Metabolic responses to a 48-h ultra-marathon run in middle-aged male amateur runners

The changes consequent on the ultra-endurance run do not pose a serious health risk in men who begin their endeavor with ultra-endurance running in mid-life. There is some circumstantial evidence that hyperventilatory hypocapnia may modulate inflammatory response by stimulating the release of interleukin-6 from working skeletal muscles.

Blood samples were taken before the race, after 12, 24, and 48 h of running, and after 24 and 48 h of recovery from male amateur runners (N = 7, age 35-59 years, VO2max mean ± SD 57.0 ± 4.0 ml kg(-1) min(-1), total distance covered 183-320 km). The samples were analyzed for morphology, acid-base and electrolyte balance, iron status, lipid profile, interleukin-6, high-sensitivity C-reactive protein, N-terminal pro-brain-type natriuretic peptide, high-sensitivity cardiac troponin T, non-enzymatic antioxidants, activities of selected enzymes including antioxidant enzymes, and total antioxidant status.

To evaluate ongoing metabolic changes during a 48-h competitive run and a 48-h recovery period, with focus on potential health risks exemplified by heart and skeletal muscle damage biomarkers and oxidative stress-related indices.

The sustained ultra-endurance run caused hypocapnic alkalosis with slight hyperkalemia and hypocalcemia, but no hyponatremia. Blood biochemistry showed severe muscle but not liver damage, and an acute inflammatory response. These effects were evidenced by leukocytosis, several fold rises in interleukin-6 and high sensitivity C-reactive protein, extreme elevations in serum levels of muscle enzymes, and marked increases in cardiac biomarker levels. Most of the changes dissolved during the 48 h post-race recovery. Neither the iron pool, nor erythropoiesis, nor pro-oxidant/antioxidant balance were substantially affected. Conclusions: The changes consequent on the ultra-endurance run do not pose a serious health risk in men who begin their endeavor with ultra-endurance running in mid-life. There is some circumstantial evidence that hyperventilatory hypocapnia may modulate inflammatory response by stimulating the release of interleukin-6 from working skeletal muscles.