Male infertility sperm motility-Male Infertility - Urology Care Foundation

There is no scientific evidence that wearing tight clothes or bike shorts affects the quality of your sperm. Diet, vitamins and supplements actually have very little impact on your sperm count - but they do help you stay healthy. Sports injuries to the groin will only have an impact on sperm production in extremely severe cases. While the effect of age on a man's fertility is not as significant as it is with women, there is a decline in the quality of sperm after the age of After this age, sperm volume, motility and morphology declines and damage to sperm DNA increases.

Male infertility sperm motility

Male infertility sperm motility

Male infertility sperm motility

Male infertility sperm motility

Male infertility sperm motility

Confirming the microarray studies, Nsun7 transcription was low in day-old testes when the majority of advanced cells are in zygonema, but increased by 14—18 days of age when most spermatocytes are in pachynema Fig. Men who work in the incertility or have jobs that include painting, driving, or repeated trauma to Proper way to use a condom pelvic area may be at risk for work-induced infertility. It also gets enough tissue for sperm extraction. Lifestyle Tips For Good Urologic Health You can get on track for good urologic health with better infertolity habits and small changes motklity your lifestyle. For the sperm to get through the cervical mucus to Male infertility sperm motility a woman's egg, they need to have progressive motility of at least 25 micrometers a second. It can exist at birth "congenital". There is moderate hyperstimulation in 5 out of women having IVF. For example, your healthcare provider may ask if you've had trouble with erections.

Artistic nudity models portfolio. Home sperm count testing kits

The difference between Grannies babes two lies in the complexity of movements, with qigong being a simpler form Male infertility sperm motility repetitive body movements and breathing techniques. If the sperm is otherwise healthy, pregnancy with low sperm motility can occur. The benefits did not persist when the glutathione was stopped. Urology Care Foundation. There are lifestyle choices people can make that will help improve the quality Male infertility sperm motility their sperm. Because of religious or cultural beliefs, some men prefer an alternative method of semen collection. Sperm motility can be affected by a number of things. Support Center Support Center. This content does not have an English version. Carnitine and its acyl esters as secondary antioxidants? Comparison of motility stimulants for cryopreserved human semen. Prolonged stress raises levels of cortisol, which has strong negative effects on testosterone. Taking 1.

There are six main criteria for healthy sperm:.

  • Infertility has long been thought of as primarily a female issue outside medical circles.
  • Many infertile couples have more than one cause of infertility, so it's likely you will both need to see a doctor.
  • Quick Definition: The definition of motility is the ability of an organism or fluid to move.
  • While we may be comfortable with an allopathic approach to male infertility, we are also responsible for knowledge about lifestyle modifications and holistic, complementary, and alternative therapies that are used by many of our patients.
  • There are six main criteria for healthy sperm:.

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Male infertility is any health issue in a man that lowers the chances of his female partner getting pregnant. About 13 out of couples can't get pregnant with unprotected sex. There are many causes for infertility in men and women. In over a third of infertility cases, the problem is with the man. This is most often due to problems with his sperm production or with sperm delivery. The man's body makes tiny cells called sperm. During sex, ejaculation normally delivers the sperm into the woman's body.

The male reproductive system makes, stores, and transports sperm. Chemicals in your body called hormones control this. Sperm and male sex hormone testosterone are made in the 2 testicles. The testicles are in the scrotum, a sac of skin below the penis.

When the sperm leave the testicles, they go into a tube behind each testicle. This tube is called the epididymis. Just before ejaculation, the sperm go from the epididymis into another set of tubes. These tubes are called the vas deferens. Each vas deferens leads from the epididymis to behind your bladder in the pelvis. There each vas deferens joins the ejaculatory duct from the seminal vesicle.

When you ejaculate, the sperm mix with fluid from the prostate and seminal vesicles. This forms semen. Semen then travels through the urethra and out of the penis.

Male fertility depends on your body making normal sperm and delivering them. The sperm go into the female partner's vagina. The sperm travel through her cervix into her uterus to her fallopian tubes.

There, if a sperm and egg meet, fertilization happens. Making mature, healthy sperm that can travel depends on many things. Problems can stop cells from growing into sperm. Problems can keep the sperm from reaching the egg. Even the temperature of the scrotum may affect fertility. These are the main causes of male infertility:.

Sperm problems can be from traits you're born with. Lifestyle choices can lower sperm numbers. Smoking, drinking alcohol, and taking certain medications can lower sperm numbers. Other causes of low sperm numbers include long-term sickness such as kidney failure , childhood infections such as mumps , and chromosome or hormone problems such as low testosterone.

Damage to the reproductive system can cause low or no sperm. About 4 out of every 10 men with total lack of sperm azoospermia have an obstruction blockage. A birth defect or a problem such as an infection can cause a blockage. Varicoceles are swollen veins in the scrotum. They're found in 16 out of of all men.

They are more common in infertile men 40 out of They harm sperm growth by blocking proper blood drainage. It may be that varicoceles cause blood to flow back into your scrotum from your belly.

The testicles are then too warm for making sperm. This can cause low sperm numbers. For more information please refer to the Varicoceles information page. Retrograde ejaculation is when semen goes backwards in the body. This happens when nerves and muscles in your bladder don't close during orgasm climax.

Semen may have normal sperm, but the semen cannot reach the vagina. Retrograde ejaculation can be caused by surgery, medications or health problems of the nervous system. Signs are cloudy urine after ejaculation and less fluid or "dry" ejaculation.

Sometimes a man's body makes antibodies that attack his own sperm. Antibodies are most often made because of injury, surgery or infection. They keep sperm from moving and working normally. We don't know yet exactly how antibodies lower fertility. We do know they can make it hard for sperm to swim to the fallopian tube and enter an egg. This is not a common cause of male infertility.

Sometimes sperm can be blocked. Repeated infections, surgery such as vasectomy , swelling or developmental defects can cause blockage. Any part of the male reproductive tract can be blocked. With a blockage, sperm from the testicles can't leave the body during ejaculation. Hormones made by the pituitary gland tell the testicles to make sperm.

Very low hormone levels cause poor sperm growth. Sperm carry half of the DNA to the egg. Changes in the number and structure of chromosomes can affect fertility. For example, the male Y chromosome may be missing parts. Certain medications can change sperm production, function and delivery.

These medications are most often given to treat health problems like:. Causes of male fertility can be hard to diagnose. The problems are most often with sperm production or delivery.

Diagnosis starts with a full history and physical exam. Your health care provider may also want to do blood work and semen tests. Your health care provider will take your health and surgical histories. Your provider will want to know about anything that might lower your fertility. These might include defects in your reproductive system, low hormone levels, sickness or accidents.

Your provider will ask about childhood illnesses, current health problems, or medications that might harm sperm production. Such things as mumps, diabetes and steroids may affect fertility.

Your provider will also ask about your use of alcohol, tobacco, marijuana and other recreational drugs. He or she will ask if you've been exposed to ionizing radiation, heavy metals or pesticides. Heavy metals are an exposure issue e. All of these can affect fertility. Your health care provider will learn how your body works during sex. He or she will want to know about you and your partner's efforts to get pregnant.

For example, your healthcare provider may ask if you've had trouble with erections. The physical exam will look for problems in your penis, epididymis, vas deferens, and testicles. Your doctor will look for varicoceles.

They can be found easily with a physical exam. Semen analysis is a routine lab test. It helps show the cause of male infertility. The test is most often done twice.

Many different tubes carry sperm. Cholesterol is a fatty substance that's needed to build cells. Reprod Health. Results from a cohort of severely obese men? Non-progressive motility refers to sperm that do not travel in straight lines or that swim in very tight circles. National Center for Complementary and Integrative Health. There are six main criteria for healthy sperm:.

Male infertility sperm motility

Male infertility sperm motility. What It Means, What's Normal, What's Not

This has also been linked to decreased sperm motility. Low sperm motility may also be due to a disorder in the male accessory sex gland secretion, which leads to the glands emptying more slowly. Sperm motility can be tested through a routine semen analysis. The sample must be kept at room temperature and delivered to the facility within 30 to 60 minutes. If less than 40 percent of your sperm are motile, your considered to have low sperm motility.

Some supplements may also help improve sperm motility. For example, one study found a 52 percent increase in sperm motility in men who took a daily supplement of micrograms of selenium along with units of vitamin E for at least days in a row. Speak to your doctor before taking supplements, and be careful about where you buy them. Supplements are not regulated, so you should only buy them from reputable vendors. If the cause of the sperm mobility issue is a medical problem, such as low hormone levels or varicocele, medication such as follicle-stimulating hormone or human chorionic gonadotropin may help.

In some cases, your doctor may recommend surgery. Many factors can affect male fertility. If the sperm is otherwise healthy, pregnancy with low sperm motility can occur. Using a reproductive technology such as in vitro fertilization or intrauterine insemination IUI can help increase the chance of pregnancy. This is because they bypass the need for the sperm to swim on their own.

Your doctor can test you and your partner to determine if there are any health conditions affecting fertility. Your doctor will then determine next steps. Infertility has long been thought of as primarily a female issue outside medical circles. Yet both male and female factor fertility issues contribute….

Alcohol, even in moderate amounts, can affect your sexual health. It can lead to loss of libido and infertility in both men and women. Learn more…. Infertility is a problem for many men. Here are 10 science-backed ways to increase sperm count and enhance overall fertility in men.

Nux vomica can affect the nervous system, and is most often used to treat conditions that are acute, or develop rapidly and have a short course. Collagen is an essential building block for the entire body, from skin to gut, and more. Here's five changes you may see or feel just by taking more….

You can do a lot of prep work to make the perfect sleep environment. But if that doesn't work, here are six other hacks to try. Identifying your triggers can take some time and self-reflection. In the meantime, there are things you can try to help calm or quiet your anxiety…. If your take on meditation is that it's boring or too "new age," then read this. Once there, the sperm must fertilize the egg, which also requires movement.

Motility is just one measurement of sperm and semen health. Other factors considered during a semen analysis include:. In the big picture of male semen health, if only motility is a problem, the odds of spontaneous pregnancy are better than if other issues are present.

Percentage motile : what percentage of all the sperm in a single ejaculate are moving. Percentage motile concentration : what percentage of sperm are moving in one measurement of semen, usually presented as millions of cells per mL. Total motile sperm count TMSC : how many sperm are swimming in a single ejaculate. This number has been shown to be most relevant to male fertility prognosis. For example, a sperm that just vibrates in place would be considered non-progressive.

A sperm that zigzags but makes forward progression would be considered progressive. Progressive motility is needed in order for the sperm to swim their way up the female reproductive tract. Total motility refers to the percentage of sperm making any sort of movement. This movement can include non-progressive movement. Not all of those sperm, however, are expected to be completely healthy. When it comes to sperm motility, for an ejaculate sample to be considered normal, at least 40 percent of the sperm should be motile, or moving.

This can include non-progressive movement. A diagnosis of poor sperm motility is usually made based on the percentage of motile sperm. However, research has found that the total motile sperm count is a more relevant measurement. A total motile sperm count over 20 million is considered to be normal.

Lower than 5 million is poor sperm motility. Less than 1 million is severe poor sperm motility. Sperm motility can be affected by a number of things. Usually, when sperm motility is poor, there are other problems found with sperm health. For example, men with poor sperm motility may also have low sperm counts or poor sperm morphology or sperm shape.

Sperm that aren't formed properly can't swim properly. Poor sperm motility may also occur if a man has infrequent sexual activity.

In this case, if the first ejaculate collected showed poor motility, a second ejaculate collected soon after should be better. Get diet and wellness tips to help your kids stay healthy and happy. More in Fertility Challenges. Why Do Sperm Swim? Motility and Semen Health.

Motility Measurements. Types of Motility. Normal Sperm Motility.

Low sperm count - NHS

Poor sperm quality is the major cause of infertility in humans. Other than sex-linked factors, the genetic basis for male infertility is poorly defined, largely due to practical difficulties in studying the inheritance of this trait in humans. As an alternative, we have conducted forward genetic screens in mice to generate relevant models. We report on the identification and characterization of a chemically-induced mutation, Ste5Jcs1 , which causes affected male mice to be sterile or subfertile.

Mutant sperm exhibited depressed progressive motility associated with a rigid flagellar midpiece but not principal piece segment, which could not be rescued by treatment with agents that stimulate cAMP or calcium signaling pathways.

Overall mutant sperm ultrastructure appeared normal, including the axoneme, although the midpiece mitochondrial sheath showed abnormal electron density patterns.

Positional cloning of Ste5Jcs1 led to the identification of a mutation in a novel gene called Nsun7 , which encodes a protein with a Sun domain that is homologous to tRNA and rRNA cytosine methyltransferases. Therefore, Ste5Jcs1 mutation uncovers a previously unrecognized biological process in sperm that underscores the functional compartmentalization of the midpiece and principal piece of the flagellum.

Some studies have suggested that at least half of the cases of idiopathic infertility in men have a genetic basis [ 2 ]. The genes underlying human infertility have been difficult to elucidate because of the nature of the phenotype, which confounds genetic analysis. An exception is interstitial deletion of the Y chromosome, which contains several genes required for fertility [ 3 ]. Most of the progress in understanding the genetics of human infertility has come from analysis of the mouse. Using gene knockout technology, more than genes causing abnormal spermatogenesis have been identified according to Mouse Genome Database, MGD.

These mutations affect a variety of spermatogenic stages, and many have been identified in studies that were originally intended to evaluate somatic defects [ 4 ]. In addition, mouse models have been generated by forward genetic approaches [ 5 — 7 ], although full exploitation of these important resources requires positional cloning of the underlying genes.

Therefore, an understanding of the mechanisms that regulate flagellar movement is crucial. Regulation of flagellar movement includes the activation of motility when sperm leave the epididymis and the hyperactivation of motility in the oviduct. Activation is primarily stimulated by cAMP signaling, whereas hyperactivation is primarily stimulated by calcium Ca signaling [ 8 ].

Proper flagellar movement is dependent upon the axoneme, which is subjected to different regulatory systems in the midpiece and principal piece of the flagellum. For example, the soluble adenylyl cyclase sAC , which is required for the activation of motility, is restricted to the midpiece [ 9 ], while the plasma membrane calcium channels CatSper1, CatSper2, and CatSper4, which are required for the hyperactivation of motility, are restricted to the principal piece [ 10 , 11 ].

Little is known about how the smooth waves of axonemal contractions are coordinated along the entire length of the flagellum, across its distinct subregions. We present the genetic and phenotypic characterization of a male infertility mutant, Ste5Jcs1 , which was isolated in a forward genetic mutagenesis screen [ 12 ].

The sperm from these animals are characterized by poor progressive motility, linked to rigidity of the midpiece but not the principal piece and apparent defects of the mitochondrial sheath therein. The Ste5Jcs1 mutation is unique in that it provides a relevant model for the most common cause of human male infertility poor sperm quality , and provides insight into the functional compartmentalization of the midpiece and principal piece of the sperm flagellum.

The Ste5Jcs1 mutation was generated as described previously [ 12 ]. Sperm were analyzed using the media and procedures described previously [ 13 ]. The cauda epididymides were removed from adult males and punctured four times at the distal end with a gauge needle in a prewarmed mm polystyrene culture dish that contained 3 ml of medium.

Sperm were allowed to swim out for 10 min before 1 ml of the sperm suspension was drawn off from the far side of the dish.

The females were checked for the presence of a copulatory plug over the first 4 days, and either removed to a holding cage or left with the male, then checked again at 3 wk for pregnancy Supplementary Table 1 , available online at www.

The JC-1 probe was diluted fold from the stock 1. The pellet was fixed in 2. Thin sections nm thickness were cut and stained with uranyl acetate and lead citrate. Specimens were examined in a Philips Transmission electron microscope at 80 kV. Experimental data generated during CASA analysis of sperm were analyzed using the Minitab statistical software. In a previous study, a forward genetic screen was conducted to isolate ENU-induced mutations that mapped to the Rw inversion region of proximal mouse Chr 5 [ 12 ].

Ste5Jcs1 was one of two male-specific infertility mutations recovered in the screen. In the original experiments, the male homozygotes were found to be sterile, as assessed by failing to impregnate a wild-type partner after about 1 mo of cohabitation, and sperm from the affected males were reported to show abnormal motility [ 12 ].

Given time often several weeks after sexual maturity , some males produced small litters average of 3. We observed no cases of such males impregnating more than one female in a 7-day period. This indicates that a small percentage of the sperm in the ejaculate although possibly not every ejaculate is capable of reaching the oviduct and penetrating the outer layers of the oocyte to achieve fertilization.

Thus, the mutation results in subfertility, rather than sterility. The subfertility phenotype was not attributable to decreased sperm counts, as similar concentrations of sperm were extracted from mutant and control males Table 1. Histological sectioning through the cauda epididymides confirmed that mutant males had high concentrations of sperm Fig.

However, when examined microscopically, sperm from mutant males displayed an obviously aberrant motility pattern, which was quantified and characterized as described below. Histological analysis of the Ste5Jcs1 mutant. Mutant males had a lower percentage of motile sperm Table 1. Most notable was that the midpiece section of the flagellum appeared abnormally rigid and did not contribute to flagellar bending see video in Supplemental material, available online at www.

Ste5Jcs1 sperm swam in a slow circular trajectory or erratically with frequent changes of direction due to the asymmetrical beating of the principal piece and the immobility of the midpiece. Incubation under conditions that resulted in a hyperactivated motility pattern for the wild-type sperm increased the straightness of the swimming pattern but not the midpiece flexibility of Ste5Jcs1 sperm Table 1.

Ste5Jcs1 sperm ultrastructure and fluorescent imaging of sperm mitochondria. Video capture of the activated motility pattern of the same sperm in two sequential frames. A Wild-type sperm exhibiting symmetrical and moderate amplitude flagellar beating. The motility pattern can be viewed online in the supplemental video footage available at www.

Transmission electron micrographs of cross-sections through the midpiece of wild-type C and mutant D sperm flagella.

Axoneme, ax; outer dense fibers, df; mitochondria, mt. The presence of active mitochondria is indicated by orange fluorescence in the midpiece arrows. Mutant sperm were treated with various pharmacological agents, to assess whether any of these agents could rescue the phenotype and thereby indicate a possible basis for the motility defect. Incubation with cAMP-AM [ 14 ] or caffeine [ 15 ], which stimulates the soluble adenylyl cyclase SACY signaling pathway to activate flagellar bending, did not ameliorate midpiece rigidity.

The nonprogressive motility phenotype was partially rescued when sperm were treated with thimerosal Table 1 , an agent that stimulates an increase in intracellular calcium in sperm [ 16 ]; however, the midpiece rigidity remained.

Other agents that raise the level of cytoplasmic calcium in sperm, such as thapsigargin [ 16 ], ionomycin [ 17 ], procaine [ 18 ], and caffeine [ 16 ], also failed to rescue midpiece rigidity data not shown. Lastly, NH 4 Cl, which elevates intracellular pH and calcium [ 15 , 19 , 20 ], did not rescue the motility defect data not shown. To uncover the ultrastructural defects in mutant sperm, sections through the middle and principal pieces were examined by transmission electron microscopy TEM.

However, the mitochondrial region of the midpiece section appeared vacuolated in the mutant compared to the wild-type Fig. We also assessed the mitochondrial membrane potential and respiratory activity in Ste5Jcs1 sperm using the JC-1 cationic dye. The mutant sperm stained normally Fig. Although the vacuolated appearance of Ste5Jcs1 mutant mitochondria bears close resemblance to that of the mitochondria of PMCA4-null sperm [ 21 ], the results of the single-sperm calcium imaging suggest that these sperm do not experience calcium overload and that they have lower basal levels of calcium than the wild-type Fig.

We mapped Ste5Jcs1 to a 2. This region contains 24 candidate genes Table 2 , only one of which is expressed predominantly in testis according to the available microarray and EST expression data , i. Microarray analysis of the mouse testicular transcriptome presented in the GermOnline database at www. This is roughly concordant with the results obtained with one Affymetrix probe set [ 24 ] indicating that transcription initiates on Day 21 after birth, at which time round spermatids are the most advanced male germ cells.

NA, not applicable; no male genital ESTs were present. Given the consistency between the timing of Nsun7 expression and the phenotype, we considered this defect to be a strong candidate for Ste5Jcs1 and thus, we sequenced the allele in mutant mice. Hereinafter, we refer to this allele as Nsun7 Ste5Jcs1.

Identification of a point mutation in Nsun7. A Sequencing traces of nucleotides to from exon 7 of Nsun7. The C to T point mutation at nucleotide of the mutant is boxed. The NSUN7 protein is presented at the top as a rectangle, and the numbers above denote amino acid positions. The location of the point mutation is indicated by the asterisk.

Underneath are schematic homology alignments to proteins encoded by the mouse paralog Nsun5 , as well as orthologs in yeast Sc , Drosophila Dm , and zebrafish Dr. The amino acid sequences of these homologs extend beyond the regions of homology to NSUN7, as indicated.

The percentages amino acid identity ID and similarity Sim; conservative amino acid differences , as computed by BLASTp alignments, are indicated on the right. Amplification of the Gapdh control lower panel. Orthologs or homologs of NSUN7 are present in vertebrates zebrafish to yeast, with most of the amino acid sequence conservation centered on the Sun domain Fig. To confirm the published microarray data alluded to above and to assess the transcript levels in mutant testes, RT-PCR analysis was performed on RNA samples obtained from prepubertal and adult mice.

Confirming the microarray studies, Nsun7 transcription was low in day-old testes when the majority of advanced cells are in zygonema, but increased by 14—18 days of age when most spermatocytes are in pachynema Fig. It is therefore possible that truncated NSUN7 is produced in mutant animals. The Ste5Jcs1 mutation led to the discovery of a novel gene that was not previously suspected to play a role in spermatogenesis.

Moreover, the phenotype is unique in terms of its effects on the sperm midpiece, which in turn affects progressive motility. Although we do not know whether mutations in Nsun7 are responsible for any cases of human infertility or subfertility, the general phenotype of poor sperm quality is a relevant one for idiopathic fertility defects, and it is possible that mutations in other genes that affect the same or related processes occur in humans.

Sperm acquire motility in the epididymis, and this motility is mediated primarily by cAMP signaling. Motility is manifested by proper function of the axoneme, which is comprised of microtubules and ATP-dependent dynein motors.

ATP, long thought to be provided by oxidative phosphorylation in the mitochondria, can nevertheless by adequately supplied by glycolytic activity in the flagellum of the mouse sperm [ 26 ]. This observation, coupled with our finding that mitochondrial function appears to be normal in Nsun7 Ste5Jcs1 sperm, indicates that something other that mitochondrial respiration is responsible for the midpiece-related motility defects and abnormal mitochondrial electron density.

Perhaps the most important aspect of the phenotype is that the flagellar beating defect is compartmentalized; the principal piece, but not the midpiece, of the mutant sperm is able to beat vigorously.

Unless the rigidity of the sperm midpiece is purely structural, it would seem that the midpiece region of the axoneme is deficient in components required for normal flagellar function.

We have previously speculated that this may be explained by a differential compromise of distinct signaling activities in these two regions of the sperm [ 27 ], citing the curious findings that the CatSper1 and CatSper2 ion channels, which are required for hyperactivated motility, are present in the principal piece [ 10 ], while the soluble adenyl cyclase sAC , which is required for activated motility, is restricted to the midpiece [ 9 ].

The identification of a mutation that is apparently responsible for Ste5Jcs1 is an important step towards elucidating the actual cause of the sperm defects. However, comparative analyses do not yield obvious clues.

Homology studies revealed that orthologs of Nsun7 are in organisms as distant as yeast S.

Male infertility sperm motility

Male infertility sperm motility

Male infertility sperm motility