Bolus propulsion during the normal oral phase of swallowing is thought to be characterised by the sequential elevation of the front, middle, and posterior regions of the dorsum of the tongue. However, the coordinated orchestration of lingual movement is still poorly understood. This study examined how pressures generated by the tongue against the hard palate differed between three points along the midline of the tongue. Specifically, we tested three hypotheses: (1) that there are defined individual patterns of pressure change within the mouth during liquid swallowing; (2) that there are significant negative pressures generated at defined moments during normal swallowing; and, (3) that liquid swallowing is governed by the interplay of pressures generated in an anteroposterior direction in the mouth. Using a metal appliance described previously, we measured absolute pressures during water swallows in six healthy volunteers (4 male, 2 female) with an age range of 25-35 years. Participants performed three 10-ml water swallows from a small cup on five separate days, thus providing data for a total of 15 separate water swallows. There was a distinct pattern to the each of the pressure signals, and this pattern was preserved in the mean obtained when the data were pooled. Furthermore, raw signals from the same subjects presented consistent patterns at each of the five testing sessions. In all subjects, pressure at the anterior and hind palate tended to be negative relative to the preswallow value; at mid-palate, however, pressure changes were less consistent between individuals. When the pressure differences between the sites were calculated, we found that during the swallow a net negative pressure difference developed between anterior and mid-palate and a net positive pressure difference developed between mid-palate and hind palate. Large, rapid fluctuations in pressure occurred at all sites and these varied several-fold between subjects. When the brief sharp reduction in pressure that occurred early in each swallow was used to determine the sequence of events, we found that activity occurred first at the anterior of the palate followed by the mid-palate and then the hind palate. There was a considerably longer and more variable delay between the start of activity at the front of the palate than at the rear of the palate. To obtain an index of the "effort" involved in generating the pressures at each site regardless of direction (positive or negative), we obtained the product of the root mean square (RMS) pressure change during each swallow (kPa) and its duration (s). Overall, the most effort appears to have occurred at the front of the palate and the least at mid-palate. Our results also showed that some participants exerted a small amount of midline pressure when swallowing, while others used a relatively large amount of tongue pressure. We conclude that while tongue behaviour during swallowing follows a classical sequence of rapid shape changes intended to contain and then propel the bolus from the oral cavity to th...

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Investigating the sequence and magnitude of tongue movements against the hard palate during swallowing is basic to understanding the process by which the bolus is moved from the front of the mouth to the pharynx. Here we outline the basic muscular anatomy of the tongue, and we report on specific pressure patterns generated at three positions along the midline: at the front, middle and back of the hard palate. We show that there are sharp amplitudinal changes from positive to negative pressures at all three locations. While these pressure patterns show large interindividual variations, they appear to be consistent within individuals, irrespective of bolus size or consistency. Tentatively, we are able to identify three basic patterns; Type I, squeezer – a mostly positive pressure cascade from the front to the back of mouth; Type II, slider – characterized by an effortless and extended swallow, and Type III, slapper – large positive and negative pressure fluctuations during each swallow. Finally, we found that the most variability in pressure fluctuations occurred in the front of the mouth, from which we conclude that the front of the tongue has a predominant organisational role, whereas the back of the tongue is mostly propulsional. PRACTICAL APPLICATIONS While tongue pressure patterns during liquid swallowing vary greatly between persons, they appear to be highly specific within individuals. While some individuals have seemingly effortless swallows, others are more forceful and either squeeze their bolus or apply rapidly changing positive and negative forces to it. The results presented here also show that these patterns remain conserved irrespective of bolus consistency or volume, suggesting that novel foodstuffs might have to be individually designed with three swallowing types in mind. We also show maximum variation at the front of the tongue, emphasising an organisational rather than purely propulsional role for this area. This knowledge will be useful in designing and formulating new food products, particularly for those suffering from dysphagia, an inability to swallow normally.

Intrinsic cardiac regulation, the direct effect of changes in right atrial pressure on heart rate, was examined in rabbits under chloralose/urethane anaesthesia. Autonomic influences on the cardiac pacemaker were eliminated by cervical vagotomy and intravenous propranolol. Right atrial transmural pressure was monitored as the difference between right atrial and pleural pressures. Blood volume expansion (5-15%) increased right atrial transmural pressure and heart rate and produced a sinus arrhythmia associated with respiration-linked fluctuations in right atrial transmural pressure. The gain of intrinsic cardiac rate regulation was calculated as 0.96 +/- 0.24 beats min-1 mmHg-1 at a heart rate of 218 +/- 6 beats min-1 (values as the mean +/- SEM, n = 12). When heart rate was reduced by electrical stimulation of the peripheral end of the right vagus nerve, gain increased to 2.25 +/- 0.57 and 4.61 +/- 1.6 beats min-1 mmHg-1 at heart rates of 180 +/- 4 and 130 +/- 4 beats min-1, respectively (n = 6 and n = 10; P < 0.05 compared with pre-stimulation values). During vagally-induced bradycardia, rapid infusion of blood into the left superior vena cava produced a brief marked cardiac acceleration. We conclude that right atrial pressure has a small direct influence on heart rate, and this is enhanced by background cardiac parasympathetic stimulation.

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We have recently shown that the intrinsic rate response to an increase in right atrial pressure is augmented when cardiac muscarinic receptors are activated. This present study examines the cardiac pacemaker response to vagal stimulation at different values of right atrial pressure in isolated rat right atrium and in the rabbit heart in situ. In the rat atrium, when pressure was raised in steps from 2 to 10 mmHg, there was a progressive reduction in the response to vagal stimulation [40.5 ± 7.2% reduction (mean ± SE) at 8 mmHg, P < 0.01], which was independent of the level of vagal bradycardia, that persisted in the presence of the β-adrenergic agonist isoproterenol. In barbiturate-anesthetized rabbits with cervical vagi cut and β-adrenergic blockade, raising right atrial pressure ∼2.5 mmHg by blood volume expansion reduced the bradycardia elicited by electrical stimulation of the peripheral end of the right vagus nerve (9.1 ± 1.1% reduction, P < 0.0001). These results demonstrate that vagal bradycardia is modulated by the level of right atrial pressure and suggest that normally right atrial pressure may interact with cardiac vagal activity in the control of heart rate.

Male rats were assigned to light (C) or strenuous (T) running programs. Both groups ran at 30 m/min, 8% elevation. Over 16 wk, T and C completed 2,939 +/- 72 and 507 +/- 7 min (mean +/- SE). In a graded running test, maximum exercise heart rates for T and C were 542 +/- 7 and 554 +/- 6 beats/min (P greater than 0.05). Heart rates elicited by maximum effective concentrations of isoproterenol (ISO) in vivo and in vitro were 483 +/- 8 and 489 +/- 11 beats/min for T and 499 +/- 5 and 502 +/- 5 beats/min for C (no difference between groups or treatments). A lower heart rate was recorded in T for both resting (353 +/- 7 vs. 373 +/- 4 beats/min) and in vitro intrinsic states (231 +/- 22 vs. 299 +/- 22 beats/min) (P less than 0.05 for both conditions). The difference between maximum ISO-stimulated and maximum exercise heart rates was attributed to a temperature difference. In a separate group of lightly trained rats, ISO was administered intravenously during hard exercise when heart rate approached exercise maximum. Heart rate after ISO did not increase beyond the maximum heart rate observed in a control run. It was concluded that the maximum chronotropic response to sympathetic stimulation can be elicited during hard exercise and that maximum exercise heart rate reflects this limit rather than a saturation of cardiac sympathetic activity.

We examined the effect of temperature and adrenergic stimulation on atrial rate in the rat. Right atrial preparations were maintained for 65 min at 38.0 degrees C and then exposed to high or moderate concentrations of isoproterenol (ISO) or left as controls. Temperature was cycled through four different values between 35.6 and 42.8 degrees C and allowed to stabilize at each value before atrial rate was measured. The rate-temperature loops exhibited a modest hysteresis; higher values for rate were obtained on the ascending limb. Hysteresis was found to result from a transient overshoot of the rate response to a temperature step. The linear response of atrial rate to temperature ranged from 20.3 +/- 1.3 to 22.6 +/- 0.7 beats.min-1.degrees C-1 (mean +/- SE) for control and high ISO (P greater than 0.05). Data were analyzed by applying the Arrhenius equation and by calculating the Q10 effect. ISO, while increasing atrial rate, reduced the measures of temperature sensitivity. Q10 and mu (temperature characteristic) were 2.1 and 59.8 +/- 2.1 for control and 1.7 and 40.0 +/- 1.5 for high ISO groups, respectively. The direct effect of an increase in temperature on sinoatrial rhythm would contribute significantly to the increase in heart rate seen in exercise.