Abstract des Autors

The precise mechanism of the fatigue which limits athletes from greater performance levels remains elusive. It is likely that the mechanism differs for different duration events. The limiting factors should therefore be considered within the intensity domains for which there is a common aerobic and acidaemic response profile. Work rates up to subject's lactate threshold are characterized by steady states of pulmonary gas exchange and little or no sustained metabolic (chiefly lactic) acidaemia. Above the lactate threshold, but below the critical power, the steady state of oxygen uptake is delayed, with an >excess< component of VO2 becoming manifest with sustained increases, or declining levels, of lactate and (H+). Work rates above critical power lead to continuous non-steady states of pulmonary gas exchange and a degree of metabolic acidaemia, resulting in maximum VO2 being attained. Proposed mechanisms of fatigue include (H+) and/or inorganic phosphate-induced reduction in muscular force generation resulting from impaired cross-bridge cycling. Other fatigue-inducing metabolites may also be contributory, such as increased oxygen free radicals and the plasma concentration of free tryptophan. For prolonged events, depletion of energetic substrates (e.g. glycogen) can be limiting. The dominant systemic limiting factor is likely to be the cardiovascular system. In some elite athletes, however, the pulmonary system may also provide a source of limitation through: a) expiratory air flow limitation; b) inadequate pulmonary capillary transit time for oxygenation; and c) possible development of interstitial pulmonary oedema and, in extreme cases, disruption of the alveolar-capillary interface. Verf.-Referat