Doy un repaso a las referencias de 2011 en las que van apareciendo conclusiones de estudios hechos en maratones o sobre corredores de maratón.
Alejandro Lucía colabora con M.Joyner y J. Ruiz en el artículo “The Two-Hour Marathon: Who and When?” y repasan las características fisiológicas de quien, en un potencial futuro, pudiese llevar más allá los records de maratón. En un breve pdf de letsrun.com se reseña: “Whoever breaks two hours will likely have outstanding running economy and small body size along with exposure to high altitude, and significant physical activity early in life. However, neither these factors nor any specific suite of genotypes appear to be obligatory for a time this fast“.
Las cagaleras de la muerte…¡ después del maratón!. Surgisphere.com ofrece el artículo del Journal of Surgical Radiology “Marathon-induced colitis” D. King y L. Avery trabajan con la evidencia que más que problemas coronarios, la principal sintomatología tras las grandes carreras es una diarrea que puede ser patológica. De entre los problemas gastrointestinales aparecidos, “Up to 20% of marathoners will have biochemical evidence of microscopic blood in their stools upon post-race fecal occult blood testing (“heme-positive”). Multiple cases and analyses of these cases suggest ischemia and reperfusion as the dominant mechanism for inducing colitis after a marathon. Shunting and redirection of cardiac output to the skeletal muscles presumably leaves the gastrointestinal tract in a state of acutely diminished blood flow for the duration of the marathon“. Así pues, no estáis solos si también os ocurre esto. En el artículo se repasa el proceso y las variables.
La canalla corporativa impide que tengamos gratis las versiones completas de muchos más, pero el abstract de “An exploration of the hydration strategies of the runners of the 2010 london marathon by questionnaire“, de Jonathan Williams et alofrece los siguienetes números, tomados como bien dice de los participantes que rellenaron el cuestionario en el maratón londinense. Resultados: 93% of the runners had read or been told about drinking fluids on marathon day. The majority of competitors had a plan regarding fluid intake prior to, during and after the marathon. 83.9% said that they knew enough about what and how much to drink on marathon day. However, 34% planned to drink a volume large enough to put themselves at higher risk of EAH. Only 21% knew the volumes of water and sports drink bottles from which they planned to drink during the marathon. 20.7% were planning to take a drink from all 24 water stations. Only 25% planned to drink according to their thirst as recommended by the international EAH conference consensus statement.
68% of runners had heard of hyponatraemia or low sodium levels, but only 35% had a basic understanding of its cause and effects.
Conclusions Runners of the 2010 London Marathon lack knowledge about appropriate fluid intake on race day. A significant proportion of participants have drinking strategies that put them at risk of EAH. Runners need to be more effectively educated about safe fluid intake prior to future London Marathons.”
De este mismo evento pero de 2003, precisamente, salen ahora en misma publicación las cifras de hiponatrenia en el artículo The incidence of exercise-associated hyponatraemia in the London marathon, de C. Kipps et al (y del que solo podemos leer el abstract) http://bjsportmed.com/content/45/1/14.abstract
“Of the 88 volunteers, 11 (12.5%) developed asymptomatic hyponatraemia (serum sodium 128–134 mmol/l). They consumed more fluid (p<0.001) and gained more weight (p<0.001) than did those without hyponatraemia.
Conclusions A significant proportion (12.5%) of healthy volunteers developed asymptomatic hyponatraemia running a marathon in cool conditions. On average, these runners consumed more fluid and gained more weight than did non-hyponatraemic runners, although fluid intake was not related to weight gain in this study. Four of the 11 hyponatraemic runners lost weight over the course of the marathon, strengthening the case for an additional factor, such as inappropriate antidiuretic hormone release during exercise, in the development of EAH“.
La medicina insiste en avisar de los daños que nuestro cuerpo experimentan después de correr durante largas distancias, como la revista Nephrology, “Changes in renal markers and acute kidney injury after marathon running“, de Peter McCullough et al. Su abstract indica que existen “Approximately 40% of marathon runners experience a transient rise in serum creatinine that meets criteria of AKI (acute kidney injury) with a parallel elevation of cystatin C, and supportive elevations of neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 in the urine. All biomarker elevations resolved by 24 h. These data suggest that AKI with a transient and minor change in renal filtration function occurs with the stress of marathon running. The impact of repetitive episodes of AKI with long-distance running is unknown“.
Millet, Tomazin et al escriben sobre los efectos de los ultras de montaña. “Neuromuscular Consequences of an Extreme Mountain Ultra-Marathon“, pero cuando uno es un ultra, ¿a quién le importan las consecuencias neuromusculares, nein? En serio, los autores desgranan “We investigated the physiological consequences of one of the most extreme exercises realized by humans in race conditions: a 166-km mountain ultra-marathon (MUM) with 9500 m of positive and negative elevation change. For this purpose, (i) the fatigue induced by the MUM and (ii) the recovery processes over two weeks were assessed. Evaluation of neuromuscular function (NMF) and blood markers of muscle damage and inflammation were performed before and immediately following (n = 22), and 2, 5, 9 and 16 days after the MUM (n = 11) in experienced ultra-marathon runners. Large maximal voluntary contraction decreases occurred after MUM (−35% [95% CI: −28 to −42%] and −39% [95% CI: −32 to −46%] for KE and PF, respectively), with alteration of maximal voluntary activation, mainly for KE (−19% [95% CI: −7 to −32%]). Significant modifications in markers of muscle damage and inflammation were observed after the MUM as suggested by the large changes in creatine kinase (from 144±94 to 13,633±12,626 UI L−1), myoglobin (from 32±22 to 1,432±1,209 µg L−1), and C-Reactive Protein […]“. El resto, en PloS One.
Que no se diga que no corremos avisados, jongens en meisjes.