In competing Masters track and field athletes, we did not find any influence of age, gender, weight, height, or impact profile on the development of Achilles tendinopathy. Additional research is required to improve our understanding of the causative factors in Achilles tendinopathy.

So far, aging studies have concentrated on endurance athletes. Master sprint-trained athletes were not the main focus of attention. We propose the novel hypothesis that the sprint model of lifelong physical training that involves high-intensity exercise is at least as beneficial as moderate-intensity endurance exercise for successful aging.

We studied relationships between age and aerobic capacity in three groups of subjects adhering to different exercise modalities. A total of 203 men aged 20-90 years were examined: 52 speed-power track and field athletes (SP), 89 endurance runners (ER) and 62 untrained individuals (UT). Maximal exercise characteristics were obtained during a graded treadmill test until exhaustion: oxygen uptake (VO2max), heart rate (HRmax), oxygen pulse (O2 Pulsemax) and maximal distance (Distmax). Information about training history and weekly training amount was collected. A linear model of regression was adopted. VO2max in SP was lower than in ER, but significantly higher than in UT. The cross-sectional rates of decline in body mass-adjusted VO2max and Distmax were significantly smaller in SP than in ER and UT. About 80 years of age, the levels of VO2max and Distmax reached similar values in SP and ER. The decline in HRmax, but not in O2 Pulsemax was suggested as a cardiac adaptation accounting for between-group differences in VO2max loss. Weekly training volume was a significant positive predictor of age-related changes in aerobic capacity. In conclusion, not only endurance, but also speed-power exercise appears adequate to ensure an elevated aerobic capacity at old age.

Purine metabolism is crucial for efficient ATP resynthesis during exercise. The aim of this study was to assess the effect of lifelong exercise training on blood purine metabolites in ageing humans at rest and after exhausting exercise. Plasma concentrations of hypoxanthine (Hx), xanthine (X), uric acid (UA) and the activity of erythrocyte hypoxanthine-guanine phosphoribosyl transferase (HGPRT) were measured in 55 sprinters (SP, 20‒90 years), 91 endurance runners (ER, 20‒81 years) and 61 untrained participants (UT, 21‒69 years). SP had significantly lower levels of plasma purine metabolites and higher erythrocyte HGPRT activity than ER and UT. In all three groups, plasma purine levels (except UA in UT) significantly increased with age (1.8‒44.0% per decade). HGPRT activity increased in SP and ER (0.5‒1.0%), while it remained unchanged in UT. Hx and X concentrations increased faster with age than UA and HGPRT levels. In summary, plasma purine concentration increases with age, representing the depletion of skeletal muscle adenine nucleotide (AdN) pool. In highly-trained athletes, this disadvantageous effect is compensated by an increase in HGPRT activity, supporting the salvage pathway of the AdN pool restoration. Such a mechanism is absent in untrained individuals. Lifelong exercise, especially speed-power training, limits the age-related purine metabolism deterioration.

The effect of anaerobic training on purine metabolism is significant despite of a very short total duration of anaerobic loads. Elevated preexercise HGPRT activity in CP suggests adaptation changes consisting in a "permanent readiness" for purine salvage. The detraining in TP leads to reverse adaptation changes. Probably, plasma Hx concentration and erythrocyte HGPRT activity may be considered as a useful measure of training status.