Hematologic, iron-related, and acute-phase protein responses to sustained strenuous exercise.
This study was undertaken to gain insight into the mechanisms responsible for the hypoferremia occurring after severe exercise. To this end, 18 athletes who were competing in a 160-km triathlon involving canoeing, cycling, and running were evaluated before the race, immediately after the finish, and thereafter at 30 min, 24 h, and 48 h. The evaluation included plasma iron, total iron-binding capacity, lactoferrin, ferritin, haptoglobin, cortisol, various enzymes, and white cell count. The cortisol, white cell count, and lactoferrin were significantly increased immediately after the race, while the plasma iron and transferrin saturation were significantly decreased. There was a 40% but nonsignificant rise in the plasma ferritin at the completion of the race, while the C-reactive protein was raised by nearly 300% at 24 h. In contrast, haptoglobin declined significantly by 24 h but was normal again 24 h later. Quantitative considerations suggested that the lactoferrin was not responsible for removing transferrin iron from circulation and hence causing the hypoferremia. Instead, it seemed more likely that the iron-related changes were occurring as part of an acute phase response initiated by muscle injury.
D000209:Acute-Phase Proteins / Q000097:blood*; D000328:Adult; D002097:C-Reactive Protein / Q000097:blood; D005293:Ferritins / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007501:Iron / Q000097:blood*; D007781:Lactoferrin / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D010807:Physical Endurance; D005082:Physical Exertion
D000209:Acute-Phase Proteins; D002097:C-Reactive Protein; D005293:Ferritins; D007501:Iron; D007781:Lactoferrin; D006854:Hydrocortisone