These notes are intended to accompany lectures in Human Physiology by Dr. Peter King at Francis Marion University, Florence, SC 29501.

Sex determination
As in most other animals (but not all), sex in humans is determined by genetics.
The 23rd chromosome pair in humans is not autosomal and there are differences in men and women - females have 2 X chromosomes (homomorphic) and males have 1 X and 1 Y chromosome (heteromorphic).

After meiosis to produce gametes all ova have an X chromosome, but only 50% of sperm have an X and 50% have a Y chromosome.

In humans there is a gene on the Y chromosome (SRY gene) that leads to the production of a protein TDF (testis determining factor).
Embryos are initially sexually indifferent and gonads can be testes or ovaries.
TDF appears to change the developmental pattern of the gonads to become testes.
In the absence of the Y chromosome (and TDF) the gonads develop as ovaries.

Developing testes produce androgens (mainly testosterone) plus mullerian inhibiting substance, MIS, which further promotes male development patterns and secondary male characteristics.
Developing ovaries produce estrogens (estradiol) and progesterone which promotes female development and secondary characteristics.
Sex hormones stimulate development of sexual behavior patterns after physical determination.

The function of gonads whether testes or ovaries is controlled by gonadotropic hormones released by the anterior pituitary, follicle stimulating hormone (FSH) and luteinizing hormone (LH). These are controlled by gonadotropin releasing hormone (GnRH).
GnRH secretion increases at the time of puberty. Reasons for puberty onset are unclear and variable. Melatonin, body fat, age, nutrition may all play a role.

The male and female sex hormones are very similar in structure and are all derivatives of cholesterol.
Estradiol 17b, an active estrogen, is a direct derivative of testosterone and is present and active in certain male cells.
Thecal cells in ovaries secrete testosterone but it is converted to estradiol in other ovarian cells where it is active.

Spermatogenesis
A major function of the testes is sperm production.
Sperm cells are formed from spermatogonia in seminiferous tubules in the testes.
Many mammals have testes located in a scrotum outside the body cavity. This is to reduce the temperature. Normal sperm development happens at about 2°C below normal body temperature in humans.

Spermatogonia (2n) undergo continual mitosis to produce spermatocytes.
Spermatocytes undergo meiosis to produce spermatids that mature to become sperm cells.

Luteinizing hormone (LH) secreted by the anterior pituitary stimulate Leydig cells to secrete testosterone.
Leydig cells are located between seminiferous tubules.
Testosterone supports meiosis in the spermatocytes and the maturation of spermatids to spermatozoa (mature sperm cells).

Sertoli cells surround the developing sperm in the seminiferous tubules. Under the influence of follicle stimulating hormone (FSH) sertoli cells produce androgen binding protein (ABP) that concentrates the testosterone around the developing sperm.
Spermatogenesis takes about 8-10 weeks in humans and is continuous after puberty.
In many other animals spermatogenesis is seasonal.

Control of the whole process is based in the hypothalmus that releases gonadotropin releasing hormone (GnRH) that causes the release of LH and FSH from the anterior pituitary.
There are feedback mechanisms that maintain optimal levels of stimulation.
Testosterone has an inhibitory effect on the secretion of FSH and LH.
Sertoli cells secrete a peptide hormone called inhibin that supresses the release of FSH.

Erection
Erection of the penis is caused by blood fl;ow to the erectile tissue in the penis, the corpora cavernosa and the corpus spongiosum.
Blood flow is controlled by parasympathetic mediated vasodilation of arterioles (parasympathetic activity is suppressed).
Expansion of arterioles compresses veins creating positive feedback and expansion of erectile tissue.

Emission and ejaculation
Emission is the movement of sperm into the urethra.
Ejaculation is the expulsion of semen from the penis, usually caused by the stimulation of the glans penis.
Peristalsis moves the sperm from the epididymus along the vas deferens. It is joined by fluid from the seminal vesicle and the prostate to form semen. Ejaculation and emission is controlled by the sympathetic ns.

Seminal vesicles' secretion makes up about 60% of semen volume. It is alkaline and contains fructose, ascorbic acid and prostaglandins.
Fructose provides fuel for sperm activity.
Ducts of the seminal vesicles connect to the vas deferens forming the ejaculatory duct.
Prostaglandins decrease the viscosity of mucus at the cervix.

The prostate gland surrounds the beginning of the urethra as it leaves the bladder. It also surrounds the ejactulatory ducts.
The prostate secretes an alkaline fluid through a number of ducts which contains enzymes that activate sperm.
Prostate secretions make up about 30-35% of semen.
Bulbourethral glands secrete a small quantity of fluid before ejaculation, lubricates erethra and is alkaline.

Alkalinity of semen counteracts acid environment of the vagina.
Semen has antibiotic characteristics.
Clotting factors (fibrinogen) cause semen to coagulate soon after ejaculation and then fibrynolysin soon breaks down the clotting.
Ejaculate is about 2-5 ml containing about 50 - 150 million sperm per ml.

The Female System

The ovaries of females has a dual role
1. To produce ova
2. To produce estrogens and progesterone
Estrogens is a collective term for a number of hormones the most active of which is estradiol.
Hormones are generally released cyclically and are under the control of the hypothalmus.

Oogenesis
During embryonic development oogonia divide by mitosis and form primary oocytes.
By birth, oogonia are no longer present and the mammalian (and bird) ovary contains its full complement of primary oocytes (about 2 million in humans of which only about 400-500 will be released).
Primary oocytes are still 2n and surrounded by follicular cells, together making up the primary follicle.

Primary oocytes are in an arrested stage of prophase I of meiosis.
Beginning at puberty a small number of primary oocytes begin development each month (ovarian cycle).
In humans normally only one oocyte from one of two ovaries will continue meiosis.
Meiosis II is only completed after sperm penetration!
Mechanism for choosing one to develop is not understood.
Ovulation cycle

Three phases
1. Follicular phase
2. Ovulation
3. Luteal phase

Follicular phase
10 - 25 primary follicles are "selected" to begin development toward ovulation.
Follicular cells in primary follicle increase in number, differentiate and become granulosa cells. Granulosa cells secrete estrogen.
Secondary follicles are formed after proliferation of granulosa cells and production os fluid filled vesicles in the follicle. Primary oocyte still in prophase I.
Outer granulosa cells further differentiate and form thecal cells.
Graafian follicle then develops after further growth, as the vesicles combine to form a single antrum. Primary oocyte completes meiosis I forming secondary oocyte.

Ovulation
Growing pressure from the expanding antrum rupture the wall of the ovary.
Secondary oocyte surrounded by some granulosa cells called the corona radiata are expelled into the peritoneal cavity.

Luteal phase.
After ovulation the granulosa cells expand and change functionally to form an endocrine gland, a corpus luteum (yellow body). It secretes estrogen and progesterone.
If no fertilization occurs the corpus luteum degenerates in 10 days to become a corpus albicans (white body).

Hormonal Control of Ovulation
Start
Rising levels of GnRH (gonadotropin releasing hormone) from the hypothalamus result in increased secretion of FSH (follicle stimulating hormone) and LH (Luetinising hormone) from the anterior pituitary.
LH and FSH stimulate follicular development.

LH causes thecal cells (surround follicle) to secrete androgens which diffuse into the FSH activated granulosa cells where they are converted into estrogens. Granulosa cells secrete estrogens and inhibin.
After initially inhibiting LH and FSH, a critical level of estrogen causes a surge of LH and a smaller surge of FSH to be releasesd from the anterior pituitary.
Granulosa cells also secrete inhibin which suppresses release of FSH from the anterior pituitary.

LH stimulates meiosis in the primary oocyte and rupture of the graafian follicle (ovulation).
LH surge also stimulates the change in the granulosa cells to form the corpus luteum.
Estrogen and progesterone levels from corpus luteum inhibit LH and FSH secretion.
If fertilization does not occur, corpus luteum degenerates due to falling LH, estrogen and progesterone fall, GnRH increases and cycle starts again.

Menstrual or Uterine cycle

Three phases
Mentrual phase - Menstruation or the shedding of the endometrium (uterine lining) following the degeneration of the corpus luteum and the drop in progesterone level.
Proliferation phase - Estrogen from growing follicle stimulates regrowth of the endometrium.
Secretory phase - Progesterone from corpus luteum increases blood supply of endometrium and causes glycogen secretion in the uterus.

If fertilization occurs (normally takes place in the fallopian tubes):
The zygote (fertilized ovum) moves toward the uterus, where the endometrium has been developing to accept it since the previous menstrual phase and the influence of progesterone.
The blastocyst attaches to and buries into the endometrium (implantation).

Implantation stimulates the blastocyst to release human chorionic gonadotropin (HCG) which supports the continuing function of the corpus luteum.
Excess HCG is excreted in urine and is the indicator of many pregnancy tests.
The placenta develops that allows diffusion of nutrients and gases between the blood of the fetus and the mother.

The placenta also takes on the endocrine function of producing estrogen and progesterone after about 6 weeks into pregnancy.

Estrogen and to lesser extent progesterone inhibit the release of FSH and LH during pregnancy (no new follicular development) and hence their use as a contraceptive.

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This webpage was created by Peter King. Please contact the the author with comments at pking@fmarion.edu.
Last edited July 20, 2010.
http://people.fmarion.edu/pking/humanphys/reproduction.html
copyright Peter King.