Biomedical subjects

O Faude

Publications and source records attributed to O Faude.

3 recordsLinked to original sources

PubMed2006

Risk factors for injuries in elite female soccer players.

OBJECTIVE: To describe risk factors for injuries in elite female soccer. METHODS: A total of 143 female soccer players from the German national league participated in the study. Baseline information on player characteristics--for example, anthropometric measurements and playing position--and medical history were recorded at the start of the study. During one outdoor season, injuries and training and match exposure times were prospectively documented for each player. RESULTS: The risk of a new anterior cruciate ligament (ACL) rupture was significantly increased in players with a previous rupture (odds ratio (OR) = 5.24, p = 0.01). This was not the case for ankle sprain (OR = 1.39) or knee sprain (OR = 1.50). In addition, no significantly increased risk of new sprains or ACL ruptures was found when the injured leg was the unit of analysis. Injury incidence was considerably higher in defenders (9.4 injuries per 1000 hours exposure) and strikers (8.4/1000 hours) than goalkeepers (4.8/1000 hours) and midfielders (4.6/1000 hours). Ten per cent of all players (n = 14) sustained more than three injuries. Most of these were defenders (n = 8) or strikers (n = 4). Significantly more injuries occurred to the dominant leg (105 v 71, p = 0.01); this was particularly true for contact injuries (52 v 29, p = 0.01). CONCLUSIONS: Injury risk should be assessed on an individual basis. Therefore it seems appropriate to individualise preventive training programmes, as is recommended for other training content. Evaluating the existing rules of soccer and their appropriate application may also help to decrease injury risk, particularly in contact situations.

Adolescent↗

PubMed2005

Does prolonged cycling of moderate intensity affect immune cell function?

BACKGROUND: Prolonged exercise may induce temporary immunosuppression with a presumed increased susceptibility for infection. However, there are only few data on immune cell function after prolonged cycling at moderate intensities typical for road cycling training sessions. METHODS: The present study examined the influence on immune cell function of 4 h of cycling at a constant intensity of 70% of the individual anaerobic threshold. Interleukin-6 (IL-6) and C-reactive protein (CRP), leukocyte and lymphocyte populations, activities of natural killer (NK), neutrophils, and monocytes were examined before and after exercise, and also on a control day without exercise. RESULTS: Cycling for 4 h induced a moderate acute phase response with increases in IL-6 from 1.0 (SD 0.5) before to 9.6 (5.6) pg/ml 1 h after exercise and CRP from 0.5 (SD 0.4) before to 1.8 (1.3) mg/l 1 day after exercise. Although absolute numbers of circulating NK cells, monocytes, and neutrophils increased during exercise, on a per cell basis NK cell activity, neutrophil and monocyte phagocytosis, and monocyte oxidative burst did not significantly change after exercise. However, a minor effect over time for neutrophil oxidative burst was noted, tending to decrease after exercise. CONCLUSIONS: Prolonged cycling at moderate intensities does not seem to seriously alter the function of cells of the first line of defence. Therefore, the influence of a single typical road cycling training session on the immune system is only moderate and appears to be safe from an immunological point of view.

Acute-Phase Reaction↗

PubMed2004

Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point?

OBJECTIVES: The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. METHODS: During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l x min(-1) oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg x m(-2); Vo(2peak) 51.3-62.1 ml x min(-1) x kg(-1)). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. RESULTS: In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l x min(-1)) compared with the first test. CONCLUSIONS: For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.

Acidosis, Lactic↗