This study investigated whether 4 weeks of daily supplementation with 500 or 1000 mg of Vitamin C and 500 or 1000 IU of Vitamin E could modify biochemical and ultrastructural indices of muscle damage following a 21 km run. Fifteen experienced male distance runners were divided into two groups (vitamin or placebo) and received supplementation for four weeks before completing the first 21 km run in as fast a time as possible. A four-week "washout" period followed before the subjects crossed over and received the alternate supplement for the next four weeks. They then completed a second 21 km run. Before, immediately after and 24 h after each run venous blood samples were taken and analysed for serum creatine kinase, myoglobin, malondialdehyde and vitamin C and E (before-samples only) concentrations. A subgroup of six subjects also had muscle biopsy (gastrocnemius) samples taken 24 h before and 24 h after each 21 km run, which were later analysed by electron microscopy. The two dosages of supplementation produced similar results, so a single vitamin group was formed for further analysis of results. Significant increases (p < 0.05) in creatine kinase and myoglobin, but not in malondialdehyde, were found post-run in both groups. However, no significant differences were found between the vitamin and placebo groups for creatine kinase, myoglobin and malondialdehyde concentrations recorded after the 21 km runs. A qualitative ultrastructural examination of pre-run muscle samples revealed changes consistent with endurance training, but little further change was seen after the 21 km run in either the vitamin or placebo groups. It was concluded that vitamin C and E supplementation (500 or 1000 mg or IU per day) for four weeks does not reduce either biochemical or ultrastructural indices of muscle damage in experienced runners after a half marathon.

Red blood cell (RBC) susceptibility to oxidative and osmotic stress in vitro was investigated in cells from trained and untrained men before and after submaximal exercise. Whilst no significant change in peroxidative haemolysis occurred immediately after 1 h of cycling at 60% of maximal aerobic capacity (VO2max), a 20% increase was found 6h later in both groups (P < 0.05). The RBC osmotic fragility decreased by 15% immediately after exercise (P < 0.001) and this was maintained for 6h (P < 0.001). There was an associated decrease in mean cell volume (P < 0.05). Training decreased RBC susceptibility to peroxidative haemolysis (P < 0.025) but it did not influence any other parameter. These exercise-induced changes were smaller in magnitude but qualitatively similar to those found in haemopathological states involving haem-iron incorporation into membrane lipids and the short-circuiting of antioxidant protection. To explore this similarity, a more strenuous and mechanically stressful exercise test was used. Running at 75% VO2max for 45 min reduced the induction time of O2 uptake (peroxidation), consistent with reduced antioxidation capacity, and increased the maximal rate of O2 uptake in RBC challenged with cumene hydroperoxide (P < 0.001). The proportion of high-density RBC increased by 10% immediately after running (P < 0.001) but no change in membrane-incorporated haem-iron occurred. In contrast, treatment of RBC with oxidants (20-50 mumol.l-1) in vitro increased cell density and membrane incorporation of haem-iron substantially. These results showed that single episodes of submaximal exercise caused significant changes in RBC susceptibility to oxidative and osmotic stress. Such responses may account for the increase in RBC turnover found in athletes undertaking strenuous endurance training.

No abstract

We studied the effects of repeated exercise and histamine challenge in asthmatic patients to determine the frequency and degree to which a state of refractoriness was induced by these stimuli. Twenty-nine patients performed three exercise tests, and on a separate day 16 of these patients had three histamine inhalational challenge tests. Forty minutes separated each challenge. Changes in airways resistance were measured using the peak expiratory flow rate (PEFR). The fall in PEFR (expressed as a percentage of the pre-challenge value) was used to quantify the response to challenge. Significant "protection" was defined as a fall in PEFR after a repeated challenge less than 50% of the fall observed on the first challenge. All patients had a fall in PEFR greater than 220% on the first challenge of the day. With repeated exercise 28 out of 29 patients had a fall in PEFR less than that observed on the first test and 12 had significant "protection". The fall in PEFR after the third exercise challenge was not significantly different to the second challenge and a "plateau" effect was observed. There was no significant difference in the fall in PEFR after the first and second histamine challenge although two of the 16 patients were significantly protected. After the third histamine challenge five of the 16 patients were significantly protected from the effects of the same dose of histamine. The degree to which repeated exercise challenge induces a diminished response is variable. With repeated challenge the response to histamine remains relatively constant in most

ABSTRACT. Thirty‐one children with asthma took part in a 10‐week period of training comprised of either swimming, a specially planned dry land exercise or a combination of both. There was no difference in the degree of bronchospasm induced by the different forms of exercise, nor was there a consistent change in the clinical pattern of asthma with either type of activity. No reduction in the bronchospastic response to exercise was noted after the 10 weeks of training but there was less tachycardia. An improvement in the mean maximum expiratory pressure occurred in both the dry land and swimming groups indicating improved chest wall function. It was concluded that provided asthma was adequately managed an appropriately planned dry land exercise programme resulted in similar advantages to swimming training without added risk of exercise induced asthma.