Heat stress can severely impact male fertility and our previous work has shown that ambient temperatures negatively affect fertility in a subset of stallions. The timing of susceptibility (0-2 weeks from heat event to subfertility) suggests that subfertility arises via mechanisms other than compromised spermatogenesis – e.g., epididymal, accessory gland or systemic responses. This study aimed to investigate interactions between climate, systemic and seminal markers of oxidative stress/inflammation, and fertility; and their role in heat-induced subfertility.
Dismount samples were collected weekly from 25 stallions across 3 stud farms, assessed for sperm quality and seminal plasma total antioxidant capacity (TAC), sperm DNA damage and oxidative DNA adducts (8-oxo-2'-deoxyguanosine; 8-oxo-dG). Blood samples were collected monthly and assessed for TAC, c-reactive protein (CRP), 8-oxo-dG and malondialdehyde. Fertility data (weekly pregnancy rates) and climate data (peak max and min temperature, heat load index [HLI] and temperature-humidity index [THI] of the preceding week) were recorded.
Peak temperatures in the week preceding sampling were inversely correlated with pregnancy rates (R=-0.19; p<0.01) across the cohort. Climate outputs correlated with plasma 8-oxo-dG and plasma CRP, most notably peak HLI in week preceding sampling (8-oxo-dG R=0.48, CRP R=0.42; p<0.01). Systemic and seminal TAC were correlated (R=0.4, p=0.0007), but only seminal TAC was responsive to temperature peaks.
Two stallions showed inverse correlations between temperature indices and pregnancy rates (R=-0.79 to -0.92, p<0.01). In these horses, seminal TAC did not increase following heat events, while systemic 8-oxo-dG correlated much more strongly with heat events than it did in non-susceptible horses (8-oxo-dG vs HLI R=0.93, p<0.01). CRP was inversely correlated with first-cycle pregnancy rate (R=-0.54, p<0.05).
These observations suggest that stallions experiencing heat induced subfertility have suboptimal adaptive responses and poorer ability to deploy antioxidant defences to mitigate heat stress. The mechanisms interlinking systemic and localised reproductive tract responses require further investigation.