Interesting, do you think maybe it has to do with muscle tone or strength? contractions are less effective at shortening muscle fibres to dilate cervix?

sent from my watzamajig so may not make sense....
You guys might like to read this paper

http://edoc.hu-berlin.de/oa/degruyter/jpm.2009.110.pdf


Other clinical evidence is in harmony with the potential for obesity to compromise the intensity or efficiency of uterine contractility. Onset of labor may be delayed by obesity, and dysfunctional labor may be abetted. Obese women have been observed to have longer-term gestations, and more post-dates pregnancies than thinner women w4, 22x. Also, in a prior analysis of labor duration, Vahratian et al. studied rates of dilatation in a data base of 612 nulliparas and found active phase labor (defined as 4–10 cm dilatation) was significantly longer in overweight and obese women, after adjusting for birth weight w24x. Zhang et al. w27x showed in a clinical study that obese women had a higher risk of cesarean, related primarily to abnormal progress in the first stage of labor.

Until recently, there has been no biologic basis to explain why simply being obese would affect labor, but accumulating evidence supports the association of
obesity with impaired uterine contractility. In one study, myometrial tissue obtained at cesarean from obese women was shown in vitro to contract with less force (as indicated by lower calcium fluxes) than those from normal weight subjects w27x.

The basis for this contractile inhibition may reside in some of the biochemical changes induced by obesity. For example, leptin, a protein with diverse metabolic and
regulatory functions, is produced in increased amounts in obese individuals. Moynihan et al. demonstrated that leptin strongly inhibited myometrial contractility in vitro w12x. Cholesterol, also increased in obesity, has similar inhibitory effects on myometrial activity and calcium signaling w21, 28x. We conclude that obesity may interfere with the progress of labor, resulting in dysfunctional patterns of dilatation. The mechanism for such an effect may be mediated through diminished uterine contractility in the active phase of labor, a consequence of increased levels of leptin, cholesterol, or other metabolic features of the obese state. Obesity should be added to the list of possible causes of abnormal labor progression.


The effect of obesity doesn't seem to reach to second stage (where similar pressure is exerted by all women regardless of obesity status): http://journals.lww.com/greenjournal...tage_of.3.aspx


And if you want to see how they have "tried" to isolate the effect of obesity from other complications in pregnancy / labour, see here:
http://www.ncbi.nlm.nih.gov/pubmed/16108107


That's scientist mcfatty, over and out for the evening .