4.7 Article

Fertility Impairment after Trekking at High Altitude: A Proof of Mechanisms on Redox and Metabolic Seminal Changes

Journal

Publisher

MDPI
DOI: 10.3390/ijms23169066

Keywords

altitude hypoxia; male infertility; redox biology; oxidative stress; sperm parameters; sperm physiology

Funding

  1. Department of Psychological, Health, and Territorial Sciences, G. d'Annunzio University of Chieti-Pescara, Italy

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This study evaluated the effects of high-altitude exposure on sperm parameters and health status in travellers. The results showed that high-altitude trekking led to a decrease in sperm concentration and seminal volume, and an increase in oxidative stress. The study also suggested that uncontrolled ROS production may be the cause of impaired sperm quality.
Many authors described negative but reversible effects of high-altitude hypoxic exposure on animal and human fertility in terms of sperm concentration, function, and biochemical alterations. The aim of this study was to evaluate the acute and chronic effects of high-altitude exposure on classical sperm parameters, redox status, and membrane composition in a group of travellers. Five healthy Italian males, all lowlanders not accustomed to the altitude, were evaluated after 19 days-trekking through low, moderate, and high altitudes in the Himalayas. Sperm samples were collected before (Pre), 10 days after (Post), and 70 days after the end of the expedition (Follow-up). Sperm concentration, cholesterol and oxysterol membrane content, and redox status were measured. Hypoxic trek led to a significant reduction in sperm concentration (p < 0.001, eta(2)p = 0.91), with a reduction from Pre to Post (71.33 +/- 38.81 to 60.65 +/- 34.63 x 10(6)/mL) and a further reduction at Follow-up (to 37.13 +/- 39.17 x 10(6)/mL). The seminal volume was significantly affected by the hypoxic trek (p = 0.001, eta(2)p = 0.75) with a significant reduction from Pre to Post (2.86 +/- 0.75 to 1.68 +/- 0.49 mL) and with partial recovery at Follow-up (to 2.46 +/- 0.45 mL). Moreover, subjects had an increase in ROS production (+86%), and a decrease in antioxidant capacity (-37%) in the Post period with partial recovery at Follow-up. These results integrated the hormonal response on thyroid function, hypothalamus-pituitary-gonadal axis, and the prolactin/cortisol pathways previously reported. An uncontrolled ROS production, rather than a compromised antioxidant activity, was likely the cause of impaired sperm quality. The reduction in fertility status observed in this study may lie in an evolutionary Darwinian explanation, i.e., limiting reproduction due to the adaptive disadvantage offered by the combined stressors of high-altitude hypoxia and daily physical exercise.

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