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1 Department of Science Applied to Biological Systems, Section of Human Physiology, University of Cagliari, Italy 2 Department of Biological Science, University of Torino, Italy
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Abstract |
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(Received 6 May 2004;
accepted after revision 12 August 2004; first published online 24 August 2004)
Corresponding author A. Crisafulli: Department of Sciences applied to Biological Systems, Section of Human Physiology, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy. Email: crisafulli{at}tiscali.it
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Introduction |
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Notwithstanding that supramaximal exercise bouts frequently occur in many sports (Bangsbo, 1996), only a few studies to date have focused on haemodynamics after this kind of exercise (Kilgour et al. 1995; Crisafulli et al. 2003a). In fact, most of the studies were concerned with exercise recovery following submaximal or maximal exercise intensity both in athletes and in sedentary individuals (Takahashi & Miyamoto, 1998; Carter et al. 1999; Takahashi et al. 2000; Raine et al. 2001; Nottin et al. 2002). Some of these studies reported postexercise hypotension and syncope during passive recovery (Fleg & Lakatta, 1986; Crisafulli et al. 2000). Our group recently reported that passive recovery from a single bout of supramaximal bicycle exercise led to a lower stroke volume (SV) and cardiac output (CO) with respect to active recovery (Crisafulli et al. 2003a). It was concluded, however, that this apparent impairment in cardiovascular function was fully explainable by reduced muscular and metabolic engagement during passive compared to active recovery, since arterial blood pressure and arterio-venous O2 difference were not different between the two recovery conditions. Nevertheless, a single bout of supramaximal exercise probably did not suffice to stress the cardiovascular homeostasis in athletes accustomed to bouts of this kind of effort. The question then arises whether repeated bouts of supramaximal exercise should be performed to sufficiently stress the cardiovascular system of athletes in order to detect any difference in haemodynamic response between active and passive recovery. To the best of our knowledge, cardiodynamics of this particular recovery situation have not been investigated.
We previously reported that five bouts of supramaximal exercise spaced by active recovery can massively elicit anaerobic metabolism, and that the amount of anaerobic energy sources recruited during high-intensity intermittent efforts correlate well with field performance (Crisafulli et al. 2002b). On this basis and because muscle activity during active recovery can sustain metaboreflex, heart rate and venous return, we hypothesized that this mode of recovery following repeated bouts of supramaximal exercise might lead to a better haemodynamic response than passive recovery and it would reduce the risk of postexercise hypotension and syncope. It can also be hypothesized that subjects accustomed to repeated bouts of supramaximal exercise may develop specific adaptation which could compensate for the cardiovascular stress induced by passive recovery (Crisafulli et al. 2003a). Thus, to verify these hypotheses and to improve our knowledge of haemodynamic adjustments during recovery periods occurring in sport activities involving bursts of supramaximal exercise, we investigated haemodynamic response during two modes of recovery (active and passive) from repeated bouts of this kind of effort.
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Methods |
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We recruited seven male volunteers (soccer players), whose mean ± S.E.M. values of age, height and weight were 28.7 ± 1.4 years, 177.8 ± 2.3 cm and 72.8 ± 2.1 kg, respectively. All subjects were free of any cardiovascular or pulmonary disease, with normal electrocardiogram during rest, exercise and recovery; no one reported suffering from postexercise intolerance or hypotension. Each subject gave written informed consent to participate to this study, which was performed according to the declaration of Helsinki and approved by the local ethics committee.
Experimental design
Before entering the study, subjects performed a preliminary bicycle incremental test on an electromagnetically braked cycle-ergometer (Tunturi EL 400, Finland) to assess the maximum workload achievable (Wmax). This test consisted of a linear increase of workload of 20 W min–1, starting from 20 W, at a pedalling frequency of 60 r.p.m., up to exhaustion (i.e. the point when the subject was unable to maintain a pedalling rate of at least 50 r.p.m). During this preliminary test oxygen consumption 
and carbon dioxide production 
were also measured. Mean ±
S.E.M. values of maximum heart rate (HR) and Wmax reached were 178.5 ± 1.5 beats min–1 and 212.7 ± 12.6 W, respectively. Maximum values of 
and 
were 3.54 ± 0.16 and 4.15 ± 0.24 l min–1, respectively.
On separate days from this preliminary test, each subject underwent the following study protocol (Fig. 1), randomly assigned to eliminate any order effect.
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(b) Passive recovery (PR) test featured the same rest–warm-up–exercise–recovery protocol employed for AR, but the subjects stopped on the bicycle without moving their legs during the recovery between and after the bouts of supramaximal exercise. As can be inferred, the total length of AR and PR tests was 22.5 min (3 min of rest; 3 min of warm-up; 6.5 min of supramaximal exercise bouts spaced by recovery periods; and 10 min more recovery).
(c) Control rest (CR) test. On this day each subject reported to the laboratory and sat quietly on the cycle-ergometer for 22.5 min in order to obtain reference control rest values in the same environmental conditions as the supramaximal exercise protocols. This protocol session was applied to verify whether this condition (i.e. seated on the cycle) per se, without any exercise, could affect haemodynamic variables and to obtain a reference control rest condition to which data from AR and PR tests could be compared.
All experiments were conducted between 09.00 and 12.00 h in a temperature-controlled room and were separated from each other by at least 3 days. Subjects had a light meal at least 2 h before the exercise tests.
Haemodynamic measurements
Haemodynamic variables were measured by means of an impedance cardiograph (NCCOM 3, BoMed Inc., Irvine, CA, USA). This device allows continuous non-invasive cardiodynamic evaluation during rest, exercise and recovery (Crisafulli et al. 2000, 2002a, 2003b) and it has already been used in a similar experiment (Crisafulli et al. 2003a). NCCOM 3 was connected to the subject by arranging eight commercially available spot electrodes. Two thoracic sensing electrodes were placed perpendicularly to the longitudinal plane of the sternum, laterally to the xiphoid process, in the mid-axillary line. Two cervical sensing electrodes were placed close to the clavicles at the base of the neck. Two pairs of current-injecting electrodes (2.5 mA, 70 kHz) were placed 5 cm above the cervical and below the thoracic sensing electrodes. Through a digital chart recorder (ADInstruments, PowerLab 8sp, Castle Hill, Australia) we stored NCCOM 3-derived analog traces of electrocardiogram, thorax impedance (Z0), and the Z0 first derivative (dZ/dt). Stored traces were later analysed, and signals affected by movement and respiratory artefacts were excluded from calculations. Stroke volume was calculated using the Sramek–Bernstein equation (Bernstein, 1986):
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| (1) |
Subjects were also connected to a standard manual sphygmomanometer for systolic (SBP) and diastolic blood pressure (DBP) assessment, which was made in the left arm by the same physician throughout all protocol sessions. Since it was found that the exercise-induced increase in HR causes a greater reduction in the diastolic than in the ejection period, to calculate mean blood pressure (MBP) we employed the formula previously described by Moran et al. (1995). This formula allows calculation of MBP, taking into account changes in the diastolic and systolic periods caused by exercise tachycardia. In particular, the fraction of systole (FS) from the heart cycle was assessed and MBP was then calculated from DBP and the pulse pressure (PP) adjusted for FS as follows: DBP + (FS x PP). We obtained systemic vascular resistance (SVR) by multiplying by 80 the MBP:CO ratio.
Data analysis
Haemodynamic data were averaged for 3 min during rest and the warm-up period, and for 1 min during the recovery periods between and after the supramaximal exercise bouts for both AR and PR tests. The corresponding time points of the CR test were averaged in the same manner. We do not show data concerning the supramaximal efforts because we could not gather artefact-free impedance traces in this condition for all seven subjects in the study, since the movements generated during the heavy efforts compromised readability of the impedance signals (see Considerations about haemodynamic measurement for more details).
Results are presented as means ± S.E.M. Statistical analysis was performed by employing commercially available software (Sigma Stat 2.03). For statistical analysis we considered changes from resting values. Comparisons were performed using two-way analysis of variance (ANOVA) for repeated measures (factors: recovery mode and time) followed by Newman–Keuls post hoc test when appropriate. Statistical significance was set at a P value of <0.05 in all cases.
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Results |
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The observations at rest did not show any significant difference between the three protocol sessions (Table 1). Throughout the CR test haemodynamic parameters were stable, so it could be stated that haemodynamic variables were unaffected by this condition (i.e. seated on the cycle).
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at the 10th minute of PR versus
+0.05 ± 0.3 and +0.3 ± 0.1 at corresponding time points of AR and CR tests, respectively, P < 0.05 in both cases; Fig. 3, middle panel). Ventricular filling rate (Fig. 3, bottom panel) was significantly higher during the AR than during the PR test starting from the last minute of recovery between exercise bouts and throughout the period of recovery after all exercise bouts. During the PR test this parameter gradually returned to values not different from the CR test (+45.7 ± 13.8 versus
–3.5 ± 7.1 ml s–1, respectively, at the 10th minute of recovery after all exercise bouts, P > 0.05). However, during AR it remained higher than the level observed during the PR and CR tests (+190.9 ± 73.1 ml s–1 at the 10th minute of recovery after all exercise bouts, P < 0.05 versus PR and CR tests).
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Discussion |
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The differences in HR behaviour between the two recovery conditions are in line with previous findings that HR decreases less during active than passive recovery following submaximal (Carter et al. 1999) or supramaximal efforts (Crisafulli et al. 2003a). These differences are likely to have been caused by the cessation of central command from the cerebral motor cortex. There may also have been a contribution to the difference in HR from the reduction in mechano-metaboreceptor activity arising from the contracting skeletal muscle which occurred during the PR compared to AR test. In fact, the neural activity responsible for recruitment of motor units and that arising from the stimulation of mechano-metaboreceptors in the contracting muscles is thought to be pivotal in increasing HR during exercise (Rowell & O'Leary, 1990), and the reduction in activity of these heart rate modulators would have induced the relative bradycardia that occurred during PR compared to AR.
Like HR, myocardial contractility (indexed by PEP:VET, which is inversely related to contractility) during PR after exercise bouts recovered faster towards baseline values than during the AR test (see Fig. 3). The different contractility behaviour between AR and PR could be explained through the same mechanisms that modulated HR, i.e. the stimuli arising from the central command and from mechano-metaboreceptor activity. It was in fact demonstrated that metaboreflex activity is capable of increasing myocardial contractility during exercise and recovery (Bonde-Petersen & Suzuki, 1982; O'Leary & Augustyniak, 1998; Crisafulli et al. 2003b).
Another finding was that SV was significantly affected by the recovery mode since, starting from the 2nd minute of recovery after bouts, it was lower during PR than during AR. This different time course was probably mediated by three mechanisms: (1) the faster restoration of in myocardial contractility; (2) the reduction in cardiac preload; and (3) the reduction in cardiac filling rate due to the cessation of muscle pump activity that occurred during PR with respect to AR. With regard to this last mechanism, it must be noted that, by creating intramuscular pressure oscillations, the muscle pump is important in maintaining central venous pressure and SV (Carter et al. 1999). Thus, in our setting, the cessation of muscle pumping that occurred during PR probably reduced cardiac filling and, consequently, decreased SV with respect to AR. In fact, there was a reduction in VFR during PR compared to AR. Moreover, an increase in Z0 took place during PR, while it was unchanged during the AR and CR tests. This thoracic impedance index is inversely related to thoracic blood volume and cardiac preload (Carter et al. 1999). Therefore, it is reasonable to assume that there was a reduction in cardiac end-diastolic volume during the PR test with respect to baseline values. As a result of heart rate, contractility and stroke volume behaviour, CO also returned faster towards baseline values during the PR than during the AR test.
Concerning MBP, during the periods of recovery between exercise bouts in the AR test, this parameter tended to progressively increase, whereas it showed stable values during the PR test. The explanation of these different trends may reside in the fact that, while SVR was the same, CO was higher during the AR than during the PR test. In particular, CO progressively increased during recovery between exercise bouts in the AR test, whereas it levelled off during the PR test, thus explaining the different MBP behaviour between the two recovery settings.
Notwithstanding that cardiac preload (inversely related to Z0) decreased below CR values, MBP did not drop below CR values at any time during the PR protocol. This can be attributed to the fact that the major determinants of cardiac performance (i.e. HR, SV, contractility and VFR), though lower than the values observed during the AR test, were all above CR values. In particular, HR was higher all the time, while the other considered parameters were higher than CR values when between AR and PR tests there was no difference in SVR. This fact indicates that the regulation of blood pressure was not compromised by motionless recovery, during which mechanisms controlling the cardiovascular system managed to regulate blood pressure by modifying HR, SV and contractility. Then, when many of these parameters recovered towards baseline values, the recovery of SVR compensated for the decreased CO. This is in line with previous findings reporting that during recovery blood pressure is regulated to a set point which provides adequate circulation for the washout of metabolic end-products and for the delivery of nutritional metabolites (Takahashi et al. 2000; Crisafulli et al. 2003b). This is also consistent with the concept that, in healthy people, mechanisms controlling the cardiovascular system manage to regulate blood pressure by modifying HR, CO, contractility and SVR under various circumstances so that blood pressure regulation is achieved even if there is a lack in response of one of these haemodynamic components (Nobrega et al. 1997; Crisafulli et al. 2002a, 2003b). Furthermore, our findings strengthen the concept that a normal MBP response could be elicited through SVR modulation even when the CO response is blunted by reduction of venous return and ventricular filling (Nobrega et al. 1995).
Hence, it can be emphasized that the lower cardiac performance occurring during PR could be explained simply by the reduced muscular engagement that motionless recovery induced with respect to active recovery. In this light, the differences between the AR and PR tests were caused by the faster return of haemodynamics towards baseline values rather by a real impairment of cardiodynamic function. This assertion is in accordance with our recent findings which suggested that the apparent impairment in cardiovascular function during passive recovery following a single bout of supramaximal exercise was the result of the reduced muscular engagement with respect to active recovery (Crisafulli et al. 2003a).
However, there is a novel finding in the present report compared to our previous one. In fact, in the present study a drop in cardiac preload, as testified by an increase in Z0, occurred during passive recovery. This phenomenon was not evident when passive recovery was studied after a single bout of supramaximal exercise (Crisafulli et al. 2003a). Therefore, it can be stated that repeated bouts of supramaximal exercise impair venous return more than a single bout, probably causing a more pronounced accumulation of end-products and muscle vasodilatation. Hence, in our setting it appears that the recovery mode could affect haemodynamics, even if our study population did not show any sign of cardiovascular impairment such as hypotension and/or CO drop below baseline values since, as stated before, the mechanisms controlling the cardiovascular system successfully regulated haemodynamic homeostasis. Thus, even if active recovery caused a better haemodynamic response than passive recovery (i.e. higher HR, SV and CO), it seems that haemodynamics were not compromised by PR and that this mode of recovery did not cause any impairment in blood pressure regulation in our study population. It would be of interest to study the cardiovascular response in a population not accustomed to performing supramaximal exercise to verify whether the findings in our subjects are the result of specific adaptations to this kind of exercise. In fact, sedentary people not accustomed to heavy effort may not tolerate motionless recovery after strenuous exercise such as five bouts of supramaximal exercise and may develop symptoms of hypotension. As a matter of fact, hypotension was observed in sedentary people following less intense effort than that achieved by the athletes in our study (Fleg & Lakatta, 1986).
Considerations about haemodynamic measurement
So far, the Fick and the dye-dilution methods have been considered the ‘gold standard’ for CO assessment at rest and during exercise (Warburton et al. 1999a). Unfortunately, both techniques are invasive and cause discomfort and risks, so that they are not suitable for haemodynamic investigations involving healthy subjects, in whom the use of non-invasive tools is more advisable. The choice among non-invasive methods is restricted to rebreathing, Doppler echocardiography and impedance cardiography, but none of them has unanimously been considered accurate and reproducible yet. For example, CO estimated by the rebreathing method requires steady-state conditions and is affected by errors arising from the difficulty in quantifying the venous–arterial difference in CO2 blood content, thereby limiting its usefulness during maximal exercise (Warburton et al. 1999a; Sun et al. 2000). On its side, CO measured by Doppler echocardiography is thought to be very hard to perform successfully and requires a lot of practice and experienced operators (Warburton et al. 1999b; Rowland & Obert, 2002). Furthermore, this method tends to underestimate CO at maximal exercise workloads compared with invasive methods (Warburton et al. 1999b). In the present study we used the impedance method which, like rebreathing and Doppler echocardiography, suffers from some limitations for application to exercise physiology (Warburton et al. 1999b), but it appears reliable in healthy subjects (Moore et al. 1992; Singer, 1998). Probably the major source of errors in CO assessment during exercise with this technique is that heavy efforts affect impedance traces by generating artefacts due to movement of the legs and chest so that the reference points of impedance waveforms may be not recognizable. Indeed, during the five bouts of supramaximal exercise we could not produce artefact-free impedance traces for all the subjects in the study, so we could not calculate SV in those cases. However, during rest, warm-up and recovery periods we could gather artefact-free traces which, as previously shown (Crisafulli et al. 2003a), were selected from stored signals by visual inspection by a skilled physician. In this way traces affected by artefacts were excluded and SV was derived only from readable impedance waves. This signal-processing procedure was time consuming, but it has been demonstrated to be reliable and reproducible for assessing SV during recovery following supramaximal exercise (Crisafulli et al. 2003a). Besides, we paid particular attention that, during the AR test, the subjects did not pedal faster than 60 r.p.m., a rate that minimized the generation of artefacts. Thus, it is our opinion that if artefacts were excluded from SV calculation, the impedance method would be suitable for haemodynamic estimation in studies such as ours.
In conclusion, the present study, performed in healthy athletes accustomed to supramaximal exercise, demonstrates that active recovery from repeated bouts of this kind of exercise induces an improvement in cardiac performance (i.e. higher levels of HR, contractility, SV and CO) with respect to passive recovery. However, this does not necessary mean that passive recovery impaired cardiovascular function. Rather, it appears that these differences are fully explainable through a faster haemodynamic recovery towards baseline values that took place during this recovery mode compared to active recovery. As a matter of fact, during passive recovery even if venous return and cardiac preload dropped below control levels, the activity of the cardiovascular regulatory mechanisms, by keeping HR, contractility, SV and CO higher than control values and then restoring SVR towards baseline values, successfully managed to defend mean blood pressure, which never dropped below control rest values.
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HR, top panel), stroke volume (
and continuous lines), PR (
and dashed lines) and CR tests (• and continuous lines) are shown. Vertical dashed lines identify the protocol periods; horizontal dashed line represents baseline level. Values are means ±
S.E.M.
*P < 0.05 versus corresponding time point of CR test; 
P < 0.05 versus corresponding time point of PR test.
P < 0.05 versus corresponding time point of AR test.
