Ibuprofen does not affect serum electrolyte concentrations after an ultradistance run.

OBJECTIVE: To determine the effects of ibuprofen on serum electrolyte concentrations after a 160 km running race. METHODS: Twenty nine subjects (mean (SD) age 47.9 (7.4) years) ingested 600 mg ibuprofen the day before, and 1200 mg ibuprofen during, a 160 km competitive trail running race (approximately every 4 h in 200 mg doses). Twenty five control subjects (mean (SD) age 46.8 (10.3) years) avoided ingestion of ibuprofen before or during the race. Blood was drawn on the day before the race and immediately after the race. Serum biochemical profiles were analysed by a clinical laboratory. Significant effects of treatment and time were determined with a general linear model with repeated measures. RESULTS: Subjects in the two groups did not differ by age, training volume, race experience, body mass index, body fat, or finishing time (25.8 (3.3) vs 25.6 (3.9) h). Body weight did not change significantly over the race (measured before, mid-race (90 km), and after). Ibuprofen ingestion did not significantly affect any of the serum markers including creatine kinase (p = 0.16). A significant decrease in serum sodium (p = 0.006), potassium (p = 0.001), chloride (p<0.001), calcium (p<0.001), albumin (p<0.001) and globulin (p<0.001) was observed after the race. Increases were seen in creatine kinase (p<0.001), creatinine (p<0.001), blood urea nitrogen (p<0.001), uric acid (p<0.001) and glucose (p<0.001) as the result of the race. CONCLUSIONS: These data suggest that the non-specific cyclo-oxygenase inhibitor, ibuprofen, does not alter serum electrolyte concentrations during ultradistance running. However, the stress of ultradistance running appears to be related to significant changes in certain serum markers.

Ibuprofen use, endotoxemia, inflammation, and plasma cytokines during ultramarathon competition.

The primary purpose of this study was to measure the influence of ibuprofen use during the 160-km Western States Endurance Run on endotoxemia, inflammation, and plasma cytokines. Subjects included 29 ultramarathoners who consumed 600 and 1200 mg ibuprofen the day before and on race day, respectively, and 25 controls that competed in the race but avoided ibuprofen and all other medications. Blood and urine samples were collected the morning prior to and immediately following the race, and subjects recorded muscle soreness during the week following the race using a 10-point Likert scale (DOMS). Race time (25.8+/-.6 and 25.6+/-.8 h, respectively) and ratings of perceived exertion (RPE, 6-20 scale) (14.6+/-.4 and 14.5+/-.2, respectively) did not differ significantly between ibuprofen users and nonusers. Ibuprofen use compared to nonuse was linked to a smaller increase in urine creatinine (P=.038), higher plasma levels of lipopolysaccharide (group effect, P=.042), and greater increases (pre-to-post race) in serum C-reactive protein and plasma cytokine levels for interleukin (IL)-6, IL-10, IL-8, IL-1 ra, granulocyte colony-stimulating factor, monocyte chemotactic protein 1, and macrophage inflammatory protein 1 beta, but not tumor necrosis factor alpha. Post-race DOMS and serum creatine kinase levels did not differ significantly between ibuprofen users and nonusers (20,621+/-3565 and 13,886+/-3068 microcal/L, respectively, P=.163). In conclusion, ibuprofen use compared to nonuse by athletes competing in a 160-km race did not alter muscle damage or soreness, and was related to elevated indicators of endotoxemia and inflammation.

Indirect calorimetry during ultradistance running: a case report.

The purpose was to determine the energy expenditure during ultradistance trail running. A portable metabolic unit was carried by a male subject for the first 64.5 km portion of the Western States 100 running race. Calibrations were done with known gases and volumes at ambient temperature, humidity and pressure (23-40.5 °C and 16-40% respectively). Altitude averaged 1692.8 ± 210 m during data collection. The male subject (36 yrs, 75 kg, VO2max of 67.0 ml·kg(-1)·min(-1)) had an average (mean ± SD) heart rate of 132 ± 9 bpm, oxygen consumption of 34.0 ± 6.8 ml·kg(-1)·min(-1), RER of 0.91 ± 0.04, and VE of 86.0 ± 14.3 L·min(-1) during the 21.7 km measuring period. This represented an average of 51% VO2max and 75% heart rate maximum. Energy expenditure was 12.6 ± 2.5 kcals·min(-1), or 82.7 ± 16.6 kcals·km(-1) (134 ± 27 kcals·mile(-1)) at 68.3 ± 12.5% carbohydrate. Extrapolation of this data would result in an energy expenditure of >13,000 kcals for the 160 km race, and an exogenous carbohydrate requirement of >250 kcal·hr(-1). The energy cost of running for this subject on separate, noncompetitive occasions ranged from 64.9 ± 8.5 to 74.4 ± 5.5 kcals·km(-1) (105 ± 14 to 120 ± 9 kcals·mile(-1)). Ultradistance trail running increases energy expenditure above that of running on nonundulating terrain, which may result in underestimating energy requirements during these events and subsequent undernourishment and suboptimal performance. Key PointsThe energy cost of running is elevated during ultradistance trail races compared to normal running conditions.This elevated energy cost results in a ~12% increase in energy expenditure for a given distance.Ad libitum energy intake may grossly underestimate the demand of ultradistance running in the conditions investigated in this paper, thus jeopardizing race performance.

Muscle damage is linked to cytokine changes following a 160-km race.

Muscle damage and perceived soreness following the 160-km Western States Endurance Run were related to changes in plasma cytokines and use of nonsteroidal anti-inflammatory drugs (NSAIDS). Subjects included 60 ultramarathoners (mean+/-SE, age 45.3 +/- 1.1 years) who finished the race in under 30 h (26.3 +/- 0.4 h). Blood samples were collected the morning prior to and immediately following the race, and subjects recorded muscle soreness during the week following the race using a 10-point Likert scale (DOMS). Seven plasma cytokines were measured including IL-6, IL-10, IL-8, IL-1ra, granulocyte colony-stimulating factor (G-CSF), monocyte chemotactic protein 1 (MCP-1), and macrophage inflammatory protein 1beta (MIP-1beta). Cytokine changes were compared between NSAID users and nonusers, and correlated with creatine phosphokinase (CPK) and DOMS. Significant increases were measured for all seven cytokines, with the greatest fold increases seen for IL-6 (125x), IL-10 (24x), and G-CSF (12x). CPK was correlated with changes in IL-6, G-CSF, IL-10, IL-1ra, and MCP-1 (r = .49-.68), (P < .001), but not IL-8 or MIP-1beta. DOMS averaged 7.1 +/- 0.3 the day after the race, and 5.0 +/- 0.3, 2.5 +/- 0.2, and 1.6 +/- 0.1 3 days, 5 days, and 7 days post-race, respectively, and each was correlated with CPK (r = .40-.63, P < .001) and changes in IL-6, G-CSF, IL-10, and MCP-1 (r = .28-.77, P < .05). A comparison of NSAID users (72% of athletes) and nonusers showed no differences in CPK or DOMS, but did reveal greater increases in five of seven cytokines in the NSAID users (P < .05). In conclusion, muscle damage in athletes competing in a 160-km race was significantly correlated with post-race DOMS and increases in five of seven cytokines. NSAID users did not experience a reduction in muscle damage or DOMS, but did have higher post-race plasma levels in five of seven cytokines.