Differently than in the small bowel and in some animal species (e.g., the dog (Sarna et al. 1984)), however, the bursts of contractions do not appear regularly spaced in the time course following a periodic pattern with specific aborally propagated contractile events such as that described in the small bowel (i.e., the migrating motor complex, MMC (Deloose et al. 2012)). In the human large bowel, propagation of the contractile bursts may be observed (Bampton et al. 2001; Hagger et al. 2002), even though most of them are nonpropagated or migrate orally (Dinning et al. 2014; Rao et al. 2001). The rectum, also, displays a peculiar motor pattern, the so-called rectal motor complex (RMC), that occurs independently from the MMC of the small bowel (Kumar et al. 1990), and it is characterized by a series of contractions featuring a frequency of 2–3 per minute, a burst duration of more than 3 min, and amplitude more than 5 mmHg (Enck et al. 1989; Orkin et al. 1989; Prior et al. 1991). The function of the RMC is unknown; however, it has been speculated that these complexes might act as a sort of braking mechanism, since they are often seen to propagate in a retrograde manner (Rao and Welcher 1996) and are accompanied by a rise in anal canal pressure (Ferrara et al. 1993) but are not related to anal events such as passage of flatus (Rønholt et al. 1999).

Propagated activity. In man, colonic propagated activity may be basically subdivided into two types of propagating contractions, the so-called low-amplitude propagated contractions (LAPC) (Bassotti et al. 2001) (Fig. 5.2) and the high-amplitude propagated contractions (HAPC) (Bassotti and Gaburri 1988; Bharucha 2012; Crowell et al. 1991; De Schryver et al. 2002) (Fig. 5.3); both events are probably the manometric equivalent of the migrating long spike bursts described by electromyographic techniques (Bueno et al. 1980; Garcia et al. 1991) and are the main factors responsible for the transport of contents within the colon.

LAPC represent the most frequent type of propagated events, occurring up to more than 120 times per day, with amplitude less than 50 mmHg and propagation over relatively short (about 20 cm) distances (Bampton et al. 2001; Bassotti et al. 2001; Rao et al. 2001). These propagated sequences have also been shown to display a spatiotemporal linkage, in that two consecutive events originating from different colonic segments overlap (Dinning et al. 2009; Dinning et al. 2010b); thus, a series of regionally linked LAPC may span the entire length of the colon (Dinning et al. 2010a). The exact physiological function of LAPC is unknown, but some studies suggest that these events may be associated with the transport of liquid colonic contents (Chauve et al. 1976; Cook et al. 2000) and of gas (Bassotti et al. 1996).

The presence of infrequent, vigorous propulsive contractions able to shift colonic contents over long tracts of the large bowel had been documented in man with radiological methods at the beginning of 1900 (Hertz 1907; Holtzkhnecht 1909) and then called mass movements (Holdstock et al. 1970); subsequently, combined radiological and manometric techniques demonstrated that the manometric equivalent of mass movements were represented by the HAPC (Torsoli et al. 1971). These contractions are less frequent compared to LAPC, have higher average amplitude (about 100 mmHg) compared to the latter, and represent a constant event in healthy subjects (Bassotti et al. 1992). The main physiological function of HAPC, that often starts in the proximal colon (Dinning et al. 2008), is that of shifting aborally relatively large amounts of contents (Ritchie 1971), creating a right-left pressure gradient able to start the mechanism of defecation and sometimes are associated with the urge to defecate, although only about one third of them travels beyond the rectosigmoid junction (see below), as shown by studies with intracolonic instillation of bisacodyl (Bassotti et al. 1999a; Kamm et al. 1992). HAPC are usually propagated in a caudal direction (although retrograde propagation is present, even in normal subjects, and is usually observed in proximal segments) and appear more frequently in daylight hours, after meals, and after morning awakening. It is also worth noting that the frequency of HAPC is significantly greater in children younger than 4 years, and this is probably correlated to the more frequent bowel movements observed in infants and toddlers (Di Lorenzo et al. 1995).

The basic mechanisms controlling the onset of LAPC and HAPC are poorly known. Some human studies suggest that colonic distension and some chemical stimulation may evoke these contractions (Bampton et al. 2002; Bassotti et al. 1994; Liem et al. 2010), that cholinergic stimulation does not elicit this kind of activity (Bassotti et al. 1991), and that physical exercise is able to stimulate both types of propulsive contractions (Cheskin et al. 1992); HAPC may also be elicited by colonic fermentation of a physiological malabsorbed amount of starch (Jouët et al. 2011).

Circadian trends of colonic motility. In humans, colonic motor activity widely fluctuates around the clock, and it is now clear that both electrical and contractile activity and muscle tone vary according to common physiological events such as eating, sleeping, and morning (or sudden) awakening (Auwerda et al. 2001; Bassotti et al. 1990; Frexinos et al. 1985; Narducci et al. 1987; Steadman et al. 1991). Thus, colonic motility is maximal during the daylight hours and reaches a minimum during night and when sleeping (Furukawa et al. 1994; Narducci et al. 1987). Food ingestion, also, is one of the more powerful physiological stimuli for large bowel motility. The colonic motor response to eating is preceded by a cephalic phase (Rogers et al. 1993), starts within 1–3 min following ingestion of the first mouthfuls of food, and lasts at least 2–3 h (Bassotti et al. 1987); it is mainly composed by segmental contractions (even though HAPC may be observed after meals (Bassotti 1990)), and it is paralleled by increased colonic smooth muscle tone (Steadman et al. 1992). The response to eating is also influenced by the caloric content and the composition of the meal , with stimulation following ingestion of fat and carbohydrates (Levinson et al. 1985; Rao et al. 2000) and inhibition following ingestion of proteins (Battle et al. 1980), and it is mediated by peptides (gastrin, neurotensin, cholecystokinin), prostaglandins, vagal cholinergic pathways, and serotoninergic pathways (Ducrotté et al. 1994). In man, proximal and distal colonic segments exhibit different properties in response to meal ingestion, as shown by the fact that the proximal ones display a relatively rapid – but less sustained in the time course – response compared to the distal ones (Bassotti et al. 1989a); proximal and distal segments of the large bowel also feature quantitatively different tonic activity, likely due to different viscoelastic properties and diameter (Ford et al. 1995). Thus, as also supported by scintigraphic studies (Krevsky et al. 1986; Picon et al. 1992), it has been hypothesized that the colon has different physiological activities, with the proximal segments deputed to the mixing and the storage of contents and the distal ones functioning as conduit apt to propel the feces toward the rectum (Bassotti et al. 1999b). Of interest, intestinal continuity seems to be essential for the elicitation of a colonic motor response to eating (Hallgren et al. 1995).

Defecation. Defecation is a complex physiological event that involves both central (cerebral) and peripheral (colorectal) stimuli (Palit et al. 2012). Thus, in physiological conditions, every individual is able to control how, where, and when to defecate, according to the needs and the social interactions, such as the availability of toileting facilities, and it has been developed in the course of human evolution (Bassotti and Villanacci 2013). Defecation may be subdivided in four different phases, represented by the basal phase, the pre-expulsive phase, the expulsive phase, and termination of defecation (Palit et al. 2012).

Basal phase. This phase is constituted by the above described colorectal motor activity that continuously moves the contents toward the rectum and acts synergically with the puborectal muscle that exerts a resting contractile traction able to maintain the anorectal angle at approximately 90° (Mahieu et al. 1984) and the anal sphincter. The latter is normally contracted, providing an airtight seal, except when the subject consciously wants to defecate or pass flatus. This function is provided by a tonic activity of both the external and the internal (the latter provides about 80 % of the overall activity) anal sphincter , in association with the anal cushions (Frenckner 1975). To allow descent of rectal contents into the upper portion of the sphincter itself, and to perceive their physical nature, the internal sphincter displays intermittent and transient relaxations. This so-called “sampling reflex,” in accordance to the nature of the contents (solid, liquid, gas) and the social opportunity, eventually induces the subject to voluntarily relax the sphincter (rectoanal inhibitory reflex) that starts the actual defecation (Miller et al. 1988).

Pre-expulsive phase. Starting with a sensation of “call to stools,” this phase shows a strict correlation between appearance of HAPC and the urge to defecate; of interest, HAPC sequences often start before actual defecation, shifting aborally discrete amounts of contents and activating distal colorectal afferents by distension of the viscus wall (Bampton et al. 2000). The progressive rectal distention causes an initial awareness of filling that becomes constant with continued distention and therefore an urge to defecate until the maximum rectal tolerable volume is reached (Broens et al. 1994).