It was not possible to verify any association between intratendinous flow and pain at the start of the season or at the follow-up (end of the season). Intratendinous flow at the start of the season could not predict symptomatic outcome at the end of the season. The decrease in Doppler flow during the season might suggest that intratendinous flow could be part of a physiological adaptive response to loading and that intratendinous flow as previously believed is not always a sign of pathological changes.

Life expectancy among individuals with spinal cord injuries (SCI) has remained lower than in the normal population, even with optimal medical management. But signi®cant improvement has been achieved, as will be illustrated in this retrospective study of an unselected group of traumatic survivors of SCI, dead or still living. There has been a complete follow-up over 4 decades, information being obtained from available medical records, death certi®cates, and post mortem records. The survey included a total of 888 individuals (713 men and 175 women) who had survived the injury and primary treatment and were rehabilitated at the centre for Spinal Cord Injured in Hornbñk, Denmark. At the end of the follow-up, 31st December 1992, 236 (197 men and 39 women) had died. The commonest causes of death were lung diseases, particularly pneumonia; suicide; and ischaemic heart disease. Among functionally complete tetraplegic individuals there was a recognizably high percentage of deaths from pneumonia, and among the least disabled individuals (Frankel class E) we found a high frequency of suicides. The Standardised Mortality Ratios (SMRs) were highest for septicaemia, followed by uraemia and pneumonia. A signi®cant decrease in the overall mortality was observed from the ®rst (1953 ± 1973) to the second half of the observation period (1972 ± 1992). Similarly the survival curves for both men and women demonstrate that the gap in survival probability between the normal population and the SCI has diminished considerably from the early to the later period. Likewise, except for suicide and ischaemic heart disease, a decrease in SMRs was seen for all causes of death. In particular there were large decreases related to lung embolus, septicaemia, pneumonia, and uraemia. The patterns of causes of death in the study group begin to approximate those of the general population, though many cause-speci®c deaths for SCI remain substantially above the normal population. Continuous improvement in preventive measures as well as treatment procedures is still necessary.

Epidemiological and experimental studies have shown increased frequency and severity of infections after intense, long-term exercise. This study examines whether an in vivo impairment of the cell-mediated immunity and antibody production can be demonstrated after intense, long-term exercise. Twenty-two male triathletes performed one-half an ironman (group A). Vaccinations with tetanus and diphtheritis toxoid and purified pneumococcal polysaccharide were given after the exercise. Furthermore, a skin test with seven different antigens was applied on the forearm. Antibody titers were measured before and 2 wk after the exercise. The skin test was read 48 h after the application. Eleven non-exercising triathletes (group B) and 22 moderately trained men (group C) were used as control groups. Group A revealed a significantly lower skin test response to the tetanus antigen than both groups B and C. In group A, a smaller cumulative response (sum of the diameters of indurations and number of positive skin test spots) was found than in both groups B and C. No differences in antibody titers were found among the three groups. Thus, the in vivo cell-mediated immunity was impaired in the first days after prolonged, high intensity exercise, whereas there was no impairment of the in vivo antibody production measured 2 wk after vaccination.