Scrotal heating and sedentary position

Testicular descent into the scrotum normally occurs by birth in boys and failure of testicular descent, especially when this extends into puberty and adulthood, results in absence of spermatogenesis. The testes descend into the scrotum in order that their temperature can be kept 3–4°C below core body temperature, as maintenance at normal body temperature is incompatible with spermatogenesis. It is probably also important that the testes are descended into the bottom of the scrotum rather than being placed at the top where their proximity to the body surface is likely to impair cooling of the testis. This is mentioned because it is reckoned that failure of the testes to descend into the bottom of the scrotum should probably be classified as a form of cryptorchidism . As well as testis position, the two other key elements in ensuring cooling of the testis are the presence of a vascular-rich corrugated scrotal surface via which heat loss can occur and the presence of an arterio-venous plexus (the pampiniform plexus) in the spermatic cord and which functions as a heat exchanger to cool incoming blood to the testis by heat exchange with the cooler venous blood that is exiting the testis . Normal functioning of this plexus is important for maintaining testicular coolness, and it is potentially susceptible to disruption by chemicals or by vascular-active drugs disorders such as varicocele in which the veins in the plexus are varicosed . However, even if the pampiniform plexus is functioning normally, it cannot cool the incoming arterial blood to the testis unless the blood leaving the testis is already itself cool, and this requires heat loss via the scrotal surface and its transmission to the underlying testes. Therefore, anything that impedes scrotal heat loss will affect testicular temperature and in turn any elevation of testicular temperature will have a harmful effect on spermatogenesis. In general, the more prolonged is the elevation in testicular temperature, then the greater will be the detrimental effect on spermatogenesis 

 

The most obvious things that can affect scrotal heat loss are a febrile illness such as influenza, exposure to an exogenous heat source, such as occupationally (bakers, welders, foundry workers) or via taking a hot bath . Based on experimental studies in laboratory animals, a 30 min soak in a moderately hot bath (40–42°C) impairs spermatogenesis  and, more importantly, it can induce germ cell apoptosis, DNA damage to the sperm and impair embryo development and fertility when ‘affected’ males are mated with normal females (Paul et al. 2008a,b). Follow-up studies have provided insight into the mechanisms involved (Paul et al. 2009). These have shown that heat exposure causes hypoxia and oxidative stress responses in the germ cells, manifest as increased expression of hypoxia inducible factor 1α, haem oxygenase 1, glutathione peroxidase 1 and glutathione-S-transferase-α, which push the germ cells towards apoptosis (Paul et al. 2009). Perhaps of more concern is if mild oxidative DNA damage is induced such that the germ cells continue their development into sperm, as this is associated with increased time for such sperm to initiate a pregnancy in humans (Loft et al. 2003). The adverse effects of scrotal heating on spermatogenesis and fertility are equally evident in non-human primates (Lue et al. 2002). Exposure to heat in other situations, such as in a hot shower, would have minimal effect as the scrotum is still able to thermo-regulate (it is not immersed in water) and a similar situation applies to saunas, although spending a long time in very hot saunas is detrimental.

 

Arguably of more concern are lifestyle and occupational factors that cause men to spend a long time in a sedentary position, something that has become common for many men working in Western countries today (figure 2). When seated, air does not circulate so easily around the scrotum and therefore there is less-efficient cooling, an effect likely to be exacerbated if wearing tight underpants or trousers. In studies of men in whom scrotal temperature was measured continuously in relation to position and activity, scrotal temperature increased progressively with duration of sedentation, and this was associated with lower sperm counts (Hjollund et al. 2000, 2002a,b). Studies in lorry and taxi drivers, who spend a long time seated, have also produced evidence for detrimental effects on semen quality (Figa-Talamanca et al. 1996; Bujan et al. 2000). However, overall, the relationship between time spent seated and poor semen quality is not suggestive of a major impact on fertility (Hjollund et al. 2000, 2002b;Stoy et al. 2004). Other studies have investigated the impact of wearing tight versus loose underwear and reached similar conclusions (Mieusset & Bujan 1995b). The most recent scenario investigated has been the impact on scrotal temperature of using a laptop computer (Sheynkin et al. 2005). It is perhaps more likely that scrotal heating may combine with or exacerbate adverse effects of other environmental/lifestyle factors and that only then will there be a significant impact on fertility (Lue et al. 2000).

 

Scrotal heating has been investigated as a potential contraceptive method in men and shown to be effective (Mieusset & Bujan 1995a). However, other studies that have tried to link more modest elevations in scrotal temperature (such as those associated with sedentary position) to infertility have not shown major or consistent associations, as outlined above. Nevertheless, it is common sense that any factor that impedes normal cooling of the scrotum/testes can only have an adverse effect on spermatogenesis, and it is therefore prudent to advise all men who are attempting to father a pregnancy, especially if they are known to have low sperm counts or low sperm motility, to take steps to minimize scrotal heating by any of the pathways mentioned above—where this has been done in a controlled way, the results have been positive (Jung et al. 2001). Such small lifestyle changes can only have a beneficial effect on spermatogenesis.