A single bout of dynamic (6,7) or static (12) exercise can result in a postexercise hypotension (PEH) lasting up to 2 h. PEH has been reported in sedentary and endurance-trained men and women (6,7,19). It is frequently caused by a single bout of submaximal exercise at 60% of maximal oxygen uptake (V̇O2max) lasting between 40 and 60 min (6,7), although it can occur at exercise intensities ranging from 40 to 70% of V̇O2max (13). PEH is especially pronounced in hypertensive patients, where it can persist up to 17 h after exercise (15), suggesting that submaximal exercise can be considered as an antihypertensive nonpharmacological treatment (13). The hypotensive effect is predominantly associated with a reduction in TPR that is not counterbalanced with increases in cardiac output (6,7,9).
Senitko et al. (19) found that endurance training did not reduce PEH, either in prevalence or magnitude of response. In endurance-trained women, hypotension was the result of peripheral vasodilatation as had been shown previously in sedentary individuals, whereas in endurance-trained men, it was caused by reduced cardiac output (because of a fall in stroke volume) and unchanged TPR. The aerobic capacity in endurance-trained men in this report, however, was not large (∼46 mL·kg−1·min−1) and was equivalent to the aerobic capacity of recreational subjects.
In most studies investigating PEH, submaximal exercise protocols were used, whereas the occurrence and the mechanism of PEH after maximal exercise in moderately endurance-trained athletes are less known. Maximal exercise to exhaustion causes physiological and psychological changes such as metabolic acidosis, hyperventilation, and severe discomfort, not encountered during submaximal exercise. The mechanism of PEH after maximal exercise has been investigated only in sedentary, normotensive individuals (11,17).
The present study investigated the occurrence and mechanisms of PEH in moderately trained athletes after short maximal exercise.
A total of 20 professional soccer players of the Croatian national champion team, Hajduk Split, were included in the study. Their mean age was 22.0 ± 2.9 (mean ± SD) yr (range 19-31), height 184.4 ± 6.3 cm (range 174-194), and weight 81.8 ± 5.8 kg (range 72-93). The subjects composed the first selection of the Hajduk Split senior team. At the time of the experiment, their averaged weekly training programs included six training sessions per week (each training lasting for approximately 90 min), mainly in soccer training. They also participated to one official game per week. The study cohort was composed of three goalkeepers, eight defenders, six midfield players, and three forwards. One subject was a medium smoker and the remaining 19 were nonsmokers. None of the subjects reported active asthma or the use of any medication. Each had normal screening physical examination, electrocardiogram, and spirometry. Informed consent was signed by all subjects and the study protocol was approved by the ethical committee of the University of Split School of Medicine.
Baseline physiological measurements of cardiopulmonary parameters were compared with identical measurements taken at 30 and 60 min after maximal exercise. The subjects reported to the soccer stadium at 10:00 a.m. after a 36-h period without intense exercise. They came to the indoor laboratory at the soccer stadium 1-2 h after a light breakfast containing no caffeinated beverages. Before the test, each subject was familiarized with the exercise testing protocol and the laboratory setting. After medical examination, 30 min of rest in the seated position was used to allow the subjects to adjust to the controlled laboratory setting and the required seated posture. At the end of resting period, baseline measurements were taken. It was previously shown that PEH occurs regardless of the body position (2,5,6). The laboratory was comfortably warm (23.8 ± 0.8°C) and quiet. After collection of baseline cardiovascular parameters, the subjects walked to the athletic field (100-m distance). This was followed by a 10-min warm-up (stretching and slow running) and after that the subjects performed the maximal exercise testing until exertion, which occurred within 9-13 min for all players. The same protocol used in the field condition was previously reported in the laboratory (1). The initial speed of running was 8 km·h−1, with an increase in running speed by 1 km·h−1 each following minute up to maximal effort. The subjects were paced on the athletic field (400 m in length) by a bicycle with an electronic chronometer and tachometer. During the entire test, heart rate (HR) was registered continuously with Polar HR monitor (Polar Vantage, Finland) and spiroergometry was monitored by portable K4 b2 breath-by-breath telemetric unit (Cosmed, Italy). After exercise testing, subjects disconnected from the K4 unit and returned to the laboratory for postexercise measurements, which were done 30 and 60 min after exercise. The subjects were restricted in water intake until all measurements were completed.
Arterial blood pressure and heart rate.
The systolic and diastolic blood pressures (SBP and DBP) were measured noninvasively by the oscillometric or auscultatory method (Tango, Sun Tech). Arterial pulse pressure (PP) was calculated as SBP-DBP. The mean arterial pressure (MAP) was calculated as two thirds DBP + one third SBP. Postexercise hypotension was defined by reduction of SBP and DBP of 4-5 mm Hg after exercise in comparison with baseline values.
Maximal oxygen uptake.
During exercise, oxygen uptake, HR, and lung ventilation were determined a with portable K4 b2 breath-by-breath telemetric unit (Cosmed). The unit was first calibrated to a known concentration of O2 and CO2, a given volume of air, and to the atmospheric pressure. Respiratory gas concentrations, HR, and the ventilatory volumes were telemetrically relayed to a portable computer. HR and the respiratory data were provided on a report once every 30 s with the values averaged over the last 10 respiratory cycles. Criteria for assessment of V̇O2max included a respiratory exchange ratio (RER) ≥1.1 and a plateau (≤150 mL increase) in V̇O2, despite an increase in workload. The highest HR attained at maximal oxygen uptake represents maximal HR. Anaerobic threshold was determined from the increase in the ventilatory equivalent for O2 (VE/V̇O2), without a concomitant increase in the ventilatory equivalent for CO2 (VE/V̇CO2) (4). The mean relative V̇O2max and the maximal HR (HRmax) at V̇O2max was 56.3 ± 4.7 mL·kg−1·min−1and 186.6 ± 6.1 bpm, respectively. The absolute V̇O2max was 4633.5 ± 523.7 mL·min−1. Duration of the field test was 11.4 ± 0.9 min, and the running speed at V̇O2max was 19.2 ± 1 km·h−1. The anaerobic threshold was at 79.7 ± 6.6% V̇O2max.
Cardiac output (Q) was estimated by the indirect Fick method of carbon dioxide (CO2) rebreathing to equilibrium, as described previously (3). The equilibrium fraction of CO2 was given by extrapolation, using the regression line between 8- and 12-s rebreathing intersects at 20 s after the start of the rebreathing maneuver (Cosmed B2, Italy). Q was measured in duplicate and the rebreathing bag was thoroughly flushed between two rebreathing periods. Stroke volume (SV) was calculated as Q/HR and TPR as MAP/Q (mm Hg·min−1·L−1). Because a single-breath DLCO maneuver causes decreases in Q, SBP, and DBP (10), in this study Q was measured in the test series before DLCO. Q measurements with CO2 rebreathing technique before exercise and during PEH have been used by others (2,5,6).
Diffusing lung capacity for carbon monoxide.
Diffusing lung capacity for carbon monoxide (CO) (DLCO) was determined by the single-breath method. Concentrations of CO were measured using an infrared analyzer (Quark PFT, Cosmed, Italy). Alveolar volume was measured by single-breath methane dilution and DLCO/VA was calculated.
Data are expressed as mean ±SD. Comparisons between preexercise and postexercise measurements were done with nonparametric Friedman and Wilcoxon rank sign tests. Associations between quantitative variables were evaluated by Pearson's coefficient of correlation. P < 0.05 was considered significant.
Baseline vital signs were normal in all subjects, with HR averaging 59.6 ± 5.9 bpm and with SBP and DBP pressure averaging 129.8 ± 8.8 and 73.0 ± 6.7 mm Hg, respectively (Table 1). All 20 subjects successfully completed the study protocol. No subject reported any symptom (e.g., fainting or lightheadedness) after exercise.
Significant lowering of SBP, DBP and MAP were found 30 and 60 min after exercise (Table 1). Interestingly, the decrease in BP was noticed in all of the goalkeepers, but was not present in forward players. The HR increased at 30 min and remained increased at 60 min after exercise, whereas SV, CO, and DLCO decreased. TPR did not change significantly after exercise. Nonsignificant increases observed, mean that a decrease (but not an increase) in TPR after exercise can be safely excluded (Table 1).
At 60 min postexercise, the lesser the V̇O2max, the greater decrease in DBP (r = −0.73, P = 0.0001, Fig. 1), but not in SBP (r = −0.03, P = 0.91) was observed. No correlations were observed at 30 min postexercise. Also, at 60 min postexercise, the greater the SBP, the greater decrease in SBP was observed (r = 0.51, P = 0.023, Fig. 2), which was not the case for DBP (r = 0.24, P = 0.31).
In the present study, we investigated the occurrence and cause of postexercise hypotension in moderately trained endurance athletes after short-term maximal exercise. The main findings are (a) there may be less PEH in the subjects with higher V̇O2max values, (b) PEH can be seen after brief but maximal exercise, (c) PEH may occur more frequently in subjects with higher baseline SBP, and (d) in more trained subjects, the mechanisms causing PEH probably differ from the mechanisms in untrained people.
Central and peripheral hemodynamics after maximal exercise.
Postexercise hypotension after a single bout of dynamic exercise in sedentary men and women and endurance-trained women is the result of a reduction in TPR (6,7,9). Our results indicate that PEH in endurance-trained soccer players is related to reduced cardiac output caused by stroke volume reduction, because the TPR was unchanged. Similar findings were reported previously by Hagberg et al. (5) in older hypertensive persons and by Senitko et al. (19) in endurance-trained men after submaximal exercise. Hagberg et al. (5) suggested that reduction in cardiac output was related to reduced myocardial contractility, whereas Senitko et al. (19) explained this effect by reduction in central venous pressure (CVP) and, thus, cardiac preload.
Possible factors affecting stroke volume are preload, afterload, and myocardial contractility. Afterload was likely to be lower after exercise in this study because of lower SBP. A single index of increased efferent sympathetic nervous activity after exercise was persistent tachycardia up to 60 min Raine et al. (17) reported increased ejection fraction from 61% at baseline to 71% after maximal exercise, indicating increased inotropy postexercise. The likely mechanism for reduction of stroke volume after exercise in the present study was a decline in cardiac filling, given that afterload was reduced and that myocardial contractility was probably increased. Cardiac preload is dependent on changes in plasma volume and venous capacitance. Plasma volume change was not measured in this study. It is unlikely that any significant changes in plasma volume occurred in this study, given the short exercise time (9-13 min), cooler environment, and unrestricted pretrial water intake. The main factor reducing cardiac filling in this study is likely the hydrostatic gradient secondary to the upright seated posture as well as pooling of blood in the previously active muscle. Other potential mechanism underlying the reduced venous return after exercise is the redistribution of cardiac output from less compliant to more compliant vascular beds such as splanchnic organs and skin (18). Halliwill et al. (8) found that whole-limb venous compliance is under negligible active sympathetic control in humans, suggesting the possibility of venous pooling in the leg vasculature in addition to splanchnic and skin beds. Similar vasodilatation in the visceral organs or lower limbs leading to pooling of blood and a decrease in venous return after submaximal exercise was proposed by Brown et al. (2). Renal and splanchnic (16) vascular beds, however, are not involved in postexercise vasodilatation.
Diffusing lung capacity for CO was reduced in this study for about 10% as was previously reported by others after exercise of different duration, intensity, and sport (14). Finding of reduced DLCO in this study appears to support the theory of peripheral pooling and reduced central blood volume after maximal exercise.
It appears that longer bouts of exercise (1 h vs 30 min) produce more PEH (6,7). The effects of exercise intensity and duration on PEH remain unresolved. Probably more sustained PEH occurs after moderate intensity, longer lasting exercise (7), but short, maximal exercise might produce a greater, but less sustained, fall in BP. This study adds to the existing knowledge of the occurrence of PEH by reporting that most of trained soccer players experienced PEH up to 1 h after the maximal field exercise. The average drop in MAP in the supine position was 4-5 mm Hg, but often ranged from 1 to 14 across individuals. The subjects with the greater decrease in SBP had its higher baseline value, which is in accord with findings in hypertensive patients (15). This finding indicates that brief maximal exercise causes a similar fall in BP as longer submaximal protocols, which may prove important in considering hypertension treatment. Future studies should address the sustainability of this effect.
Our subjects had mean V̇O2max of 56 mL·kg−1·min−1, which places them in the lower range of elite soccer players (10). This was partly because three goalies had relative V̇O2max of approximately 51 mL·kg−1·min−1. We are lacking data to differentiate between the lack of training (more probably) and limited capacity for higher V̇O2max. We therefore suggest that the occurrence of PEH in trained subjects is dependent on the cardiopulmonary fitness and is more frequent in the subjects with lower fitness status.
The endurance-trained subjects in this study were only moderately trained. Future study therefore needs to evaluate postexercise hypotension in highly trained athletes (e.g., cyclists, rowers, or runners).
This study indicates that in more trained men, the mechanisms causing PEH probably differ from the mechanisms in those who are untrained. We suggest that PEH in trained men is associated with reduced cardiac output, because of reduced cardiac filling. The main factor reducing cardiac filling in this study is likely the hydrostatic gradient secondary to the upright posture as well as the pooling of blood in the previously active muscle. The lower fitness level or higher baseline SBP is associated with higher occurrence of postexercise hypotension.
The authors wish to express their thanks to Jolanda Zlokovic` for her technical assistance. This study was financially supported by the Croatian National Council for Research grant no. 0216006.
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