27Moderate physical exercise does not cause any changes in the plasma levels of the catabolic hormone cortisol and the anabolic hormone testosterone compared with the concentrations during a control day. In studies on army recruits, however, fit compared to unfit men tended to have smaller mean decreases in plasma testosterone and free testosterone index during the day both during a control day and during a day with submaximal marching exercise. After 4 months training, the mean plasma testosterone and free testosterone index tended to decrease less during both control and marching exercise days, and this was more evident in the well-conditioned subjects. However, very fit male athletes, who have been training for many years, and sedentary men have identical plasma testosterone levels and serum sex hormone binding globulin binding capacities (SHBG). Intense physical exercise invariably leads to an increase in plasma cortisol and a decrease in plasma testosterone compared with the concentrations during a control day. However, the percentage of free testosterone seems to increase cornpensatorily, which in many individuals keeps the absolute free testosterone level constant or even higher despite no change or slight increase in SHBG. Prolonged exhaustive physical exercise in men results in a decrease in plasma testosterone even down to normal female levels, and there is a constant increase in SHBG resulting in very low free testosterone concentrations. It is known from studies in rats that a low level of androgens results in an increase in the binding of cortisol in muscle tissue probably due to an increase in the number of cortisol receptors. This in combination with the high level of cortisol during prolonged exhaustive physical exercise may lead to a situation in which the protein catabolic events in the muscle cells supersedes the anabolic ones. Rats trained on a treadmill and sedentary rats have identical plasma and testicular testosterone concentrations, identical plasma LH levels, and training has no effect on Leydig cell LH and prolactin receptors. When these rats ran until exhaustion, the trained rats were able to run much longer (up to 3 h) than the untrained rats. In this experiment, the decrease in plasma testosterone was greater in the trained rats compared with the untrained ones, and also the testicular concentration of testosterone, androstenedione, and progesterone fell to lower levels in the trained rats after the exhaustive exercise. The plasma LH levels remained unchanged. This suggests that the decrease in plasma testosterone is due to a reduction in testicular testosterone production and a depletion of the testosterone stores and that the testosterone-LH feedback mechanism is no longer functioning in these exhausted animals. However, when the Leydig cells were incubated in vitro with HCG at different concentrations, it could be shown that in trained rats Leydig cell testosterone and cyclic AMP production was significantly greater than in sedentary rats. All these results are in good agreement w...

Muscle ATP, creatine phosphate and lactate, and blood pH and lactate were measured in 7 male sprinters before and after running 40, 60, 80 and 100 m at maximal speed. The sprinters were divided into two groups, group 1 being sprinters who achieved a higher maximal speed (10.07 +/- 0.13 m X s-1) than group 2 (9.75 +/- 0.10 m X s-1), and who also maintained the speed for a longer time. The breakdown of high-energy phosphate stores was significantly greater for group 1 than for group 2 for all distances other than 100 m; the breakdown of creatine phosphate for group 1 was almost the same for 40 m as for 100 m. Muscle and blood lactate began to accumulate during the 40 m exercise. The accumulation of blood lactate was linear (0.55 +/- 0.02 mmol X s-1 X l-1) for all distances, and there were no differences between the groups. With 100 m sprints the end-levels of blood and muscle lactate were not high enough and the change in blood pH was not great enough for one to accept that lactate accumulation is responsible for the decrease in running speed over this distance. We concluded that in short-term maximal exercise, performance depends on the capacity for using high-energy phosphates at the beginning of the exercise, and the decrease in running speed begins when the high-energy phosphate stores are depleted and most of the energy must then be produced by glycolysis.

No abstract

Background. Only a few reported studies focus on the natural history and course of advanced and severe chronic atrophic gastritis. Methods. In this study we followed 47 men (mean age 62 years) with advanced (moderate or severe) Helicobacter pylori-positive atrophic corpus gastritis. Duration of endoscopic follow-up was 6 years and follow-up based on serum levels of pepsinogen I and antibodies to H. pylori covered a period of 10 years. None of the patients was treated for H. pylori infection prior to end of follow-up. Results. The median H. pylori antibody titre declined (IgG from 4000 to 1300; IgA from 200 to 50) in the study population, and 11 men (23%) converted to seronegative (p=0.0005, Fisher's exact test). There was a small but significant (p=0.0004, Page's test) declining trend in mean atrophy score of the corpus during follow-up (from 2.5 to 2.2). However, no significant changes were observed in grade of atrophy or intestinal metaplasia of the antral mucosa or in grade of intestinal metaplasia in the corpus. The mean SPGI level remained at the initial low level during the entire follow-up. Conclusions. H. pylori antibodies disappear spontaneously within 10 years in almost one fourth of patients with advanced atrophic corpus gastritis. The disappearance of H. pylori antibodies is accompanied by no or more than a mild improvement of the gastric mucosa.

Blood ketone bodies are elevated in CHF in proportion to the severity of cardiac dysfunction and neurohormonal activation. This may be at least partly attributable to increased free fatty acid mobilization in response to augmented neurohormonal stimulation. Additional studies are needed to identify the detailed mechanisms and clinical implications of CHF ketosis.