Hyperthermia is more important than hypoxia as a cause of disrupted spermatogenesis and abnormal sperm

Abstract We tested the hypothesis that hypoxia replicates effects of hyperthermia on reducing number and quality of sperm produced, whereas hyperoxia mitigates effects of hyperthermia. Forty-eight CD-1 mice (∼50 d old), inspired air with 13, 21, or 95% O 2 and were exposed to ambient temperatures of 20 or 36 °C (3 × 2 factorial, six groups) twice for 12 h (separated by 12 h at 20 °C and 21% O 2 ), with euthanasia 14 or 20 d after first exposure. Combined for both post-exposure intervals, there were primarily main effects of temperature; mice exposed to 20 vs 36 °C had differences in testis weight (110.2 vs 96.9 mg, respectively; P  6 sperm/g testes, P  2 (from 13 to 95%) affected morphologically abnormal heads (15.4, 10.8 and 17.6%, respectively; P  per se and not secondary hypoxia was the fundamental cause of heat-induced effects on spermatogenesis and sperm. These findings are of interest to develop evidence-based efforts to mitigate effects of testicular hyperthermia, as efforts should be focused on hyperthermia per se and not on hyperthermia-induced hypoxia.