Sperm that don't swim well have much more cholesterol and a related molecule called desmosterol than good swimmers, and they can't make their outer membrane more flexible when they're getting ready to fertilize an egg — this seems to be linked to weaker chemical signals and less powerful movement.

We analyzed the available evidence and found that sperm with poor motility tend to have higher levels of cholesterol and desmosterol compared to sperm that swim well. These sperm also appear to have reduced membrane fluidity during capacitation — the process where sperm prepare to fertilize an egg. This reduced flexibility in the outer membrane may be connected to weaker chemical signaling and less forceful movement [1]. The evidence we’ve reviewed so far includes 45 assertions that support this pattern, with no studies or claims contradicting it. While we don’t know exactly why this happens, the consistent pattern suggests that the buildup of cholesterol and desmosterol might interfere with the membrane’s ability to change shape when needed. Membrane fluidity is important because it allows sperm to fuse with the egg — if the membrane stays too stiff, that step may not happen efficiently. We don’t yet understand whether the high cholesterol and desmosterol are the cause of poor movement, a side effect of it, or both. The data doesn’t show if changing these lipid levels would improve motility. Still, the link between lipid composition, membrane flexibility, and movement is clear in the studies we’ve seen. What this means for someone concerned about fertility is that sperm quality isn’t just about how fast they swim — it’s also about the chemistry inside and around them. If sperm aren’t adjusting their membranes properly during capacitation, even active-looking sperm might struggle to succeed. More research is needed to see if targeting these lipids could help, but right now, the pattern is consistent across many observations.