Vaginal ultrasonography of uterine peristalsis during the follicular phase of the menstrual cycle demonstrates an increasing frequency and intensity of subendometrial and myometrial peristaltic waves as the follicular phase progresses. During this time the numbers of contraction waves with a fundo-cervical direction decrease considerably in favour of waves of contraction with a cervico-fundal direction. There is evidence that rapid sperm transport through the female genital tract is passive and is provided by these uterine contractions. Using hysterosalpingoscintigraphy, rapid sperm transport was studied by placing technetium-labelled albumin macrospheres of sperm size at the external os of the uterine cervix and following their path through the female genital tract. Ascension of the macrospheres occurred immediately following deposition at the external os of the cervix. As early as 1 min thereafter, the macrospheres had reached the intramural and isthmical part of the tube. Quantitatively, the extent of ascension increased with progression of the follicular phase. While only a few macrospheres entered the uterine cavity and even fewer the tubes during the early follicular phase, the proportion of macrospheres that entered the uterine cavity increased dramatically during the mid-follicular phase despite continuing limited entry into the tube. During the late follicular phase there was considerable ascension of the macrospheres which was directed preferentially into the tube ipsilateral to the dominant follicle. These data indicate that rapid transport of the spermatozoa through the female genital tract is under the endocrine control of the dominant follicle, ensuring the preferential accumulation of spermatozoa at the site of fertilization.

Women suffering from infertility in association with mostly mild endometriosis were subjected to vaginal sonography of uterine peristalsis during the menstrual period, the early, mid- and late follicular phases, and the mid-luteal phase of the menstrual cycle. The data obtained were compared with those of healthy controls. Women with endometriosis displayed a marked uterine hyperperistalsis that differed significantly from the peristalsis of the controls during the early and mid-follicular and mid-luteal phases. During the late follicular phase of the cycle, uterine peristalsis in women with endometriosis became dysperistaltic, arrhythmic and convulsive in character, while in controls peristalsis continued to show long and regular cervico-fundal contractions. Hysterosalpingoscintigraphy during the early, mid- and late follicular phases revealed that hyperperistalsis in the early and mid-follicular phases of patients with endometriosis resulted in a dramatic increase in the transport of inert particles from the vaginal depot, through the uterus into the tubes and also into the peritoneal cavity. During the late follicular phase of the cycle, the dysperistalsis observed in women with endometriosis resulted in a dramatic reduction of uterine transport capacity in comparison with the healthy controls. We consider uterine hyperperistalsis to be the mechanical cause of endometriosis rather than retrograde menstruation. Dysperistalsis in the late follicular phase of patients with endometriosis may compromise rapid sperm transport. Uterine hyperperistalsis and dysperistalsis are considered to be responsible for both reduced fertility and the development of endometriosis.

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