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Changes in Male Reproductive Function after High Altitude Mountaineering
The male reproductive functions of the members of the Masherbrum (7821 m) Expedition in 1999 were examined via semen analyses and endocrine tests. Specimens were collected from three subjects who had stayed above 5100 m for 21 to 24 days and above 6700 m for 4 to 5 days before departure and 1 month, 3 months, and 2 yr after returning from the expedition. Semen analyses showed no change in the semen volume. Sperm counts decreased after 1 month and had not recovered after 3 months, but they had recovered after 2 yr in all subjects. An increase in abnormally shaped sperm was also observed after 1 month, but had nearly recovered to the preexpedition state after 3 months. Endocrine tests revealed slightly decreased testosterone in the blood after 1 month, which had decreased still further after 3 months. The tests were completely normal after 2 yr. We suggest that a high altitude sojourn may induce reversible spermatogenic and Leydig cell dysfunction.
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Effects of chronic hypobaric hypoxia on testis histology and round spermatid oxidative metabolism
In order to evaluate the effects of the exposition to continuous chronic hypobaric hypoxia (CCHH) and intermittent chronic hypobaric hypoxia (ICHH) on testis histology and on oxidative metabolism of spermatogenic cells (SC), male rats were exposed to a 4600-m simulated altitude (PO2: 89.6 mmHg). After 60 days, ICHH and CCHH groups presented a significant decrease in testicular mass, an increase in interstitial space, a decrease in height of the seminiferous epithelium, depletion of cellular elements, vacuolization in epithelial cells and folding of the basal membrane. Round spermatids from animals exposed to CCHH presented a significant decrease in energy-dependent cell shape changes. Round spermatid mitochondria of CCHH rats seem to be limited in their ability to handle reducing equivalents. These mitochondria also appear to be uncoupled under basal conditions. Round spermatids from CCHH rats evidence large oxygen consumption (QO2) insensitive to inhibition by cyanide, a process that could be partly related to lipoperoxidation. Thus, exposure of male rats to CCHH and ICHH induced evident changes in testicular morphology and loss of spermatogenic cells, in all stages of the spermatogenic cycle. This post-meiotic spermatogenic cell loss in the testis correlated well with metabolic changes in round spermatids that evidenced a strong metabolic stress in these cells.