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.
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).
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.
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.
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:Copyright © 2013 by the National Strength & Conditioning Association.
ultrarunning; long-distance running; exercise; body composition; biochemistry