A 246-km continuous running race causes significant changes in bone metabolism

Department of Physical Medicine and Rehabilitation, Medical University of Vienna, 1090 Vienna, Waehringer Guertel 18-20, Austria.
Bone (Impact Factor: 3.97). 09/2009; 45(6):1079-83. DOI: 10.1016/j.bone.2009.07.088
Source: PubMed


Regular physical exercise exerts a favorable effect on the skeleton. However, excessive physical exercise may have detrimental effects. A low bone mineral density (BMD) has been registered in highly trained runners. The aim of the present study was to evaluate potential effects of the Spartathlon, an annual ultramarathon race of 246 km, on bone metabolism.
Venous blood samples were taken before and within 15 min after the end of the race as well as three days after the start of the race. The following variables of bone metabolism were studied: osteocalcin (Oc), cross-linked-C-telopeptide of type I collagen (CTX), osteoprotegerin (OPG), and its ligand, receptor activator of nuclear factor kappaB ligand (RANKL).
Blood samples were taken from 18 runners (16 men and 2 women) at the three time points. The median time taken by the runners to complete the race was 32 h and 52 min. Serum levels of CTX were significantly increased immediately after the race as well as three days after the start of the race compared with the time prior to the race. Oc was transiently suppressed after the race. Serum levels of RANKL and OPG were increased three days after the start of the race compared to the time before the start of the race.
This study showed that an ultra-distance run of nearly 250 km induced changes in RANK/RANKL/OPG interaction, which suggests a transient uncoupling of bone metabolism, increased bone resorption, and suppressed bone formation.

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    • "e l s e v i e r . c o m / l o c a t e / b o n e Prolonged, endurance exercise increases β-CTX [15] [16] [17] [18] [19] but again, bone formation markers are largely unresponsive [15] [16] [18] [19], suggesting that prolonged exercise might result in a transient negative remodelling balance. This acute response may be of significance to athletic populations as the net effects of changes in bone resorption and formation have been implicated in both stress fractures [20] and changes in bone mineral density (BMD) [21]. "
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    ABSTRACT: Individuals often perform exercise in the fasted state, but the effects on bone metabolism are not currently known. We compared the effect of an overnight fast with feeding a mixed meal on the bone metabolic response to treadmill running. Ten, physically-active males aged 28±4y (mean±SD) completed two, counterbalanced, 8d trials. After 3d on a standardised diet, participants performed 60min of treadmill running at 65% VO(2max) on Day 4 following an overnight fast (FAST) or a standardised breakfast (FED). Blood samples were collected at baseline, before and during exercise, for 3h after exercise, and on four consecutive follow-up days (FU1-FU4). Plasma/serum were analysed for the c-terminal telopeptide region of collagen type 1 (β-CTX), n-terminal propeptides of procollagen type 1 (P1NP), osteocalcin (OC), bone alkaline phosphatase (bone ALP), parathyroid hormone (PTH), albumin-adjusted calcium, phosphate, osteoprotegerin (OPG), cortisol, leptin and ghrelin. Only the β-CTX response was significantly affected by feeding. Pre-exercise concentrations decreased more in FED compared with FAST (47% vs 26%, P<0.001) but increased during exercise in both groups and were not significantly different from baseline at 1h post-exercise. At 3h post-exercise, concentrations were decreased (33%, P<0.001) from baseline in FAST and significantly lower (P<0.001) than in FED. P1NP and PTH increased, and OC decreased during exercise. Bone markers were not significantly different from baseline on FU1-FU4. Fasting had only a minor effect on the bone metabolic response to subsequent acute, endurance exercise, reducing the duration of the increase in β-CTX during early recovery, but having no effect on changes in bone formation markers. The reduced duration of the β-CTX response with fasting was not fully explained by changes in PTH, OPG, leptin or ghrelin.
    Bone 08/2012; 51(6):990-9. DOI:10.1016/j.bone.2012.08.128 · 3.97 Impact Factor
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    • "Bone formation was transiently suppressed by cortisol and PTH. Since studies have shown that RANKL, a marker of osteoclast activities, was continuously increased immediately and 3 days after the race,15 it was estimated that both bone formation and resorption rates increased for higher bone metabolism turnover and increased OC instead of recovering to the pre-race state from 100 km to 308 km. "
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    ABSTRACT: To evaluate the potential effects of a 308-km ultra-marathon on bone and cartilage biomarkers. Venous blood samples were collected at pre-race, 100 km, 200 km, and 308 km checkpoints. The following markers of cartilage damage and bone metabolism were studied: osteocalcin (OC), osteoprotegerin (OPG), and calcium, phosphorous, and cartilage oligomeric matrix protein (COMP). Blood samples were taken from 20 male runners at four different checkpoints. Serum COMP was increased by 194.1% (130.7% at 100 km and 160.4% at 200 km). Serum OPG was significantly increased by 158.57% at 100 km and 114.1% at 200 km compared to the pre-race measures. OC was transiently suppressed at 200 km. Serum calcium and phosphorous concentrations decreased compared to the pre-race measures. This study showed that the 308-km ultra-marathon induced several changes, including transient uncoupling of bone metabolism, increased bone resorption, suppressed bone formation, and bone turnover and had a major impact on cartilage structure.
    Annals of Rehabilitation Medicine 02/2012; 36(1):80-7. DOI:10.5535/arm.2012.36.1.80
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    • "In humans, osteocalcin has been reported to be inversely associated with fat mass and fasting plasma glucose (Kanazawa et al. 2009, 2010; Kindblom et al. 2009; Pittas et al. 2009), serum leptin (Guadalupe-Grau et al. 2009; Reinehr and Roth 2010) and insulin resistance (Fernandez- Real et al. 2009; Pittas et al. 2009; Reinehr and Roth 2010; Shea et al. 2009). Serum osteocalcin may be increased (Herrmann et al. 2007; Maimoun et al. 2006) reduced (Healy et al. 2005; Herrmann et al. 2007; Kerschan-Schindl et al. 2009; Malm et al. 1993; Mouzopoulos et al. 2007) or remain unchanged after high-intensity (Ehrnborg et al. 2003; Kristoffersson et al. 1995) or mild-intensity exercise (Wallace et al. 2000; Welsh et al. 1997). After prolonged exercise most studies report reduction in serum osteocalcin concentration (Kerschan-Schindl et al. 2009; Malm et al. 1993; Mouzopoulos et al. 2007). "
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    ABSTRACT: Osteocalcin is a hormone produced by osteoblasts which acts as a negative regulator of fat mass, protecting against diet induced obesity and insulin resistance in rodents. To determine if an acute increase in osteocalcin concentration is associated with opposed changes in circulating leptin levels and insulin resistance we studied 15 middle and long distance male triathletes, (age 32.1 ± 6.9 years), before and 48 h after an Olympic (OT) or an Ironman (IT) triathlon competition. Muscle power, anaerobic capacity, body composition (dual-energy X-ray absorptiometry), and serum concentrations of testosterone, dihydrotestosterone, osteocalcin, leptin, glucose, insulin and insulin resistance (HOMA) were determined pre- and post-race. Pre- and 48 h post-race total and regional lean body mass was not altered, but fat mass was similarly increased (~250 g) 48 h after the competitions. This elicited an increase in plasma leptin of 33% after the IT while it remained unchanged after the OT, likely due to a 25% increase in plasma osteocalcin which occurred only after the OT (all p < 0.05). Post-race HOMA remained unchanged in OT and IT. Performance was normalized 48 h after the competitions, with the exception of a slightly lower jumping capacity after the IT. Serum testosterone concentration tended to decrease by 10% after the IT whilst dihydrotestosterone was reduced by 24% after the IT. In conclusion, an acute increase in serum osteocalcin concentration blunts the expected increase of serum leptin concentration that should occur with fat mass gain. This study provides evidence for osteocalcin as a negative regulator of serum leptin in humans.
    Arbeitsphysiologie 10/2010; 110(3):635-43. DOI:10.1007/s00421-010-1550-3 · 2.19 Impact Factor
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