G Model JSAMS-1113; No. of Pages 5
ARTICLE IN PRESS Journal of Science and Medicine in Sport xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Journal of Science and Medicine in Sport journal homepage: www.elsevier.com/locate/jsams
Original research
Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? Kuno Hottenrott a,b,∗ , Sebastian Ludyga b , Stephan Schulze a,b , Thomas Gronwald a,b , Frank-Stephan Jäger c a
Department Sport Science, Martin-Luther-Universität Halle-Wittenberg, Germany Institute of Performance Diagnostics and Health Promotion, Martin-Luther-Universität Halle-Wittenberg, Germany c Cardiological Clinic Kassel, Germany b
a r t i c l e
i n f o
Article history: Received 2 September 2014 Received in revised form 15 October 2014 Accepted 7 November 2014 Available online xxx Keywords: Marathon Recreational runners Cardiac troponin Brain natriuretic peptide Pacing strategy
a b s t r a c t Objectives: Although alternating run/walk-periods are often recommended to novice runners, it is unclear, if this particular pacing strategy reduces the cardiovascular stress during prolonged exercise. Therefore, the aim of the study was to compare the effects of two different running strategies on selected cardiac biomarkers as well as marathon performance. Design: Randomized experimental trial in a repeated measure design. Methods: Male (n = 22) and female subjects (n = 20) completed a marathon either with a run/walk strategy or running only. Immediately after crossing the finishing line cardiac biomarkers were assessed in blood taken from the cubital vein. Before (−7 days) and after the marathon (+4 days) subjects also completed an incremental treadmill test. Results: Despite different pacing strategies, run/walk strategy and running only finished the marathon with similar times (04:14:25 ± 00:19:51 vs 04:07:40 ± 00:27:15 [hh:mm:ss]; p = 0.377). In both groups, prolonged exercise led to increased B-type natriuretic peptide, creatine kinase MB isoenzyme and myoglobin levels (p < 0.001), which returned to baseline 4 days after the marathon. Elevated cTnI concentrations were observable in only two subjects. B-type natriuretic peptide (r = −0.363; p = 0.041) and myoglobin levels (r = −0.456; p = 0.009) were inversely correlated with the velocity at the individual anaerobic threshold. Run/walk strategy compared to running only reported less muscle pain and fatigue (p = 0.006) after the running event. Conclusions: In conclusion, the increase in cardiac biomarkers is a reversible, physiological response to strenuous exercise, indicating temporary stress on the myocyte and skeletal muscle. Although a combined run/walk strategy does not reduce the load on the cardiovascular system, it allows non-elite runners to achieve similar finish times with less (muscle) discomfort. © 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
1. Introduction Benefits of regular running on cardiorespiratory fitness are known to reduce all-cause and cardiovascular mortality.1 In contrast, sudden death in marathon runners with no prior documentation of heart disease shows that prolonged endurance exercise can have the opposite effect in exceptional cases.2
∗ Corresponding author. E-mail addresses: [email protected] (K. Hottenrott), [email protected] (S. Ludyga), [email protected] (S. Schulze), [email protected] (T. Gronwald), [email protected] (F.-S. Jäger).
Especially in recreational endurance runners with less training the risk for cardiac dysfunction and injury is increased after completing a marathon.3–5 In this respect, the steadily growing number of participants in running events6 emphasizes the need to assess biochemical markers that allow the prediction of the cardiovascular risk during prolonged exercise at submaximal intensity. Previous studies have shown that prolonged running evokes abnormal elevations in creatine kinase MB isoenzyme (CK-MB), cardiac troponin (cTnI), and B-type natriuretic peptide (BNP).5 In clinical settings, increased serum levels of these cardiac markers are strong prognostic indicators of cardiac events.3,7 However, there is still an ongoing debate whether elevations in CK-MB, TNP and BNP after strenuous exercise reflect irreversible cardiac damage or just a reversible cardiac fatigue.8–10 In this respect,
http://dx.doi.org/10.1016/j.jsams.2014.11.010 1440-2440/© 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Hottenrott K, et al. Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? J Sci Med Sport (2014), http://dx.doi.org/10.1016/j.jsams.2014.11.010
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ARTICLE IN PRESS K. Hottenrott et al. / Journal of Science and Medicine in Sport xxx (2014) xxx–xxx
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Fortescue et al.11 argue that high BNP and TNP concentrations after a marathon, particularly in non-elite runners, might be due to an incomplete myocardial adaptation to training in which vulnerable myocytes are selectively eliminated. Furthermore, increases in cardiac markers correlate with post-race diastolic dysfunction, increased pulmonary pressures and right ventricular dysfunction after 2000 m rowing.3 Compared to running, walking is associated with lower energy expenditure and less physiological stress.12 Therefore, fitness experts still recommend walking breaks to make novice runners complete a marathon successfully and safely.13 Referring to the stress on the cardiovascular system, this recommendation is hardly based on evidence, as the effect of intermittent running on selected cardiac markers has not been investigated yet. However, a previous study has shown that regular walking breaks do not reduce fatigue and muscular stress during a 24 km run,14 whereas hormonal (e.g. testosterone and cortisol) responses seem to differ from continuous running.15 Furthermore, a high variability of pacing impairs marathon performance,16 possibly due to a higher energy demand, which is associated with an uneconomical running strategy. The aim of the study was to compare the effects of a run/walk strategy (RWS) vs running only (RUN) on selected markers of cardiovascular injury and stress (CK-MB, BNP, cTnI & myoglobin) as well as marathon performance. Additionally, it was examined whether or not the pacing strategy during a marathon influences the restoration of maximal aerobic performance. Higher serum concentrations of CK-MB, BNP and myoglobin, which are associated with an increased cardiovascular risk, were expected after the run/walk protocol (RWS).
2. Methods In response to a newspaper advertisement, recreational athletes applied for the study by submitting personal data including age, weight, profession and exercise experience. Only runners with a regular training volume of 10–20 km/week, who did not participate in marathons before, were included. Exclusion criteria were any chronic or acute cardiovascular, neuronal and orthopedic diseases that could jeopardize the performance and safety of participants during the marathon. Prior to the study they received a medical check-up including a detailed personal anamnesis, ECG at rest and during exercise, echocardiography as well as measurement of blood pressure. At baseline cardiac parameters (BNP, CK-MB, cTnI and myoglobin) were assessed in a venous blood sample. Out of 127 volunteers, 48 male and female recreational runners were randomly selected to participate in this investigation. The anthropometric data of the study participants, who completed all measurements, are shown in Table 1. They all read and signed an informed-consent approved by the ethics committee. Prior to the experimental trial participants engaged in a familiarization period including three months of aerobic training to prepare for the marathon and build up a comparable exercise performance. For the experimental trial recreational athletes were randomly assigned to two groups completing a marathon either by running only (RUN; n = 21) or with a run/walk strategy (RWS; n = 21). In a laboratory setting, participants completed exercise testing 7 days before (baseline) and 4 days after the marathon. At rest, a blood sample was taken from the cubital vein to assess cTnI, BNP, CK-MB and myoglobin levels. The blood analysis was performed with MeterPro (Alere Triage, Australia) providing high sensitivity by using a 99th percentile cTnI with a cut off at 0.02 ng ml−1 . Regarding the assessment of CK-MB, myoglobin and BNP the applied assay uses a sensitivity of 1.0 ng ml−1 , 5.0 ng ml−1 and 5 pg ml−1 , respectively. Following the assessment of body composition with a bioimpedance device (Data Input, BIA 2000s, Germany),
participants’ aerobic performance was measured in an incremental running test under continuous registration of the heart rate. Therefore, they gradually increased speed from initial 7.0 km h−1 by 1.5 km h−1 after each 1200 m until exhaustion. The test was stopped when participants were unable to maintain the speed. At rest and after each increment, lactate and glucose concentration were assessed with enzymatic-amperometic method (Dr. Müller Gerätebau, SUPER GL Ambulance, Germany) in 10 l blood taken from an earlobe. Heart rate, lactate and glucose concentration were processed with WinLactat 4.6 (Mesics GmbH, Germany) to derive individual target zones for the marathon. Additionally, the Dickhuth17 model was applied to the lactate-velocity curve to determine the individual aerobic and anaerobic threshold. Four days after the marathon the exercise test was repeated to assess whether or not aerobic performance was recovered and cardiac markers returned to baseline levels. All recruited recreational runners participated in the EON Mitte Kassel Marathon (May 2013 in Kassel, Germany). The course had 180.8 m difference in altitude including a maximal incline of 7% over a distance of 500 m (starting at 37 km). Using the water stations as reference, the RWS switched from running to walking every 2.5 km. Each walking period was compromised of 60 s at a selfchosen velocity in which participants felt comfortable. In contrast, the RUN completed the marathon by running only. During the event heart rate and velocity were recorded continuously with heart rate monitors with integrated GPS (RCX3 GPS, Polar Electro GmbH, Finland). Immediately after crossing the finishing line, lactate was measured in 10 l blood taken from an earlobe and participants were asked to rate muscle pain (5-point scale: 0 = none, 4 = worst pain) and exhaustion (5-point scale: 0 = none, 4 = extreme). Additionally, a blood sample was taken from the cubital vein to assess cTnI, BNP, CK-MB and myoglobin. The statistical analysis was performed with SPSS Statistics 19.0. In advance, the Shapiro–Wilk test was applied to check whether or not the data were normally distributed. As our variables followed a Gaussian distribution, analysis of variance was used for comparison between and within participants. To calculate possible interaction effects between groups a two-way ANOVA (factors: group, time) with repeated measures on the second factor was applied. Cardiac markers, aerobic performance, heart rate and blood lactate were selected as dependent variables. By using Student’s t test for unpaired samples mean and maximal heart rates during marathon, perceptual measures (selfreported muscle pain & fatigue) and finish times were compared between RWS and RUN. Furthermore, possible relationships between cardiac markers (BNP in ng l−1 , CK-MB in ng ml−1 & myoglobin in g l−1 ) and performance parameters (maximal velocity in km h−1 & velocity at the individual anaerobic threshold) were investigated by calculating the Pearson correlation coefficient. The level of significance was set at p ≤ 0.05.
3. Results Due to cramps two participants in RUN were not able to continue running and cross the finishing line. The RWS and RUN completed the marathon in 04:14:25 ± 00:19:51 (hh:mm:ss) and 04:07:40 ± 00:27:15 (hh:mm:ss), respectively. The difference in marathon time was not significant between the groups (F = 0.80; p = 0.377). Furthermore, participants’ mean (158 ± 7 min−1 vs 154 ± 6 min−1 ; F = 2.22; p = 0.146) and maximal heart rate (174 ± 8 min−1 vs 173 ± 7 min−1 ; F = 2.22; p = 0.888) did not differ significantly between RWS and RUN. The average marathon speed was correlated with velocity at the individual aerobic (r = 0.653; p < 0.001) and anaerobic threshold (r = 0.761; p < 0.001) as well as the maximal velocity during the treadmill test (r = 0.805;
Please cite this article in press as: Hottenrott K, et al. Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? J Sci Med Sport (2014), http://dx.doi.org/10.1016/j.jsams.2014.11.010
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Table 1 Subjects’ characteristics. RUN (n = 10 male/9 female)
Age (years) Height (cm) Weight (kg) HRMAX (min−1 ) VIANS (km h−1 ) VMAX (km h−1 )
46 172.5 69.1 180 11.5 13.4
± ± ± ± ± ±
6 8.5 15.1 11 0.9 1.3
RWS (n = 11 male/10 female)
44 173.4 67.8 179 11.8 14.0
± ± ± ± ± ±
8 6.9 11.3 9 1.1 1.4
Group
Group * sex
F
p
F
p
0.61 0.12 0.08 0.14 0.64 1.85
0.441 0.735 0.775 0.710 0.430 0.182
0.05 1.01 0.86 1.87 0.20 0.01
0.825 0.323 0.360 0.181 0.661 0.923
HRMAX = maximal heart rate; VIANS = velocity at individual anaerobic threshold; VMAX = maximal velocity.
p < 0.023). Immediately after the running event, participants in the RWS reported less muscle pain (1.3 ± 1.1 vs 2.3 ± 1.1; p = 0.006) and fatigue (1.6 ± 0.6 vs ± 2.3 0.8; p = 0.006) despite similar marathon times. In detail, more than 40% of RUN reported strong to extreme exhaustion compared to less than 5% of RWS. The results displayed in Table 2 confirm a global effect of time on biochemical markers. From baseline (7 days before the marathon) to the assessment immediately after the marathon BNP (RUN: 324.5%; p = 0.013; RWS: 267.2%; p < 0.001), CK-MB (RUN: 538.9%; p < 0.001; RWS: 423.8%; p < 0.001) and myoglobin (RUN: 1008.4%; p < 0.001; RWS: 870.6%; p < 0.001) increased significantly within groups. After 4 days plasma concentration of CK-MB (RWS, RUN: p < 0.001) and myoglobin (RWS, RUN: p < 0.001) dropped to a level that was not significantly different from baseline. Whereas BNP levels in RUN remained elevated in comparison to 7 days before the marathon (p = 0.146), plasma concentration of BNP in RWS also lowered to baseline values 4 days after the running event (p < 0.001). Over the measurement time points the concentration of biochemical markers was not significantly different between groups. The cTnI levels of all participants remained below the detection limit of 0.05 ng ml−1 at baseline and 4 days after the marathon. The running event did not cause any changes in cardiac troponins, apart from two exceptions: in each group there was one case with increased cTnI levels immediately after finishing the marathon (RWS: cTnI = 0.28 ng ml−1 ; RUN: cTnI = 0.15 ng ml−1 ). BNP levels immediately after the marathon were inversely correlated with velocity at the individual aerobic (r = −0.363; p = 0.041) and anaerobic threshold (r = −0.364; p = 0.040). Additionally, there was a correlation between plasma concentration of myoglobin and velocity at the individual aerobic threshold (r = −0.456; p = 0.009). Among the assessed biochemical markers a direct relation of CKMB and myoglobin levels was confirmed (r = 0.609; p < 0.001). With regard to perceptual measures, rating of muscle pain was correlated with postmarathon concentration of myoglobin (r = 0.314; p = 0.033). Compared to baseline participants’ maximal velocity and heart rate during the treadmill test was lower in both RWS and RUN 4 days after the marathon. In contrast, velocity at the individual anaerobic threshold and maximal blood lactate concentration did not differ significantly between the measurements. Furthermore, the results displayed in Table 3 show that there were no differences in aerobic performance and exhaustion criteria between RWS and RUN at pre- and post-marathon assessments. 4. Discussion Despite different pacing strategies, both groups completed the marathon with no differences in mean heart rate and finishing time. Consequently, the RWS must have compensated the lower velocity during the walking periods with a higher velocity than RUN during the running phases. Due to the decrease in limb mechanical advantage and increase in knee extensor impulse, running
requires higher metabolic cost than walking.18 However, similar mean and maximal heart rates between the groups suggest that the strain on the cardiovascular system in RWS and RUN did not differ. This notion is further supported by the lack of differences in BNP, CK-MB and myoglobin levels between groups immediately after the marathon. Despite the objectively measured cardiovascular stress was similar in RWS and RUN, muscle pain and fatigue was rated lower by runners completing the marathon with the run/walk strategy. In general, the variation of pace during a marathon is seen as intentionally chosen strategy designed to minimize the physiological strain during strenuous exercise and to prevent a premature termination of effort.19 However, an analysis by Haney and Mercer16 showed that best marathon performance is achieved by low variations in running velocity, provided that athletes choose a sustainable initial speed.20 Elite athletes are considered to maintain an economical/efficient running strategy with few variations in pacing. In contrast, a low variability of pacing in the RUN compared to a run/walk strategy (RWS) did not elicit performance benefits. Furthermore, the different pacing strategies did not affect recovery as RUN and RWS completed pre- and post-marathon performance assessments with no significant differences between groups. However, the decreased maximal velocity and velocity at the individual anaerobic threshold post-marathon as well as BNP and CK-MB levels remaining above baseline indicate that participants of both groups were not able to fully recover in 4 days. In previous studies the normalization of cardiac markers has been reported one to two weeks following a marathon.4 Running competitions have been reported to elicit temporal abnormalities in cardiac function.21 Similarly, this study showed a transient but reversible increase in cardiac biomarkers in both RWS and RUN immediately after the marathon. As elevations in BNP, CKMB and myoglobin were inversely correlated with velocity at the individual anaerobic threshold, the increase in these cardiac markers was more pronounced in runners of a lower training status. In this respect, previous studies also found more biochemical and echocardiographic evidence of cardiac injury and dysfunction after a marathon in runners of low fitness levels.3,4,22,23 Siegel et al.23 even consider running competitions a serious risk for myocardial infarction and cardiac death, particularly in the elderly. In contrast, Lucia et al.5 found no evidence of cardiac injury despite elevations of CK, CK-MB and troponin-I. In the present study the observed elevations of CK-MB and myoglobin levels beyond the normal range are consistent with the results of previous investigations.8,22 According to Saenz et al.24 , an increased concentration of CK-MB and myoglobin reflect acute muscle injury, which is expected from prolonged running, due to exertional rhabdomyolysis. With regard to myoglobin, this assumption is further supported by the present study results as a correlation between postmarathon myoglobin concentration and self-reported muscle pain has been confirmed. Lippi et al.8 also attributed rises in CK-MB and myoglobin levels to reversible muscle damage rather than biochemical signs of serious myocardial
Please cite this article in press as: Hottenrott K, et al. Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? J Sci Med Sport (2014), http://dx.doi.org/10.1016/j.jsams.2014.11.010
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Table 2 Biochemical markers before (pre), immediately after the marathon and 4 days after the marathon (post) in the RWS- (n = 21) and RUN-group (n = 19). Group
Pre (−7 days)
BNP (ng l−1 )
RWS RUN
11.6 ± 8.3 10.6 ± 6.3
31.0 ± 25.3 34.4 ± 22.8
CK-MB (ng ml−1 )
RWS RUN
2.1 ± 1.7 1.8 ± 1.0
8.9 ± 6.4* 9.7 ± 6.9*
RWS RUN
46.9 ± 25.0 41.7 ± 19.9
408.3 ± 134.5 420.5 ± 145.8*
Myo-globin (g l−1 ) *
Marathon
Post (+4 days)
*
Time p
Time * group p
17.8 ± 16.6 15.2 ± 19.7
100 ng l−1 ).
damage, although its magnitude resembles the elevations observable after acute myocardial infarction.25 Compared to CK-MB and myoglobin, the exercise-related release of BNP was lower after the marathon. The results of a previous study imply that the magnitude of the increase in BNP levels depends on duration rather than intensity.26 As there were no differences in marathon time between RUN and RWS, this might account for similar elevations in BNP. In clinical settings, BNP is seen as a strong prognostic indicator of cardiac events and death for asymptomatic patients and patients with heart failure.7 The exercise-related increase in BNP reported in multiple studies seems to be physiological rather than pathological.9 However, Neilan et al.3 have reported a strong association between elevated BNP levels and the postrace development of cardiac abnormalities shown on two-dimensional echocardiography. In this respect, the authors attributed elevations in cardiac biomarkers to changes in diastolic filling, reflecting subtle degrees of left ventricular dysfunction. Saenz et al.24 suggest that increased BNP levels might reflect a physiological response to natriuresis. However, a lack of change in serum sodium despite high BNP levels does not support this theory.3 The response of cardiac troponin levels to prolonged running varies among studies. A recent meta-analysis by Regwan et al.10 showed an incidence of post-marathon cTnI elevation in 51% of all runners. In contrast, a lack of change in cTnl levels after a marathon has been reported by other authors.21,22 In the present study, prolonged running caused elevations in cTnI above the AMI cut-off (0.05 ng ml−1 ) in only two cases. Conventional knowledge suggests that this increase reflects acute myocardial injury indicative of myocardial stunning or minor myocardial damage.21 According to Koller27 , the kinetics of cTnI release might be explained by a transient increase in membrane permeability, so that cytosolic troponins leak into the circulation. The transitory reversible shift in membrane permeability could be due to a stress-induced overload of free radicals.27
Furthermore, a relationship between cTnI elevations and functional decrements of the heart, such as left ventricular dysfunction, was not observable in the majority of previous studies.28 This indicates that the exercise-related increase in cardiac troponins might be due to the cytosolic release of the biomarker and not to the true breakdown of the myocyte.10 Therefore, several authors suggest that a clinical significance of exercise-related elevations in cTnI seems unlikely.3,21 In contrast to coronary patients, cardiac biomarkers of healthy athletes remain within the normal limit at rest, increase during exercise and return to baseline postexercise.29 The present results have to be interpreted with caution as this study is not without limitations. The plasma levels of cardiac biomarkers might have been influenced by participants’ fluid intake, which was not assessed in the study. Possibly, the RWS consumed more fluid as they had better conditions for the fluid intake during the walking periods. Furthermore, the present results do not allow identifying the cause of elevated cardiac biomarkers. As electrolytes were not assessed, it was unclear whether or not the increase in BNP levels was due to natriuresis. It also remains unclear, how elevated cardiac biomarkers were related to functional properties of the heart, because echocardiography was not performed. Another methodological concern was the use of the Alere system. Although it provides a quick assessment of cardiac biomarkers and can be used in field tests, the exercise-related elevations of BNP were restricted by the upper detection limit. Therefore, the real magnitude of changes in cardiac biomarkers after a marathon might have been higher than those measured in the study. Moreover, the present study design does not provide full insight into the time-course of regeneration after a marathon event, as the levels of CK-MB, myoglobin, BNP and cTnI returned to baseline after 4 days. An additional assessment after 2 days might have been necessary to quantify the time-course of changes in cardiac biomarkers following a running event.
Table 3 Aerobic performance, maximal heart rate and blood lactate concentration 7 days before (pre) and 4 days after completing the marathon (post) with different pacing strategies. RUN (n = 19)
RWS (n = 21)
Time p
Time * group p
VMAX (km h−1 )
Pre Post
13.4 ± 1.3 12.9 ± 1.3
14.0 ± 1.4 13.7 ± 1.3
0.002
0.753
VIAS (km h−1 )
Pre Post
9.5 ± 0.8 9.6 ± 0.6
8.6 ± 0.7 8.8 ± 0.6
ARTICLE IN PRESS Journal of Science and Medicine in Sport xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Journal of Science and Medicine in Sport journal homepage: www.elsevier.com/locate/jsams
Original research
Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? Kuno Hottenrott a,b,∗ , Sebastian Ludyga b , Stephan Schulze a,b , Thomas Gronwald a,b , Frank-Stephan Jäger c a
Department Sport Science, Martin-Luther-Universität Halle-Wittenberg, Germany Institute of Performance Diagnostics and Health Promotion, Martin-Luther-Universität Halle-Wittenberg, Germany c Cardiological Clinic Kassel, Germany b
a r t i c l e
i n f o
Article history: Received 2 September 2014 Received in revised form 15 October 2014 Accepted 7 November 2014 Available online xxx Keywords: Marathon Recreational runners Cardiac troponin Brain natriuretic peptide Pacing strategy
a b s t r a c t Objectives: Although alternating run/walk-periods are often recommended to novice runners, it is unclear, if this particular pacing strategy reduces the cardiovascular stress during prolonged exercise. Therefore, the aim of the study was to compare the effects of two different running strategies on selected cardiac biomarkers as well as marathon performance. Design: Randomized experimental trial in a repeated measure design. Methods: Male (n = 22) and female subjects (n = 20) completed a marathon either with a run/walk strategy or running only. Immediately after crossing the finishing line cardiac biomarkers were assessed in blood taken from the cubital vein. Before (−7 days) and after the marathon (+4 days) subjects also completed an incremental treadmill test. Results: Despite different pacing strategies, run/walk strategy and running only finished the marathon with similar times (04:14:25 ± 00:19:51 vs 04:07:40 ± 00:27:15 [hh:mm:ss]; p = 0.377). In both groups, prolonged exercise led to increased B-type natriuretic peptide, creatine kinase MB isoenzyme and myoglobin levels (p < 0.001), which returned to baseline 4 days after the marathon. Elevated cTnI concentrations were observable in only two subjects. B-type natriuretic peptide (r = −0.363; p = 0.041) and myoglobin levels (r = −0.456; p = 0.009) were inversely correlated with the velocity at the individual anaerobic threshold. Run/walk strategy compared to running only reported less muscle pain and fatigue (p = 0.006) after the running event. Conclusions: In conclusion, the increase in cardiac biomarkers is a reversible, physiological response to strenuous exercise, indicating temporary stress on the myocyte and skeletal muscle. Although a combined run/walk strategy does not reduce the load on the cardiovascular system, it allows non-elite runners to achieve similar finish times with less (muscle) discomfort. © 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
1. Introduction Benefits of regular running on cardiorespiratory fitness are known to reduce all-cause and cardiovascular mortality.1 In contrast, sudden death in marathon runners with no prior documentation of heart disease shows that prolonged endurance exercise can have the opposite effect in exceptional cases.2
∗ Corresponding author. E-mail addresses: [email protected] (K. Hottenrott), [email protected] (S. Ludyga), [email protected] (S. Schulze), [email protected] (T. Gronwald), [email protected] (F.-S. Jäger).
Especially in recreational endurance runners with less training the risk for cardiac dysfunction and injury is increased after completing a marathon.3–5 In this respect, the steadily growing number of participants in running events6 emphasizes the need to assess biochemical markers that allow the prediction of the cardiovascular risk during prolonged exercise at submaximal intensity. Previous studies have shown that prolonged running evokes abnormal elevations in creatine kinase MB isoenzyme (CK-MB), cardiac troponin (cTnI), and B-type natriuretic peptide (BNP).5 In clinical settings, increased serum levels of these cardiac markers are strong prognostic indicators of cardiac events.3,7 However, there is still an ongoing debate whether elevations in CK-MB, TNP and BNP after strenuous exercise reflect irreversible cardiac damage or just a reversible cardiac fatigue.8–10 In this respect,
http://dx.doi.org/10.1016/j.jsams.2014.11.010 1440-2440/© 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Hottenrott K, et al. Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? J Sci Med Sport (2014), http://dx.doi.org/10.1016/j.jsams.2014.11.010
G Model JSAMS-1113; No. of Pages 5
ARTICLE IN PRESS K. Hottenrott et al. / Journal of Science and Medicine in Sport xxx (2014) xxx–xxx
2
Fortescue et al.11 argue that high BNP and TNP concentrations after a marathon, particularly in non-elite runners, might be due to an incomplete myocardial adaptation to training in which vulnerable myocytes are selectively eliminated. Furthermore, increases in cardiac markers correlate with post-race diastolic dysfunction, increased pulmonary pressures and right ventricular dysfunction after 2000 m rowing.3 Compared to running, walking is associated with lower energy expenditure and less physiological stress.12 Therefore, fitness experts still recommend walking breaks to make novice runners complete a marathon successfully and safely.13 Referring to the stress on the cardiovascular system, this recommendation is hardly based on evidence, as the effect of intermittent running on selected cardiac markers has not been investigated yet. However, a previous study has shown that regular walking breaks do not reduce fatigue and muscular stress during a 24 km run,14 whereas hormonal (e.g. testosterone and cortisol) responses seem to differ from continuous running.15 Furthermore, a high variability of pacing impairs marathon performance,16 possibly due to a higher energy demand, which is associated with an uneconomical running strategy. The aim of the study was to compare the effects of a run/walk strategy (RWS) vs running only (RUN) on selected markers of cardiovascular injury and stress (CK-MB, BNP, cTnI & myoglobin) as well as marathon performance. Additionally, it was examined whether or not the pacing strategy during a marathon influences the restoration of maximal aerobic performance. Higher serum concentrations of CK-MB, BNP and myoglobin, which are associated with an increased cardiovascular risk, were expected after the run/walk protocol (RWS).
2. Methods In response to a newspaper advertisement, recreational athletes applied for the study by submitting personal data including age, weight, profession and exercise experience. Only runners with a regular training volume of 10–20 km/week, who did not participate in marathons before, were included. Exclusion criteria were any chronic or acute cardiovascular, neuronal and orthopedic diseases that could jeopardize the performance and safety of participants during the marathon. Prior to the study they received a medical check-up including a detailed personal anamnesis, ECG at rest and during exercise, echocardiography as well as measurement of blood pressure. At baseline cardiac parameters (BNP, CK-MB, cTnI and myoglobin) were assessed in a venous blood sample. Out of 127 volunteers, 48 male and female recreational runners were randomly selected to participate in this investigation. The anthropometric data of the study participants, who completed all measurements, are shown in Table 1. They all read and signed an informed-consent approved by the ethics committee. Prior to the experimental trial participants engaged in a familiarization period including three months of aerobic training to prepare for the marathon and build up a comparable exercise performance. For the experimental trial recreational athletes were randomly assigned to two groups completing a marathon either by running only (RUN; n = 21) or with a run/walk strategy (RWS; n = 21). In a laboratory setting, participants completed exercise testing 7 days before (baseline) and 4 days after the marathon. At rest, a blood sample was taken from the cubital vein to assess cTnI, BNP, CK-MB and myoglobin levels. The blood analysis was performed with MeterPro (Alere Triage, Australia) providing high sensitivity by using a 99th percentile cTnI with a cut off at 0.02 ng ml−1 . Regarding the assessment of CK-MB, myoglobin and BNP the applied assay uses a sensitivity of 1.0 ng ml−1 , 5.0 ng ml−1 and 5 pg ml−1 , respectively. Following the assessment of body composition with a bioimpedance device (Data Input, BIA 2000s, Germany),
participants’ aerobic performance was measured in an incremental running test under continuous registration of the heart rate. Therefore, they gradually increased speed from initial 7.0 km h−1 by 1.5 km h−1 after each 1200 m until exhaustion. The test was stopped when participants were unable to maintain the speed. At rest and after each increment, lactate and glucose concentration were assessed with enzymatic-amperometic method (Dr. Müller Gerätebau, SUPER GL Ambulance, Germany) in 10 l blood taken from an earlobe. Heart rate, lactate and glucose concentration were processed with WinLactat 4.6 (Mesics GmbH, Germany) to derive individual target zones for the marathon. Additionally, the Dickhuth17 model was applied to the lactate-velocity curve to determine the individual aerobic and anaerobic threshold. Four days after the marathon the exercise test was repeated to assess whether or not aerobic performance was recovered and cardiac markers returned to baseline levels. All recruited recreational runners participated in the EON Mitte Kassel Marathon (May 2013 in Kassel, Germany). The course had 180.8 m difference in altitude including a maximal incline of 7% over a distance of 500 m (starting at 37 km). Using the water stations as reference, the RWS switched from running to walking every 2.5 km. Each walking period was compromised of 60 s at a selfchosen velocity in which participants felt comfortable. In contrast, the RUN completed the marathon by running only. During the event heart rate and velocity were recorded continuously with heart rate monitors with integrated GPS (RCX3 GPS, Polar Electro GmbH, Finland). Immediately after crossing the finishing line, lactate was measured in 10 l blood taken from an earlobe and participants were asked to rate muscle pain (5-point scale: 0 = none, 4 = worst pain) and exhaustion (5-point scale: 0 = none, 4 = extreme). Additionally, a blood sample was taken from the cubital vein to assess cTnI, BNP, CK-MB and myoglobin. The statistical analysis was performed with SPSS Statistics 19.0. In advance, the Shapiro–Wilk test was applied to check whether or not the data were normally distributed. As our variables followed a Gaussian distribution, analysis of variance was used for comparison between and within participants. To calculate possible interaction effects between groups a two-way ANOVA (factors: group, time) with repeated measures on the second factor was applied. Cardiac markers, aerobic performance, heart rate and blood lactate were selected as dependent variables. By using Student’s t test for unpaired samples mean and maximal heart rates during marathon, perceptual measures (selfreported muscle pain & fatigue) and finish times were compared between RWS and RUN. Furthermore, possible relationships between cardiac markers (BNP in ng l−1 , CK-MB in ng ml−1 & myoglobin in g l−1 ) and performance parameters (maximal velocity in km h−1 & velocity at the individual anaerobic threshold) were investigated by calculating the Pearson correlation coefficient. The level of significance was set at p ≤ 0.05.
3. Results Due to cramps two participants in RUN were not able to continue running and cross the finishing line. The RWS and RUN completed the marathon in 04:14:25 ± 00:19:51 (hh:mm:ss) and 04:07:40 ± 00:27:15 (hh:mm:ss), respectively. The difference in marathon time was not significant between the groups (F = 0.80; p = 0.377). Furthermore, participants’ mean (158 ± 7 min−1 vs 154 ± 6 min−1 ; F = 2.22; p = 0.146) and maximal heart rate (174 ± 8 min−1 vs 173 ± 7 min−1 ; F = 2.22; p = 0.888) did not differ significantly between RWS and RUN. The average marathon speed was correlated with velocity at the individual aerobic (r = 0.653; p < 0.001) and anaerobic threshold (r = 0.761; p < 0.001) as well as the maximal velocity during the treadmill test (r = 0.805;
Please cite this article in press as: Hottenrott K, et al. Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? J Sci Med Sport (2014), http://dx.doi.org/10.1016/j.jsams.2014.11.010
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Table 1 Subjects’ characteristics. RUN (n = 10 male/9 female)
Age (years) Height (cm) Weight (kg) HRMAX (min−1 ) VIANS (km h−1 ) VMAX (km h−1 )
46 172.5 69.1 180 11.5 13.4
± ± ± ± ± ±
6 8.5 15.1 11 0.9 1.3
RWS (n = 11 male/10 female)
44 173.4 67.8 179 11.8 14.0
± ± ± ± ± ±
8 6.9 11.3 9 1.1 1.4
Group
Group * sex
F
p
F
p
0.61 0.12 0.08 0.14 0.64 1.85
0.441 0.735 0.775 0.710 0.430 0.182
0.05 1.01 0.86 1.87 0.20 0.01
0.825 0.323 0.360 0.181 0.661 0.923
HRMAX = maximal heart rate; VIANS = velocity at individual anaerobic threshold; VMAX = maximal velocity.
p < 0.023). Immediately after the running event, participants in the RWS reported less muscle pain (1.3 ± 1.1 vs 2.3 ± 1.1; p = 0.006) and fatigue (1.6 ± 0.6 vs ± 2.3 0.8; p = 0.006) despite similar marathon times. In detail, more than 40% of RUN reported strong to extreme exhaustion compared to less than 5% of RWS. The results displayed in Table 2 confirm a global effect of time on biochemical markers. From baseline (7 days before the marathon) to the assessment immediately after the marathon BNP (RUN: 324.5%; p = 0.013; RWS: 267.2%; p < 0.001), CK-MB (RUN: 538.9%; p < 0.001; RWS: 423.8%; p < 0.001) and myoglobin (RUN: 1008.4%; p < 0.001; RWS: 870.6%; p < 0.001) increased significantly within groups. After 4 days plasma concentration of CK-MB (RWS, RUN: p < 0.001) and myoglobin (RWS, RUN: p < 0.001) dropped to a level that was not significantly different from baseline. Whereas BNP levels in RUN remained elevated in comparison to 7 days before the marathon (p = 0.146), plasma concentration of BNP in RWS also lowered to baseline values 4 days after the running event (p < 0.001). Over the measurement time points the concentration of biochemical markers was not significantly different between groups. The cTnI levels of all participants remained below the detection limit of 0.05 ng ml−1 at baseline and 4 days after the marathon. The running event did not cause any changes in cardiac troponins, apart from two exceptions: in each group there was one case with increased cTnI levels immediately after finishing the marathon (RWS: cTnI = 0.28 ng ml−1 ; RUN: cTnI = 0.15 ng ml−1 ). BNP levels immediately after the marathon were inversely correlated with velocity at the individual aerobic (r = −0.363; p = 0.041) and anaerobic threshold (r = −0.364; p = 0.040). Additionally, there was a correlation between plasma concentration of myoglobin and velocity at the individual aerobic threshold (r = −0.456; p = 0.009). Among the assessed biochemical markers a direct relation of CKMB and myoglobin levels was confirmed (r = 0.609; p < 0.001). With regard to perceptual measures, rating of muscle pain was correlated with postmarathon concentration of myoglobin (r = 0.314; p = 0.033). Compared to baseline participants’ maximal velocity and heart rate during the treadmill test was lower in both RWS and RUN 4 days after the marathon. In contrast, velocity at the individual anaerobic threshold and maximal blood lactate concentration did not differ significantly between the measurements. Furthermore, the results displayed in Table 3 show that there were no differences in aerobic performance and exhaustion criteria between RWS and RUN at pre- and post-marathon assessments. 4. Discussion Despite different pacing strategies, both groups completed the marathon with no differences in mean heart rate and finishing time. Consequently, the RWS must have compensated the lower velocity during the walking periods with a higher velocity than RUN during the running phases. Due to the decrease in limb mechanical advantage and increase in knee extensor impulse, running
requires higher metabolic cost than walking.18 However, similar mean and maximal heart rates between the groups suggest that the strain on the cardiovascular system in RWS and RUN did not differ. This notion is further supported by the lack of differences in BNP, CK-MB and myoglobin levels between groups immediately after the marathon. Despite the objectively measured cardiovascular stress was similar in RWS and RUN, muscle pain and fatigue was rated lower by runners completing the marathon with the run/walk strategy. In general, the variation of pace during a marathon is seen as intentionally chosen strategy designed to minimize the physiological strain during strenuous exercise and to prevent a premature termination of effort.19 However, an analysis by Haney and Mercer16 showed that best marathon performance is achieved by low variations in running velocity, provided that athletes choose a sustainable initial speed.20 Elite athletes are considered to maintain an economical/efficient running strategy with few variations in pacing. In contrast, a low variability of pacing in the RUN compared to a run/walk strategy (RWS) did not elicit performance benefits. Furthermore, the different pacing strategies did not affect recovery as RUN and RWS completed pre- and post-marathon performance assessments with no significant differences between groups. However, the decreased maximal velocity and velocity at the individual anaerobic threshold post-marathon as well as BNP and CK-MB levels remaining above baseline indicate that participants of both groups were not able to fully recover in 4 days. In previous studies the normalization of cardiac markers has been reported one to two weeks following a marathon.4 Running competitions have been reported to elicit temporal abnormalities in cardiac function.21 Similarly, this study showed a transient but reversible increase in cardiac biomarkers in both RWS and RUN immediately after the marathon. As elevations in BNP, CKMB and myoglobin were inversely correlated with velocity at the individual anaerobic threshold, the increase in these cardiac markers was more pronounced in runners of a lower training status. In this respect, previous studies also found more biochemical and echocardiographic evidence of cardiac injury and dysfunction after a marathon in runners of low fitness levels.3,4,22,23 Siegel et al.23 even consider running competitions a serious risk for myocardial infarction and cardiac death, particularly in the elderly. In contrast, Lucia et al.5 found no evidence of cardiac injury despite elevations of CK, CK-MB and troponin-I. In the present study the observed elevations of CK-MB and myoglobin levels beyond the normal range are consistent with the results of previous investigations.8,22 According to Saenz et al.24 , an increased concentration of CK-MB and myoglobin reflect acute muscle injury, which is expected from prolonged running, due to exertional rhabdomyolysis. With regard to myoglobin, this assumption is further supported by the present study results as a correlation between postmarathon myoglobin concentration and self-reported muscle pain has been confirmed. Lippi et al.8 also attributed rises in CK-MB and myoglobin levels to reversible muscle damage rather than biochemical signs of serious myocardial
Please cite this article in press as: Hottenrott K, et al. Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners? J Sci Med Sport (2014), http://dx.doi.org/10.1016/j.jsams.2014.11.010
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Table 2 Biochemical markers before (pre), immediately after the marathon and 4 days after the marathon (post) in the RWS- (n = 21) and RUN-group (n = 19). Group
Pre (−7 days)
BNP (ng l−1 )
RWS RUN
11.6 ± 8.3 10.6 ± 6.3
31.0 ± 25.3 34.4 ± 22.8
CK-MB (ng ml−1 )
RWS RUN
2.1 ± 1.7 1.8 ± 1.0
8.9 ± 6.4* 9.7 ± 6.9*
RWS RUN
46.9 ± 25.0 41.7 ± 19.9
408.3 ± 134.5 420.5 ± 145.8*
Myo-globin (g l−1 ) *
Marathon
Post (+4 days)
*
Time p
Time * group p
17.8 ± 16.6 15.2 ± 19.7
100 ng l−1 ).
damage, although its magnitude resembles the elevations observable after acute myocardial infarction.25 Compared to CK-MB and myoglobin, the exercise-related release of BNP was lower after the marathon. The results of a previous study imply that the magnitude of the increase in BNP levels depends on duration rather than intensity.26 As there were no differences in marathon time between RUN and RWS, this might account for similar elevations in BNP. In clinical settings, BNP is seen as a strong prognostic indicator of cardiac events and death for asymptomatic patients and patients with heart failure.7 The exercise-related increase in BNP reported in multiple studies seems to be physiological rather than pathological.9 However, Neilan et al.3 have reported a strong association between elevated BNP levels and the postrace development of cardiac abnormalities shown on two-dimensional echocardiography. In this respect, the authors attributed elevations in cardiac biomarkers to changes in diastolic filling, reflecting subtle degrees of left ventricular dysfunction. Saenz et al.24 suggest that increased BNP levels might reflect a physiological response to natriuresis. However, a lack of change in serum sodium despite high BNP levels does not support this theory.3 The response of cardiac troponin levels to prolonged running varies among studies. A recent meta-analysis by Regwan et al.10 showed an incidence of post-marathon cTnI elevation in 51% of all runners. In contrast, a lack of change in cTnl levels after a marathon has been reported by other authors.21,22 In the present study, prolonged running caused elevations in cTnI above the AMI cut-off (0.05 ng ml−1 ) in only two cases. Conventional knowledge suggests that this increase reflects acute myocardial injury indicative of myocardial stunning or minor myocardial damage.21 According to Koller27 , the kinetics of cTnI release might be explained by a transient increase in membrane permeability, so that cytosolic troponins leak into the circulation. The transitory reversible shift in membrane permeability could be due to a stress-induced overload of free radicals.27
Furthermore, a relationship between cTnI elevations and functional decrements of the heart, such as left ventricular dysfunction, was not observable in the majority of previous studies.28 This indicates that the exercise-related increase in cardiac troponins might be due to the cytosolic release of the biomarker and not to the true breakdown of the myocyte.10 Therefore, several authors suggest that a clinical significance of exercise-related elevations in cTnI seems unlikely.3,21 In contrast to coronary patients, cardiac biomarkers of healthy athletes remain within the normal limit at rest, increase during exercise and return to baseline postexercise.29 The present results have to be interpreted with caution as this study is not without limitations. The plasma levels of cardiac biomarkers might have been influenced by participants’ fluid intake, which was not assessed in the study. Possibly, the RWS consumed more fluid as they had better conditions for the fluid intake during the walking periods. Furthermore, the present results do not allow identifying the cause of elevated cardiac biomarkers. As electrolytes were not assessed, it was unclear whether or not the increase in BNP levels was due to natriuresis. It also remains unclear, how elevated cardiac biomarkers were related to functional properties of the heart, because echocardiography was not performed. Another methodological concern was the use of the Alere system. Although it provides a quick assessment of cardiac biomarkers and can be used in field tests, the exercise-related elevations of BNP were restricted by the upper detection limit. Therefore, the real magnitude of changes in cardiac biomarkers after a marathon might have been higher than those measured in the study. Moreover, the present study design does not provide full insight into the time-course of regeneration after a marathon event, as the levels of CK-MB, myoglobin, BNP and cTnI returned to baseline after 4 days. An additional assessment after 2 days might have been necessary to quantify the time-course of changes in cardiac biomarkers following a running event.
Table 3 Aerobic performance, maximal heart rate and blood lactate concentration 7 days before (pre) and 4 days after completing the marathon (post) with different pacing strategies. RUN (n = 19)
RWS (n = 21)
Time p
Time * group p
VMAX (km h−1 )
Pre Post
13.4 ± 1.3 12.9 ± 1.3
14.0 ± 1.4 13.7 ± 1.3
0.002
0.753
VIAS (km h−1 )
Pre Post
9.5 ± 0.8 9.6 ± 0.6
8.6 ± 0.7 8.8 ± 0.6
