Infertility is a worldwide issue impacting 15% of couples' population. Male‐related infertility results in almost 50% of these cases. Considering lifestyle factors associated with infertility, here in this literature review article, we aimed to discuss training/sport effects on male‐related infertility. Regarding this issue, human and animal model studies related to the subject were gathered and analysed. Exercise is well known as a general improving factor, however, excessive exercise can result in male infertility due to reduced hypothalamus–pituitary–gonadal axis (HPT) function, increased oxidative stress and chronic inflammation. Consequently, these underlying impacts result in a low testosterone production, and reduced semen quality, and can lead to infertility. In contrast, it has been revealed that exercise can improve male fertility status in lifestyle‐induced infertility condition such as obesity and diabetes. Indeed, exercise, by increasing testicular antioxidant defence, reducing pro‐inflammatory cytokines level and enhancing the steroidogenesis process, leads to improved spermatogenesis and semen quality in lifestyle‐induced infertility. In fact, it seems that individual health status as well as exercise volume, intensity and duration are effective‐involved co‐factors that influence the impact that exercise will promote on male fertility. Regarding these findings, it is important to study exercise different impacts in further clinical trials in order to generate preservative guidelines for exercise and also considering exercise as a treatment option in lifestyle‐induced disease management.

Foeniculum vulgare (FVE; fennel) is an aromatic plant belonging to Umbelliferae family, which is widely used in traditional societies because of its different pharmaceutical properties. To uncover the fennel-derived essential oil (FVEO)-induced effects on male reproductive potential, 24 mature male albino mice were divided into, control, 0.37, 0.75, and 1.5 mg kg FVEO-received groups. Following 35 days, the animals were euthanized and the testicular tissue and sperm samples were collected. The histological alterations, tubular differentiation (TDI), spermiogenesis (SPI) indices, apoptosis ratio, and RNA damage of germinal cells were analyzed. Moreover, the sperm count, motility, viability, chromatin condensation, and DNA fragmentation were assessed. Finally, the pre-implantation embryo development including; the percentage of zygote, 2-cell embryos and blastocysts were assessed. Observations showed that the FVEO, dose dependently, increased histological damages, resulted in germ cells dissociation, depletion, nuclear shrinkage and significantly (P < .05) decreased tubular differentiation and spermiogenesis ratios. Moreover, the FVEO-received animals (more significantly in 1.5 mg kg -received group) exhibited decreased sperm count, viability, and motility and represented enhanced percentage of sperms with decondensed chromatin and DNA fragmentation. Finally, the animals in FVEO-received group showed diminished zygote formation and represented decreased pre-implantation embryo development compared to control animals. In conclusion, our data showed that, FVEO albeit at higher doses, is able to adversely affect cellular DNA and RNA contents, which in turn is able to negatively affect the sperm count and morphology. All these impairments are able to negatively affect the fertilization potential as well as pre-implantation embryo development.

Testicular torsion (TT) is an emergency complication that leads to oxidative stress and adversely affects spermatogenesis. Although immediate treatment consists of testicular detorsion (TD) to reverse TT-induced ischemia, mechanisms underlying recovery have yet to be fully understood. The current study aimed to investigate TD effects after a one-hour experimental TT by evaluating testicular antioxidant status and apoptosis-related proteins. Forty male Wistar rats were submitted to TT by testicular rotation, for one hour. Following TT, 32 rats were submitted to TD for 1, 2, 4, and 8 h (N = 8/group), the other 8 rats euthanized as TT-only. For controls, 8 rats were sham-operated. Testicular tissues were aseptically dissected for biochemical, histopathological, and immunohistochemistry analyses. The TD groups, especially after 4 h of TD, exhibited diminished MDA and increased TAC and GPX levels in testicular tissue. Levels of p53 and Caspase-3 were down-regulated in T1D4 and T1D8 groups versus torsion group. Bcl-2 was increased in T1D4 and T1D8 groups compared to the TT group. Moreover, spermatogenesis was recovered in T1D4 and T1D8 groups compared to the TT group. It can be concluded that after 1 h TT in rats, at least 4 h post-TD is needed for testicular tissue to initiate recovery.

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