AbstractAcclimatisation to a decreased inspiratory partial pressure of oxygen (Pr02) initiates a series of physiological adaptations that influence oxygen transport and utilisation. \Vhilst it is clear that adequate acclimatisation is necessary to achieve optimal physical performance at altitude, scientific evidence to support the potentiating effects following return to sea-level is at present equivocal due to the inconclusive findings of a large number of uncontrolled studies. Previous research has focused on the optimisation of the theoretically beneficial aspects of altitude acclimatisation. However, not all aspects of altitude acclimatisation are beneficial which has important implications for the health and fitness of the elite competitor.
Two separate investigations were conducted to determine the physiological implications of 4 weeks of moderate altitude training at New Mexico, USA or Krugersdorp, S.A:fiica (1,500 m to 2,000 m) for selected indices of submaximal, maximal and supramaximal running performance at altitude and following return to sea-level.
Resting haemoglobin concentration (Hb) did not change at altitude or following return to sea-level. An insufficient hypoxic stimulus (intensity and duration) and/or the already depressed iron stores that were observed at sea-level (serum ferritin concentration: 48 ± 35 ng.mr 1) may have been implicated in the general lack of haematological adaptation.In contrast, chronic hypobaric hypoxia (~Pi02 of 115 mmHg to 125 mmHg) was associated with adverse changes in immune function. A significant decrease in resting plasma glutamine concentration (P < 0.001 vs pre-altitude mean) may have been implicated in an increased frequency of infectious illnesses (upper respiratory and gastrointestinal tract infections: URTI/GTI) observed at altitude. Two male subjects who had contracted an URTI/GTI during the New Mexico sojourn were subsequently diagnosed with infectious mononucleosis shortly following return to sea-level. The evidence would suggest that these subjects were exposed to the Epstein-Barr virus during the initial stages of acclimatisation, presumably when they were most susceptible to antigenic invasion. The physical symptoms of one male subject who contracted an infectious illness during the S.Africa sojourn continued to persist even 17 months following return to sea-level.
Physiological performance during and following recovery from both maximal and supramaximal exercise was affected at altitude probably due to a more pronounced alveolar-end-capillary diffusion limitation. Supramaximal running velocity during a track session decreased by 3 to 4% at 1,500 m to 1,640 m (P < 0.05). Running time to exhaustion during a maximal exercise test decreased by 21% at 1,640 m (P < 0.05 vs pre altitude mean). Maximal heart rate was 12 b.min-1 lower at altitude (P < 0.01) and despite a 31.2 L.min-1 (P < 0.01) increase in maximum minute ventilation (frE STPD), maximal oxygen consumption (V02max) expressed in both absolute and relative terms decreased by 14% (P < 0.05).
The lactate threshold and other cardiorespiratory determinants of submaximal and maximal running performance at sea-level were not improved by altitude training. In contrast, supramaximal running velocity decreased by 2% (P < 0.05) following 3 weeks return to sea level in the altitude-trained group only.
In conclusion, the present research findings suggest that the elite athlete who trains at altitude is more susceptible to physical injury and infectious illness which may have a negative impact on physiological performance following return to sea-level. The potentially adverse effects of chronic hypoxia and the subsequent implications for the health and fitness of the elite competitor need to be considered if altitude training is to be incorporated into an elite athlete's training programme.
|Date of Award||1997|
|Supervisor||Bruce Davies (Supervisor)|