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Daily Marathon Running for a Week—The Biochemical and Body Compositional Effects of Participation

Karstoft, Kristian; Solomon, Thomas P.; Laye, Matthew J.; Pedersen, Bente K.

Journal of Strength and Conditioning Research: November 2013 - Volume 27 - Issue 11 - p 2927–2933
doi: 10.1519/JSC.0b013e318289e39d
Original Research
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Karstoft, K, Solomon, TP, Laye, MJ, and Pedersen, BK. Daily marathon running for a week—The biochemical and body compositional effects of participation. J Strength Cond Res 27(11): 2927–2933, 2013—Although long-distance running, such as ultramarathons and multistage races, is increasingly popular, it maybe potentially harmful to health, despite sparse evidence. We studied 8 experienced recreational runners participating in a multiple-marathon running event in which 7 marathons were completed on consecutive days. Fasting blood chemistry and body composition were assessed before and 20–24 hours after the race. The total finish time for the 7 marathons ranged between 23:25:42 and 34:25:21 (hours:minutes:seconds). Only minor increases in circulating skeletal muscle cell damage markers, liver cell damage markers, and inflammatory markers occurred after the race. No other significant adverse biochemical effects were observed. The homeostasis model assessment of insulin resistance decreased markedly, and an improved lipid profile was found. A decrease in fat mass and increase in lean body mass was observed, resulting in no overall weight changes. In summary, the race did not cause any major adverse effects, whereas some traditional markers of cardiovascular disease improved acutely after the race.

The Center of Inflammation and Metabolism, Department of Infectious Diseases, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

Address correspondence to Kristian Karstoft, k_karstoft@dadlnet.dk.

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Introduction

Long-distance running, such as ultramarathons and multistage races, are increasingly popular. Although the classic marathon distance attracts many runners every year, and many large marathon races have long waiting lists, longer races are also experiencing increased participation with several thousand ultra races organized every year (http://www.ultrarunning.com/calendar.html). The races are very heterogeneous with distances ranging from just above the 42.195-km marathon distance to well above 1,000 km, terrain ranging from flat to mountainous, climate ranging from tropical to arctic, and events ranging from single-stage to multistage races.

Marathon running has been found to cause reversible muscle cell damage (14) and to change a broad range of biochemical variables the day after the race (10). Special concerns have been put into reported increases in markers of cardiac muscle cell damage and cardiac dysfunction after marathon running (10,21), but whether these findings represent cardiac pathology is still debated (15,19).

Long-distance running events are regarded as being potentially harmful and even dangerous to health. This is primarily based on case studies reporting rhabdomyolysis and hyponatremia after various races (1,3), and studies suggesting that long-distance running can potentially cause severe skeletal muscle cell damage and liver damage (5,8). However, few studies have prospectively examined the biochemical effects of long-distance running. Such studies have reported different degrees of biochemical damage, ranging from moderate changes of only skeletal muscle markers to profound changes in markers of many different organs in the body (5,10,22,24). Some of the differences maybe explained by factors like race distance, change in altitude, race track surface, single/multistage event, and the time between the end of the race and the post-race investigation, but the evidence base is too limited to conclude whether the acute effects of long-distance running are harmful or indeed beneficial to one's health.

Most of the published literature reporting biochemical and body compositional changes after ultraendurance events has evaluated continuous races. Theoretically, one would expect that multistage races, where participants have mandatory resting and sleeping time, including the opportunity to rehydrate and “reenergize” are less stressful on the biochemical system.

The Bornholm Multiple-Marathon Race Event was held in the summer of 2010. The race consisted of consecutive daily marathons for 1 week—7 marathons in total. To our knowledge, no studies have evaluated the effects of daily marathon running. We took advantage of this event and conducted a study of some of its participants. The aim was to report the biochemical and body compositional changes to determine whether such an event would cause major risk to the participants. We chose to let the subjects be completely free-living with regard to nutritional and fluid intake during, and after the event, to have the most realistic real-world perspective of the changes such an event would cause. We hypothesized that daily marathon running for a week would not cause severe biochemical damage and that weight loss without changes in lean body mass would occur.

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Methods

Experimental Approach to the Problem

The event took place on the Danish island Bornholm at sea level on a flat 1,032-m track consisting roughly of half dirt and half asphalted road. A marathon (42,195 km) was completed each day, 7 days in a row. The temperature was between 10 and 18° C, and the humidity was between 60% and 90% with no precipitation. Subjects had free access to liquids (water and energy drink) and various types of food (fruit, snacks, bread, etc.) during the race. Other parts of the study have been published elsewhere (11).

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Subjects

Out of a total of 17 participants in the multiple-marathon race event, 9 (8 males and 1 female) accepted to participate in the study. The study was approved by the Ethical Committee of the Capital Region of Denmark, and written informed consent was gained from all subjects. Baseline characteristics, including running history, are reported in Table 1.

Table 1

Table 1

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Procedures

Within 2 weeks before the race, subjects came to the laboratory for pre-race measurements after having refrained from running or other vigorous physical activity for the previous 2 days. Subjects fasted 8 hours before the measurements but had free access to water. After 10 minutes of resting, a 25 ml blood draw was obtained from an antecubital vein and analyzed for standard clinical parameters (hematological markers, inflammatory markers, skeletal and cardiac muscle markers, liver markers, kidney markers and electrolytes, glucose, metabolic hormones, and lipids), as described below.

Subjects filled out a questionnaire regarding their training habits and marathon history. Height and weight were measured barefooted using standard procedures. Body composition was assessed by dual-energy x-ray absorptiometry (DXA, Lunar Prodigy Advance; GE Healthcare, Madison, WI, USA).

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Post-race Procedures

Between 20 and 24 hours after the end of the last marathon, subjects came in for the post-race measurements. All measurements mentioned above were performed in the exact same way and at the same time of the day as at the pre-race visit.

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Blood Analyses

Plasma tubes were immediately placed on ice and subsequently centrifuged (2,000g, 15 minutes, 4° C). Serum tubes were left at room temperature for 30 minutes and centrifuged. Samples were analyzed the same day as they were obtained using the following methods: hematocrit—packed cell volume measurement (Sysmex XE-2100; Sysmex Corporation, Kobe, Japan); hemoglobin—absorption photometry (Sysmex XE-2100); reticulocytes—fluorescence flow cytometry (Sysmex XE-2100); albumin, bilirubin, and phosphate—chemical colorimetric assay (P-Modular; Roche, Basel, Switzerland); haptoglobin, C-reactive protein, orosomucoid, and myoglobin—turbidimetric immunoassay (P-Modular); lactate dehydrogenase, total creatine kinase (CK), aspartase transaminase (AST), alanine transaminase (ALT), alkaline phosphatase, γ-glutamyl transferase, creatinine, urate, cholesterols, and triglycerides—enzymatic colorimetric assay (P-Modular); myocardial-specific creatine kinase (CK-MB), pro-BNP, troponin T, cortisol, insulin, and C-peptide—electrochemiluminescence immunoassay (E-Modular; Roche); urea—absorption photometry (P-Modular); Na+ and K+—potentiometry (Modular ISE; Roche); coagulation factor II+VII+X—nephelometry (ACL top; Instrumentation Laboratory Company, Bedford, MA, USA); Ca2+—potentiometry (Konelab 30i; Thermo Scientific, Dreieich, Germany); Cl-—potentiometry (Radiometer ABL 725/735; Radiometer, Herlev, Denmark).

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Statistical Analyses

Data are presented as mean values ± SEM. Pre- and post-race values were compared using Student's paired t-tests. Race finish times were analyzed by 1-way repeated-measures analysis of variance with Bonferroni post hoc tests. Statistical analyses were performed using Prism (v3; Graph Pad, San Diego, CA, USA). Significance was accepted when p < 0.05.

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Results

Subjects

One male did not finish the race because of knee problems; therefore, data from 8 subjects (7 males, 1 female) are reported.

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Race Results

For each subject, the single marathon finish times are shown in Figure 1. The overall finish time for the 7 marathons was 28:13:32 ± 1:21:10 (range 23:25:42–34:25:21; hours:minutes:seconds), and the last 3 marathons were significantly faster than the first 2 marathons (p < 0.05). The mean best single marathon finish time was 3:39:32 ± 0:09:11 (range 3:11:50–4:40:46 hours:minutes:seconds). As a group, the fastest marathon occurred on day 7 (3:50:28 ± 0:11:28, range 3:14:44–4:42:58 hours:minutes:seconds) and the slowest on day 2 (4:10:24 ± 0:14:11, range 3:27:08–5:21:28 hours:minutes:seconds).

Figure 1

Figure 1

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Biochemistry

Biochemical markers before and after the race are shown in Table 2. Small, but significant, decreases in hematocrit (5%, p < 0.05) and hemoglobin (5%, p < 0.05) were seen along with a comparable decrease in albumin (5%, p < 0.05). No changes were found for haptoglobin or reticulocytes (data not shown) or bilirubin. Increases were seen in the inflammatory markers C-reactive protein (Figure 2A, p < 0.05) and orosomucoid (p < 0.001).

Table 2

Table 2

Figure 2

Figure 2

Markers of skeletal muscle damage were significantly increased, including lactate dehydrogenase (∼twofold, p < 0.05), myoglobin (∼twofold, p < 0.05), and CK increased 4-fold (Figure 2B, p < 0.05). Furthermore, CK-MB was increased (∼3.5-fold, p < 0.05), whereas neither troponin T nor pro-BNP were affected. Traditional markers of liver damage were increased, including AST (∼twofold, p < 0.05), ALT (∼1.5-fold, Figure 2C, p < 0.05), and alkaline phosphatase (∼1.1-fold, p < 0.05), whereas no increase was seen in γ-glutamyl transferase or coagulation factor II+VII+X. No changes were seen in markers of kidney damage or electrolytes. No subject experienced huge fluctuations in any of the parameters, and no specific values were found to be crucial out of the normal range after the race (Table 2).

Markers of metabolic health were significantly improved after the race including 54% decrease in fasting insulin (p < 0.05), 54% decrease in insulin resistance (homeostasis model assessment; HOMA-IR (12)) (Figure 3A, p < 0.05), 10% decrease in total cholesterol (p < 0.05), and 12% increase in high-density lipoprotein (HDL) cholesterol (Figure 3B, p < 0.05). No significant changes (p > 0.05) in fasting glucose, low-density lipoprotein cholesterol, or triglycerides occurred.

Figure 3

Figure 3

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Body Composition

Whole-body fat mass decreased in all subjects, with an average loss of 1.6 ± 0.4 kg (Table 2, p < 0.05), corresponding to a decrease in body fat percent of 12.7 ± 2.3% (Figure 3C, p < 0.05). Conversely, a mean increase of 1.9 ± 0.3 kg in lean body mass (Table 2, p < 0.05) occurred, resulting in no changes in the overall weight of the subjects (Table 2, 74.8 ± 2.5 vs. 75.1 ± 2.6 kg, p > 0.05).

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Discussion

The most important finding of this study is that daily marathon running for a week did not result in severe damage as indicated by a broad range of biochemical variables and that certain health-related parameters, such as fat percentage, total cholesterol, and HDL improved substantially.

Previous studies have reported large increases in circulating biochemical markers of muscle damage after running events. For instance, 24 hours after a single marathon race, Ostrowski et al. (14) found a 16-fold increase in CK, whereas Kratz et al. (10) found a 19-fold increase in CK and a fivefold increase in myoglobin. Even more pronounced effects have been reported in ultramarathon races. A continuous 200-km ultrarace resulted in a 90-fold increase in CK immediately after the race (8), whereas a striking 246-fold CK increase was seen after a 246-km continuous race (22). In contrast, our subjects on average only experienced a fourfold increase in circulating CK. Insight into this relatively low CK response may potentially be gained from a 14-day continuous ultrarace event (1,600 km) where blood samples were taken before, during, and immediately after the race. On day 4, runners had 22-fold increase in CK, which then fell to only a fivefold increase compared with pre-race values at the end of the event, potentially indicative of some kind of “time adaptation” with regard to CK to the more or less constant daily workload (5). Moreover, our subjects daily rest period and low eccentric muscle contractions (because of the flat route) may account for the discrete changes seen in muscle markers in our study, together with the fact that the subjects were very experienced runners highly adapted to prolonged exercise, which limits the muscle damage and CK increase seen after exercise (4). Moreover, because we performed post-race measurements at least 20 hours after the last marathon, it is possible that CK levels peaked before our measurements. In this context, it is, however, important to note that the main pathological condition in relation to elevated CK is rhabdomyolysis with acute renal failure, and this severe condition rarely happens after exercise if CK values <20,000 U·L−1 and no other aggravating factors are present (2). We found that the mean CK after the event was very far from dangerous levels with a mean value of 640 ± 99 U·L−1 and a highest measured value of 990 U·L−1.

The twofold increase in myoglobin is somewhat interesting. Because plasma myoglobin clearance occurs within a few hours in subjects with normal kidney function (6), it is unlikely that the muscle damage during the event causes this increase. Instead, we speculate that ongoing low-grade muscle damage takes place some time after the event.

Myocardial-specific creatine kinase was elevated to a similar extent as total CK, whereas none of the other cardiac markers (Pro-BNP and troponin T) changed. Several studies have measured cardiac markers consecutively after long-distance running and found similar patterns 24 hours after a race (10,21), and today it is well known that CK-MB is not as specific for myocardial damage as previously expected but may also rise as a result of skeletal muscle damage (20). It is expected that the increase in CK-MB would have returned to baseline if blood sampling were repeated 48 hours post-race.

In addition to increases in circulating markers of muscle damage, increases in circulating markers of liver damage have also been described in response to endurance exercise (5,8,24). Similarly, we found small increases in ALT, AST, and alkaline phosphatase. In general, the degree to which the liver enzymes (ALT and AST) are elevated correlates to the degree of muscle damage and maybe related to muscle-derived AST and, to a lesser extent, muscle-derived ALT (13,23). Thus, it is difficult to ascertain the direct role of extreme endurance events on liver status merely from circulating AST and ALT levels. In this context, it is important to note that the liver-specific marker γ-glutamyl transferase was unchanged as well as the liver function markers bilirubin and coagulation factor II+VII+X, suggesting that no serious liver injury took place.

Previous studies have reported varying degree of disturbances in various electrolytes after long-distance running (1,3,5,10). We did not encounter any electrolyte changes after the event. We believe that the moderate temperature and humidity, and the daily rest period were important for the lack of changes. Furthermore, the delay between the last marathon and our post-race measurements probably limited possible disturbances. However, any major derangements at the end of the race would still be evident when measurements were performed.

To sum up the biochemical variables measured, the overall picture was that very minor changes occurred after the event. Supporting this is the minimal changes seen in inflammatory markers and the unchanged physical stress level indicated by no differences in cortisol levels before and after the event.

Surprisingly, our subjects not only lost fat mass but also gained lean body mass during the event. A plausible explanation of this finding is that DXA scans are dependent on hydration status and body water content. Thus, the accumulated inflammation and likely edema may increase the water content of the muscle and seemingly increase lean body mass (9). This is supported by the hemodilution (decreased hematocrit, hemoglobin, and albumin) seen after the race. An alternative explanation is that repeated bouts of endurance exercise are likely to increase the water mass associated with increased glycogen storage (17). Thus, it is unlikely that the increased lean body mass reported is because of an increased muscle protein mass. To support this speculation, a follow-up scan 3–5 days later would have been sensible but in retrospect not possible to obtain.

We also found beneficial adaptations in lipid profile. This has previously been shown, and the effect is probably sustained for several days (7,18). Furthermore, it is well established that exercise increases insulin sensitivity (16). This is probably reflected in our study by a decrease in HOMA-IR. However, changes in insulin or C-peptide clearance were not accounted for, and insulin sensitivity was not measured directly. Furthermore, we cannot determine for how long these beneficial adaptations persist from this study.

A limitation of our study is that we only had 1 repeated measurement of our variables. A more detailed picture of the effects of the race would have been interesting to obtain with measurements during, immediately after, and some days/weeks after the race. The main purpose of the study was however to report the overall effects of participation in the race, including assessment of whether the race imposed any major risk to its participants. We find that this purpose is fulfilled with the measurements obtained and reported.

Hydration status was probably different for pre- and post-race measurements, indicated by the hemodilution seen after the race. In this context, we did not collect diet records before, during, and after the race. It is likely that subjects changed their nutritional and fluid intake during the race as compared to before and that this played a role for the biochemical and body compositional outcome of the study. Yet, because we wanted to explore the effects of this unusual event under as normal and free-living circumstances as possible, we find this approach more appropriate than if subjects were provided with a standardized diet. Importantly, in line with our overall aim, this allows our findings to be directly applied to “real-world” races.

In summary, we found that daily marathon running for 7 days did not impose large adverse effects on blood biochemistry in recreational athletes and that some beneficial effects on traditional risk markers of cardiovascular disease were evident up to 24 hours after the race.

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Practical Applications

This article reports the effects of daily marathon running for 7 consecutive days. Overall, trivial adverse effects including minor muscle cell damage and minor increases in liver cell damage markers were found. This implies that daily marathon running for a week does not impose any major health risk at the biochemical level. Based on this, and given that the subjects are experienced long-distance runners without any known diseases, only very minimal health risks arise when undertaking a multistage ultrarace event under temperate weather conditions.

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Acknowledgments

Hanne Villumsen, Ruth Rovsing, Anders Rinnov Nielsen, Peter Plomgaard, and Louise Lehrskov-Schmidt are acknowledged for their technical assistance. The Centre of Inflammation and Metabolism (CIM) is supported by a grant from the Danish National Research Foundation (02-512-55). This study was further supported by the Danish Council for Independent Research—Medical Sciences, the Commission of the European Communities (Grant Agreement no. 223576—MYOAGE). CIM is part of the UNIK Project: Food, Fitness & Pharma for Health and Disease, supported by the Danish Ministry of Science, Technology, and Innovation. CIM is a member of DD2—the Danish Center for Strategic Research in Type 2 Diabetes (the Danish Council for Strategic Research, grant no. 09-067009 and 09-075724). The Copenhagen Muscle Research Centre is supported by a grant from the Capital Region of Denmark.

The authors declare no professional relationships with companies or manufacturers who will benefit from the results of the present study, and the results of the present study do not constitute endorsement of the product by the authors or the NSCA.

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Keywords:

ultrarunning; long-distance running; exercise; body composition; biochemistry

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