were performed in a laboratory with room temperature between 20-22oC and relative humidity of the air between 50-60%.

 

Prior to the beginning of the experiment, the subjects were told to: 1) abstain from the ingestion of products containing caffeine for the 72h preceding each experimental session; 2) avoid any type of vigorous physical activity; 3) avoid ingestion of alcohol in the 24h before the days of data collection; 4) eat a light meal 2h before the sessions. Moreover, they were asked to urinate before the sessions.


Diet recall

The subjects were requested to fill out the diet recall forms in detail immediately after eating a meal, using standardized measures to quantify each food and drink consumed, in order to determine the amount of caffeine ingested before and during the experiment for each individual. These details were recorded on two occasions, and the subjects were advised not to change their dietary habits during this period. First, in the week prior to the beginning of the experimental sessions, two days of the week and one day of the weekend were recorded, with the objective of quantifying the habitual consumption of caffeine. Then during the three days preceding each session, a check was done for the possible ingestion of caffeine during the 72h period of abstinence.

 

Maximum effort testing

Subjects submitted to an ergospirometric test of continuous and gradual maximum effort respectively, in a mechanically braked cycle ergometer (Monark, Ergometric), according to the Bird and Davison's protocol 9, for the determination of VO2peak, following the recommendations of the American College of Sports Medicine 10. Each individual did a 5-minute warm-up at light intensity (minimum resistance), and the test began a 50W load, and increments of 25W every two minutes until voluntary exhaustion, defined as the point at which the subject could no longer keep up the work rate (≥ 60rev.min-1). The analysis of the expired gases was made by means of a portable telemetric gas analysis system K4b2 (COSMED, Italy), sampling every 10s.  The VO2peak was represented by the highest consumption of oxygen reached during the test. Later the oxygen consumption was plotted against work rates and the corresponding exercise load (60% VO2peak) was calculated using a linear regression equation.

 

Blood pressure and heart rate

The BP was measured using an automatic oscillometric monitor (Omron HEM-711, USA). MAP was calculated as the DBP plus one-third of the pulse pressure (MAP = DBP + [(SBP - DBP) ÷ 3]). During the whole experiment, BP was measured according to the recommendations of the 7th Joint National Committee 3. Heart rate was recorded at rest and post-exercise, using an electronic heart monitor (Polar RS800 CX, Finland) before the measurements of BP were undertaken.


Heart rate variability

In addition to the measures of BP and HR, the HRV was also analysed, as a means of interpreting the autonomic activity of the heart. This variable was monitored continuously, before, during and after the sessions using a heart rate monitor (Polar RS800 CX, Finland). During the recording of this data, the subjects were seated and breathing freely. All data was recorded to the equipment and immediately downloaded to a computer in order to be analysed with the Polar Pro Trainer 5 software (Kempele, Finland). The Fourier Transform was used to quantify the high and low frequency bands.  The time and frequency domain analyses were performed with five-minute windows using the HRV Analysis software version 1.1 (Kuopio, Finland). HRV was analysed on the frequency domain, using the components of low (LF) and high frequency (HF) and the ratio between both (LF/HF) 11. The HRV data considered for the present study were those recorded before the BP measurements.


Statistical analysis

The Shapiro-Wilk test was used to analyse the distribution of the data and the Levene's test for the homogeneity of variances. For the comparison between sessions of the pre-intervention data of all variables analysed, the Student's t-test for dependent samples was used. The sphericity of the data was verified by the Mauchly's test of sphericity, using the Greenhouse-Geisser correction where necessary. The Two-Way Repeated-Measures ANOVA (session x time) was used for intra- and inter-subject comparisons, followed by the Fisher's LSD post-hoc test, where necessary. All the statistical analyses were conducted using the STATISTICA 7.0 (StatSoft Inc., U.S.A.) software, and the determined statistical significance criterion was P < 0.05.

 

Results

The characteristics of the subjects in the study are described in Table 1. The behaviour of the HR, SBP, DBP and MAP variables at rest, during the pre-exercise period, before and after the ingestion of caffeine or placebo is presented in Table 2. No statistically significant differences were detected for the baseline variables in either of the sessions.


 

Table 1: General characteristics of the sample

Characteristics

Sample (n=10)

Age (years)

24.4 ± 4.5

Body mass (kg)

74.3 ± 11.8

Height (cm)

172.8 ± 8.6

VO2peak (ml.kg-1.min-1)

36.8 ± 5.7

Values on mean ± standard deviation

 


The repeated-measures ANOVA detected a HR reduction (F=4,65; degrees of freedom=6) 20 min (P=0.01) after PLA ingestion and 40, 50 and 60min (P=0.01, P=0.001 and P=0.003, respectively) after caffeine ingestion. There was a reduction of SBP (F=12, 49; degrees of freedom=6) 20min (P=0.03) after the administration of PLA. Conversely, no change was detected after caffeine ingestion.

 

No effect could be observed in DBP after the consumption of placebo; however, the use of caffeine raised DBP (F=8,33; degrees of freedom=6) after 20, 30, 40, 50 and 60min (P=0.01, P<0.001, P<0.001, P<0.001 and P<0.001, respectively). The same pattern of changes was identified in MAP (F=11,01; degrees of freedom=6), with increases after 30, 40, 50 and 60 min (P=0.001, P=0.003, P<0.001 and P=0.001, respectively). In the comparison between the pre-ingestion measurement and the average of the records 60min after ingestion, differences were observed for DBP (P=0.001) and MAP (P=0.003), only with the consumption of caffeine. No difference was detected in the comparison between sessions (PLA vs. CAF).

 


Table 2: Cardiovascular behaviour at rest, before and after caffeine or placebo ingestion

 

 

Pre-ingestion

Post-ingestion

 

 

 

Baseline

10 min

20 min

30 min

40 min

50 min

60 min

Average of 60 min

HR (bpm)

Placebo

76.2 ± 2.1

72.1 ± 3.1

70.3 ± 3.1*

76.0 ± 3.1

74.2 ± 4.2

74.1 ± 3.2

75.5 ± 4.1

73.2 ± 3.3

 

Caffeine

76.4 ± 4.3

75.5 ± 4.3

73.7 ± 5.2

72.2 ± 4.4

70.2 ± 5.1*

68.2 ± 5.2*

68.4 ± 4.2*

71.6 ± 4.3

SBP (mmHg)

Placebo

120.0 ± 4.2

115.9 ± 3.2

114.5 ± 5.3*

117.0 ± 4.3

119.0 ± 5.8

117.1 ± 5.4

118.7 ± 5.0

117.3 ± 4.5

 

Caffeine

116.1 ± 3.1

118.0 ± 3.5

116.7 ± 3.7

121.2 ± 2.4

116.1 ± 4.4

121.0 ± 2.1

120.6 ± 3.1

119.3 ± 2.4

DBP (mmHg)

Placebo

71.8 ± 3.3

72.3 ± 5.3

75.2 ± 3.4

73.1 ± 3.9

73.4 ± 3.6

70.5 ± 3.0

73.0 ± 3.8

73.2 ± 3.4

 

Caffeine

70.1 ± 4.1

74.6 ± 2.8

75.9 ± 3.6*

77.3 ± 3.3*

78.2 ± 4.3*

79.4 ± 2.3*

77.2 ± 2.3*

77.6 ± 3.3*

MAP (mmHg)

Placebo

87.5± 3.7

86.2 ± 4.7

88.5 ± 3.2

87.2 ± 3.4

88.8 ± 3.5

86.3 ± 4.2

88.1 ± 4.2

87.5 ± 3.0

 

Caffeine

85.2 ± 3.3

89.7 ± 2.1

89.0 ± 3.2

92.4 ± 2.1*

91.1 ± 4.3*

93.2 ± 2.4*

92.2 ± 2.1*

91.4 ± 2.2*

Values in mean ± standard error. HR - heart rate; SBP - systolic blood pressure; DBP - diastolic blood pressure; MAP - mean arterial pressure

* p<0,05 vs. rest

 


 


The analysis of the variables' behaviour 10, 20, 30, 40, 50 and 60min after aerobic exercise, in both sessions (CAF and PLA), can be observed in Table 3. The last recorded values (60min) after ingestion were considered as the pre-exercise data for the analysis. During the post-exercise period, in the PLA condition, an increase in HR at 10min (P<0.001) of observation was detected. During the CAF, HR was higher at 10, 20 and 40min of recovery (P<0.001, P=0.007 and P=0.01, respectively). Reductions in SBP were observed 40 and 50min after exercise during the PLA (P=0.009 and P=0.02, respectively), while in the CAF, PEH for SBP was not detected. No alteration could be detected for DBP and MAP during both sessions. No differences were found in the comparison of the baseline measurements and the average of the 60min post-exercise measurements for all the variables. The differences between the sessions were not observed.


 


Table 3: Cardiovascular behaviour before and after an aerobic exercise

 

 

 

Pre-exercise

Post-exercise

 

 

 

Baseline

10 min

20 min

30 min

40 min

50 min

60 min

Average of 60 min

HR (bpm)

Placebo

75.5 ± 4.1

83.2 ± 8.2*

79.2 ± 9.1

78.2 ± 7.3

76.2 ± 7.3

78.4 ± 7.1

74.3 ± 7.3

78.3 ± 7.3

 

Caffeine

68.4 ± 4.2

81.2 ± 5.1*

75.2 ± 4.1*

73.2 ± 4.4

75.3 ± 4.0*

72.3 ± 4.2

73.2 ± 5.3

75.3 ± 4.4

SBP (mmHg)

Placebo

118.7 ± 5.0

118.2 ± 5.0

114.3 ± 5.2

114.1 ± 5.2

111.4 ± 5.8*

112.6 ± 3.2*

116.1 ± 4.3

114.2 ± 4.2

 

Caffeine

120.6 ± 3.1

119.9 ± 2.4

118.1 ± 2.4

120.9 ± 2.5

118.1 ± 3.2

119.0 ± 3.9

118.7 ± 4.3

119.1 ± 2.0

DBP (mmHg)

Placebo

73.0 ± 3.8

73.4 ± 3.3

74.0 ± 3.6

75.3 ± 3.2

72.8 ± 3.4

72.1 ± 3.4

73.3 ± 4.1

73.5 ± 3.1

 

Caffeine

77.2 ± 2.3

77.3 ± 3.6

74.3 ± 2.7

75.3 ± 2.0

80.4 ± 3.5

76.3 ± 3.3

79.4 ± 2.5

77.6 ± 2.7

MAP (mmHg)

Placebo

88.1 ± 4.2

88.7 ± 3.4

87.2 ± 3.4

88.8 ± 4.1

85.7 ± 3.3

85.2 ± 3.2

88.5 ± 4.6

87.6 ± 3.6

 

Caffeine

92.2 ± 2.1

91.3 ± 2.2

89.1 ± 2.3

90.3 ± 2.7

92.3 ± 2.9

90.1 ± 2.7

92.6 ± 2.5

91.3 ± 2.4

Values in mean ± standard error. HR - heart rate; SBP - systolic blood pressure; DBP - diastolic blood pressure; MAP - mean arterial pressure

* p<0,05 vs. rest

 


Table 4 shows the average of the observation period for the measurements at rest, post-ingestion and post-exercise periods for the HRV components (LF, HF, LF/HF, LFnu and HFnu) in both sessions (PLA and CAF). The post-ingestion value corresponds to the pre-exercise value. No differences in the HRV components were observed between experimental sessions. However, increases in the LF component (F=3,54; degrees of freedom=6), after ingestion, were detected at rest (PLA; P=0.04 and CAF; P< 0.001, respectively) and after exercise (CAF; P=0.002). For the HF component, only CAF caused changes on the HRV parameters (F=4,21; degrees of freedom=6), with an increase after ingestion in relation to both rest (P< 0.001) and post-exercise periods (P=0.005).


 


Table 4: Components of heart rate variability at baseline and average of 60min post-ingestion and post-exercise

 

PLACEBO

CAFFEINE

 

Baseline

Post-ingestion/

Pre-exercise

Post-exercise

Baseline

Post-ingestion/

Pre-exercise

Post-exercise

LF (ms2)

483.7 ± 221.2

721.9 ± 284.7 *

555.9 ± 314.5

501.8 ± 351.5

1045.7 ± 579.9 *

659.5 ± 354.7 †

HF (ms2)

199 ± 138.4

262.5 ± 151.7

209.5 ± 132.4

226 ± 188.5

379.9 ± 209.5 *

255.8 ± 188.2 †

LF/HF

3.06 ± 1.5

3.7 ± 2.6

3.2 ± 1.2

3.17 ± 1.7

3.1 ± 0.8

2.9 ± 1.1

LF (nu)

71.6 ± 10.7

72.9 ± 9.6

72.5 ± 6.9

72.3 ± 11.1

72.7 ± 4.2

71.1 ± 8.4

HF (nu)

28.3 ± 10.7

26.3 ± 9.5

27.1 ± 7.1

27.6 ± 11.1

27.2 ± 4.2

28.1 ± 7.9

Values in mean ± standard error; * P ≤ 0,05 vs. rest; †  P ≤ 0,05 vs. average of 60min post-ingestion

Discussion

The results of the present study show that CAF did not change HR, SBP, DBP and MAP responses at rest or after exercise in comparison to PLA. Similarly, the indicators of the autonomic activity of the heart showed no differences between the experimental sessions.

 

With regard to the analyses of BP at rest, average rises of 5mmHg in SBP, 7-8mmHg in DBP and 6-7mmHg in MAP were detected, with statistical significance from the 20th-60thmin in the DBP and from the 30th-60thmin in MAP, after CAF ingestion. For both variables, higher values were reached for the average of the 60min measurement in comparison to the pre-caffeine ingestion value.

 

These results are in accordance with the scientific evidence for the acute effect of the administration of a dose of CAF in raising resting BP 1,2, occurring approximately 30min after the ingestion 2,12. For instance, the papers of James 1 and Nurminem et al. 2 about the acute impact of CAF on BP indicated increases in the SBP ranging from 3-15mmHg and 4-13mmHg in the DBP. The main mechanism by which CAF influences BP appears to be the rise of the peripheral vascular resistance by its antagonistic effect on adenosine 1,13. It is possible that this effect could be observed in the present study, because rises in BP were detected, mainly in the DBP, concomitantly with reductions in the HR over the same period.

 

The reduction of HR may have occurred due to a baroreflex adjustment in an attempt to compensate for the rise of BP. These results corroborate the findings of some researchers who had verified a reduction in HR after CAF administration 6,14-16. However, the results observed in the literature regarding the effect of CAF on resting HR show that the substance may have a weak association with this variable, presenting controversial results of increase 1, reduction 6,14-16 or no change 19-20. Consequently, the HRV analysis revealed higher values of LF and HF after CAF ingestion in comparison to the rest.

 

Independently of the values found in isolated measurements, the analysis of the average of the whole monitoring period after CAF ingestion did not show inter-group differences. Accordingly, although the values of BP and HR had been modified in certain measurements, such behaviour was not long-lasting. Therefore these researchers cannot affirm that CAF has definitely contributed to the changes in HR or BP during the 60min post-ingestion period.

 

Regarding the behaviour of BP after a single session of exercise, particularly with regard to aerobics some studies showed reductions in SBP after effort 8,21-26. In contrast, there is the possibility that the consumption of a dose of CAF, equivalent to the daily habitual adult caffeine consumption (approximately 4mg.kg-1) 27 might attenuate the reductions of BP after exercise. However, previous research tracked the cardiovascular variables for only 10min after the exercise. Considering that PEH can be detected for many hours 28, extremely short periods of observation may be insufficient to provide an adequate understanding of the cardiovascular responses. With this in mind, for the present research, the monitoring of BP for 60min after exercise in the laboratory environment was chosen. The present authors understand that the control of the variables in this period is reasonable in order to analyse possible cardiovascular changes.

 

Accordingly, during the PLA session, reductions in the SBP were detected during the average magnitude of 5-7mmHg, significant for the 40th and 50thmin and a rise in HR during the 10thmin of observation. In DBP and MAP no significant differences were observed post-exercise in comparison with the pre-exercise period. These results agree with the findings of previous studies involving the post-aerobic-exercise hypotension in normotensive individuals, which detected reductions in SBP without significant alterations in DBP and MAP 8,21,22,24-26. Conversely, some studies show significant reductions in both SBP and DBP, in the first minutes 29-33, first hours 29,31,34-36 and up to 24 hours of monitoring 28. Additionally, some researchers report increases 37 or no alteration 38,39 in the post-aerobic-exercise SBP.

 

It is important to notice that the conflicting data involving PEH may result from factors for the different characteristics of the studied samples (age-group and initial levels of BP), the period of post-exercise monitoring (from a few minutes up to 24h) and the different forms of exercise prescription (intensity and duration), making it difficult to contrast findings between the studies 5.

In the present study, the ingestion of CAF resulted in increases of HR in 10, 20 and 40min of monitoring. Information about the effect of CAF on post-exercise HR is scarce.  Some experiments that investigated the influence of CAF on this variable during exercise have shown an increase 14, reduction 14,16 or no change 19,20,40 in HR. Thus the change in HR during exercise could have some repercussions in the behaviour observed after the effort.

 

No differences in the baseline pre-exercise records for SBP, DBP and MAP were detected. These results corroborate those previously found by Notarius et al. 6, who observed attenuation in the reductions of BP after a session of moderate aerobic exercise, interfering with the occurrence of the PEH. Although biochemical variables that could explain these results were not measured, based on the evidence in the scientific literature, the main mechanism by which caffeine acts on the cardiovascular system is the antagonism of adenosine 27, a vasodilator substance produced during exercise that appears to have an important role in the post-aerobic-exercise hypotension in middle-aged normotensive individuals 6, as previously observed, and in adults, in accordance with the presented results in this study.

 

Although there were changes in some measurements of BP and HR, the average of the post-exercise 60min monitoring period showed no difference between groups. As a result, these researchers cannot affirm that caffeine influenced the HR and BP responses. On the other hand, in the average of the post-exercise 60min monitoring period, the HRV components (LF and HF) were lower when compared to the post-caffeine ingestion period. Yet these values showed no differences in relation to the values at rest. Additionally, there were no observed differences in the three sections (rest, post-ingestion and post-exercise) between the experimental sessions, a fact that does not confirm the affirmation that there was a predominance of the sympathetic component (LF) in the post-exercise period after caffeine ingestion.

 

Although the sample size was calculated, it is possible that the number of subjects has influenced the results of the present study. Furthermore, the laboratory monitoring allows the monitoring of the cardiovascular variables without the influence of potentially confounding variables, the 60min period of monitoring hinders the extrapolation of the results with regard to the behaviour of these variables outside the laboratory environment.

 

Conclusion

Based on the results of the present study, the ingestion of a 4mg.kg-1 dose of caffeine apparently does not significantly interfere, continuously, on the cardiovascular behaviour in the rest (post-ingestion) or in the attenuation of PEH, as the levels of post-exercise BP were different between the CAF and PLA sessions at specific moments. Similarly, the behaviour of the HRV components did not differ between the experimental sessions at all times.

 

Address for correspondence:

Dr Marcos Doederlein Polito, Departamento de Educação Física - Universidade Estadual de Londrina - Rod. Celso Garcia Cid, km 380 - CEP 86051-980 - Londrina - PR – Brazil

Email: marcospolito@uel.br or marcospolito@bol.com.br

 

References

1.      James JE. Critical review of dietary caffeine and blood pressure: a relationship that should be taken more seriously. Psychosom Med 2004; 66 (1): 63-71.

2.      Nurminen ML, Niittynen L, Korpela R et al. Coffee, caffeine and blood pressure: a critical review. Eur J Clin Nutr 1999; 53 (11): 831-839.

3.      Chobanian AV, Bakris GL, Black HR et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42: 1206-1252.

4.      Pescatello LS, Franklin BA, Fagard R et al. American College of Sports Medicine position stand: exercise and hypertension. Med Sci Sports Exerc 2004; 36 (3): 533-553.

5.      Casonatto J, Polito MD. Post-exercise hypotension: a systematic review. Rev Bras Med Esporte 2009; 15 (2): 152-158.

6.      Notarius CF, Morris BL, Floras JS. Caffeine attenuates early post-exercise hypotension in middle-aged subjects. Am J Hypertens 2006; 19 (2): 184-188.

7.      Yeragani VK, Krishnan S, Engels HJ, Gretebeck R. Effects of caffeine on linear and nonlinear measures of heart rate variability before and after exercise. Depress Anxiety 2005;21(3):130-134.

8.      Bird S, Davison R. Physiological testing guidelines. Leeds: B.A.S.E.S., 1997.

9.      Jones H, George K, Edwards B et al. Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done? Eur J Appl Physiol 2007; 102 (1): 33-40.

10.   Armstrong LE, Balady GJ, Berry MJ et al. ACSM's guidelines for exercise testing and prescription. 7th. New York: Lippincott, Williams & Wilkins, 2006.

11.   Heart rate variability: standards of measurement, physiological interpretation and clinical use. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Circulation. 1996;93(5):1043-1065

12.   Mort JR, Kruse HR. Timing of blood pressure measurement related to caffeine consumption. Ann Pharmacother 2008; 42 (1): 105-110.

13.   Farag NH, Vincent AS, Mckey BS et al. Hemodynamic mechanisms underlying the incomplete tolerance to caffeine's pressor effects. Am J Cardiol 2005; 95 (11): 1389-1392.

14.   Notarius CF, Atchison DJ, Rongen GA et al. Effect of adenosine receptor blockade with caffeine on sympathetic response to handgrip exercise in heart failure. Am J Physiol Heart Circ Physiol 2001; 281 (3): H1312-H1318.

15.   Corti R, Binggeli C, Sudano I et al. Coffee acutely increases sympathetic nerve activity and blood pressure independently of caffeine content: role of habitual versus nonhabitual drinking. Circulation 2002; 106 (23): 2935-2940.

16.   McClaran SR, Wetter TJ. Low doses of caffeine reduce heart rate during submaximal cycle ergometry. J Int Soc Sports Nutr 2007; 4:11.

17.   Hibino G, Moritani T, Kawada T et al. Caffeine enhances modulation of parasympathetic nerve activity in humans: quantification using power spectral analysis. J Nutr 1997; 127 (7): 1422-1427.

18.   Sondermeijer HP, Van Marle AGJ, Kamen P et al. Acute effects of caffeine on heart rate variability. Am J Cardiol 2002; 90 (8): 906-1007.

19.   Daniels JW, Molé PA, Shaffrath JD et al. Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise. J Appl Physiol 1998; 85 (1): 154-159.

20.   Engels HJ, Wirth JC, Celik S et al. Influence of caffeine on metabolic and cardiovascular functions during sustained light intensity cycling and at rest. Int J Sport Nutr 1999; 9 (4): 361-370.

21.   Halliwill JR, Taylor JA, Eckberg DL. Impaired sympathetic vascular regulation in humans after acute dynamic exercise. J Physiol 1996; 495 (pt 1) 279-288.

22.   Pescatello LS, Fargo AE, Leach CNJ et al. Short-term effect of dynamic exercise on arterial blood pressure. Circulation 1991; 83 (5): 1557-1561.

23.   Headley SA, Claiborne JM, Lottes CR et al. Hemodynamic responses associated with post-exercise hypotension in normotensive black males. Ethn Dis 1996; 6 (1-2): 190-201.

24.   Raglin JS, Turner PE, Eksten F. State anxiety and blood pressure following 30 min of leg ergometry or weight training. Med Sci Sports Exerc 1993; 25 (9): 1044-1048.

25.   MacDonald JR, MacDougall JD, Interisano SA et al. Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise. Eur J Appl Physiol Occup Physiol 1999; 79 (2): 148-154.

26.   Terziotti P, Schena F, Gulli G et al. Post-exercise recovery of autonomic cardiovascular control: a study by spectrum and cross-spectrum analysis in humans. Eur J Appl Physiol 2001; 84 (3): 187-194.

27.   Fredholm BB, Bättig K, Holmén J et al. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 1999; 51 (1): 83-133.

28.   Forjaz CLM, Tinucci T, Ortega KC et al. Factors affecting post-exercise hypotension in normotensive and hypertensive humans. Blood Press Monit 2000; 5 (5-6): 255-262.

29.   MacDonald JR, MacDougall JD, Hogben CD. The effects of exercise duration on post-exercise hypotension. J Hum Hypertens 2000; 14 (2): 125-129.

30.   MacDonald JR, MacDougall JD, Hogben CD. The effects of exercise intensity on post exercise hypotension. J Hum Hypertens 1999; 13 (8): 527-531.

31.   Moraes MR, Bacurau RF, Ramalho JD et al. Increase in kinins on post-exercise hypotension in normotensive and hypertensive volunteers. Biol Chem 2007; 388 (5): 533-540.

32.   Jones H, Pritchard C, George K et al. The acute post-exercise response of blood pressure varies with time of day. Eur J Appl Physiol 2008; 104 (3): 481-489.

33.   Brown SP, Clemons JM, He Q et al. Effects of resistance exercise and cycling on recovery blood pressure. J Sports Sci 1994; 12 (5): 463-468.

34.   Forjaz CLM, Matsudaira Y, Rodrigues FB et al. Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans. Braz J Med Biol Res 1998; 31 (10): 1247-1255.

35.   Forjaz CLM,Santaella DF,Rezende LO et al. Effect of exercise duration on the magnitude and duration of post-exercise hypotension. Arq Bras Cardiol 1998; 70 (2): 99-104.

36.   Forjaz CLDM, Cardoso CGJ, Rezk CC et al. Postexercise hypotension and hemodynamics: the role of exercise intensity. J Sports Med Phys Fitness 2004; 44 (1): 54-62.

37.   Pescatello LS, Guidry MA, Blanchard BE et al. Exercise intensity alters postexercise hypotension. J Hypertens 2004; 22 (10): 1881-1888.

38.   Wallace JP, Bogle PG, King BA et al. A comparison of 24-h average blood pressures and blood pressure load following exercise. Am J Hypertens 1997; 10 (7 Pt 1): 728-734.

39.   Wallace JP, Bogle PG, King BA et al. The magnitude and duration of ambulatory blood pressure reduction following acute exercise. J Hum Hypertens 1999; 13 (6): 361-366.

40.   Sung BH, Lovallo WR, Pincomb GA et al. Effects of caffeine on blood pressure response during exercise in normotensive healthy young men. Am J Cardiol 1990; 65 (13): 909-913.