A semen analysis comes back and the count looks reasonable. But then there’s another number, the motility percentage, and that’s the one flagged. Low sperm motility. Sometimes called asthenozoospermia. And suddenly a result that looked like it might be fine isn’t quite as straightforward as expected.
This is actually one of the more common patterns in male fertility investigations. Normal or near-normal count, but motility below the reference range. And because most people focus on count when they think about male fertility, the motility finding can catch them off guard.
Why motility matters as much as count
Sperm count gets most of the attention, partly because it’s the most intuitive metric. More sperm, better chance of fertilisation. That logic isn’t wrong, but it’s incomplete.
A sperm that isn’t moving isn’t going to fertilise anything, regardless of how many of them are present. After ejaculation, sperm need to travel through the cervix, into the uterus, up the fallopian tube, and reach the egg, a journey of several centimetres that takes between 45 minutes and several hours. Only progressively motile sperm, those swimming forward in a purposeful direction, can make that journey. Sperm that are moving erratically, in circles, or not at all, don’t contribute meaningfully to natural conception.
The WHO 2021 reference values set total motility at 42% or above, and progressive motility at 30% or above. Progressive motility is the more clinically relevant figure. A result with 50% total motility but only 12% progressive motility is a different picture from one with 50% total and 40% progressive. The numbers need to be read together.
The terminology question
Asthenozoospermia is the clinical term for reduced sperm motility below reference values. It can occur in isolation, where count and morphology are normal but motility is low, or alongside other parameter deficits. When count, motility, and morphology are all below reference simultaneously, the term used is oligoasthenoteratozoospermia, or OAT syndrome.
Knowing the terminology matters less than understanding what the pattern means clinically. Isolated low motility with otherwise normal parameters is a different conversation from low motility occurring alongside severely reduced count.
Why this happens
Low sperm motility has a range of causes, and identifying the underlying one matters for what can be done about it.
Varicoceles are among the most commonly identified structural causes. These are dilated veins in the scrotum that raise testicular temperature, which impairs spermatogenesis and sperm quality including motility. Varicoceles are found in a meaningful proportion of men investigated for infertility, and their surgical or radiological treatment has evidence supporting improvement in semen parameters in selected patients, though the benefit varies.
Infections, both past and present, can affect motility. Certain bacterial infections directly impair sperm function. Chronic low-grade genital tract infections sometimes go undetected but can affect sperm quality over time.
Hormonal imbalances, including low testosterone, elevated prolactin, or thyroid dysfunction, affect sperm production and maturation. A hormonal profile is a standard part of the workup for significant motility reduction.
Oxidative stress is increasingly recognised as a factor in low motility. Reactive oxygen species, produced by the body in greater quantities under conditions of inflammation, infection, lifestyle factors, and environmental exposures, damage sperm cell membranes and DNA, reducing motility and fertilisation capacity. Sperm DNA fragmentation, which isn’t measured on a standard semen analysis, is associated with oxidative damage and can be elevated even when standard motility parameters appear borderline.
Certain medications affect motility, including anabolic steroids, some antifungals, and some antibiotics. Recreational drug use, including cannabis, has been associated with reduced motility in some studies, though the evidence is inconsistent.
Lifestyle factors with reasonable evidence behind them: smoking is associated with reduced progressive motility. Obesity is associated with altered hormonal profiles that affect sperm production. Prolonged scrotal heat exposure, from laptops, hot baths, or sedentary occupations, is a modifiable factor.
In some cases, no specific cause is identified. The motility is low, the investigation doesn’t find a clear explanation, and the clinical approach focuses on optimising what can be optimised and adapting the treatment pathway accordingly.
The test and what it tells you
A semen analysis is the starting point. Ideally, it’s done twice, with a gap of at least 10 to 12 weeks, before drawing clinical conclusions. Sperm parameters vary between samples, and a single result, particularly an unexpected one, should be confirmed before significant decisions are made.
The sample needs to be produced correctly. The recommended abstinence window is 2 to 7 days. Shorter than that and concentration may be lower; longer and motility often drops as older sperm accumulate in the reproductive tract. The sample should reach the lab quickly if produced at home, within 30 to 60 minutes at body temperature.
If motility is consistently low on two analyses, further investigation typically includes a hormonal profile covering FSH, LH, testosterone, prolactin, and thyroid function. A scrotal ultrasound can identify varicoceles and assess testicular structure. Sperm DNA fragmentation testing may be considered, particularly in couples where female investigations are normal but IVF cycles have produced poor embryo development or recurrent early pregnancy loss.
What can be done about it
Sperm motility treatment depends on what’s driving it. That’s the honest starting point. A low motility result without an identified cause is treated differently from one with a clear underlying factor.
Where a varicocele is found in a man with abnormal semen parameters, treatment, either surgical or through radiological embolisation, is associated with improvement in motility and other parameters in a proportion of patients. The evidence is most consistent for clinically detectable varicoceles rather than subclinical ones, and the magnitude of benefit varies.
Hormonal optimisation is relevant where a hormonal abnormality is identified. Treating elevated prolactin or correcting thyroid dysfunction can improve semen parameters. Low testosterone from exogenous testosterone use is a specific case: testosterone supplements suppress the body’s own production of sperm. Stopping exogenous testosterone, and allowing the hormonal axis to recover, often significantly improves parameters over several months.
For oxidative stress and DNA fragmentation, antioxidant supplementation is the area with the most evidence, though the quality of that evidence is mixed. Coenzyme Q10, vitamin C, vitamin E, and folate are the most studied. Some trials have shown modest improvements in motility and DNA fragmentation scores with supplementation. The effect size is generally not large, and supplements alone are not a treatment for significant low motility, but they may be used as adjuncts alongside other interventions.
Lifestyle modifications with reasonable evidence: stopping smoking, reducing alcohol, correcting obesity, avoiding anabolic steroids, and reducing scrotal heat exposure are all supported by the literature to varying degrees. None of these is a quick fix, and because sperm take around 70 to 74 days to develop, any changes made now won’t show in a semen analysis for approximately three months.
Two hypothetical profiles that show where this leads
A 33-year-old with a semen analysis showing normal concentration at 22 million per millilitre, but progressive motility at 18%, below the 30% reference. Count is fine. Morphology is borderline. A varicocele is identified on scrotal ultrasound, clinically palpable on one side. Hormones are normal. He’s a smoker. In a profile like this, the reasonable approach involves treating the varicocele, stopping smoking, and rescanning in three to four months. Motility improvement after varicocele treatment in this kind of profile is plausible, and the combination of structural treatment and lifestyle change gives the best chance of seeing an improvement before deciding whether assisted reproduction is needed.
A different hypothetical: a 38-year-old with progressive motility at 11%, moderate DNA fragmentation on a fragmentation test, and no identified structural cause. Hormones normal. Non-smoker. Healthy BMI. Antioxidant supplementation is recommended. The couple has been trying for 18 months. His partner’s investigations are normal. In this profile, the motility and fragmentation combined, with no reversible structural cause found, shifts the conversation toward IUI or IVF with ICSI rather than continuing to wait for natural improvement. ICSI, which selects a single sperm and injects it directly into the egg, bypasses the motility requirement for fertilisation entirely. For couples where male factor is the primary identified issue, it’s often the most direct clinical response.
How motility interacts with fertility treatment
In IUI (intrauterine insemination), the sperm sample is processed in the lab before use, a step called sperm washing that concentrates the most motile sperm and removes seminal fluid. The post-wash total motile sperm count is what determines whether IUI is a viable option. Consistently very low motility may produce a post-wash count that’s too low for IUI to have a meaningful success rate.
In IVF with conventional insemination, sperm are placed near eggs in a dish, and fertilisation occurs naturally. Low motility increases the risk of fertilisation failure in this setting. ICSI removes that risk by injecting sperm directly into the egg, which is why it’s the standard approach when significant male factor is present.
For very severely affected motility, particularly where few or no progressively motile sperm are found, a test called the hypo-osmotic swelling test can identify living but non-motile sperm, which may still be usable for ICSI despite not moving.
The thing worth saying directly
Low sperm motility is not a condition that exists on its own in a vacuum. It’s a finding that, depending on severity, the other parameters it accompanies, and the clinical history, either warrants monitoring and lifestyle change, further investigation, medical or surgical treatment, or a shift toward assisted reproduction.
What it’s not is a definitive verdict on what’s possible. Men with significantly reduced motility father children, through natural conception in mild cases and through assisted reproduction in more severe ones. The clinical response depends on having an accurate picture of what’s driving it and what options that picture opens up.
If you’ve had a semen analysis flagging low motility and you want to understand what it means for your specific situation, the next step is a conversation with someone who can look at the full results, not just the flagged number.
Book a consultation at 9M Fertility.
→ Also read: What to Expect from a Semen Analysis: A Complete Guide for Men
→ Also read: TESA Procedure: A Complete Guide for Men with Zero Sperm Count
