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To monitor human EE from breath measurements, ideally the breaths sampled should represent a normal breath for each subject; the subject should not need to force an

exhalation nor deliberately breathe at a slower rate than normal. The volume of O2 and

CO2 exhaled and the rate of breathing effect the EE calculated over a given period, by

the relationship shown in equation 2.4. Unfortunately, with the current gas sensor technology, in order to measure purely exhaled gas the subject needs to breathe through either a mask or a mouthpiece (with nose-clip). The effect of breathing with the addition of a mask or mouthpiece has previously been studied, as discussed in the following section.

2.3.2.1 Effect of Breath Monitoring

Breathing through a mouthpiece has been reported to increase tidal volume and decrease breathing frequency, perhaps caused by one or more of the follow three reasons: Influence of the additional dead space of the apparatus; stimulation of nasal and oral mucosa and shift of the respiratory route from the nose and mouth to just the mouth [103]. Similar findings have been discovered when sampling using a mask, where Cope et al. report that tidal volume and minute ventilation were effected [104]. It is commonly believed that the psychological load or sensor stimulation are the main culprits for the degradation in breathing rate [105]. Ventilation is normally controlled ‘automatically’, but on occasions it can be consciously controlled [106]. The contribution of each of the three effects mentioned above on breathing is a cause of disagreement in the literature.

The use of breath sampling apparatus can prevent the subject from being able to maintain a normal breathing pattern. Wearing a mask or exhaling through a mouthpiece stimulates the trigeminal receptors in the face, shown in Fig. 2.11 a), and/or oral cavity [103]. The area of the face around the mouth/nose is particularly sensitive to an applied force. Fig 2.11 b) shows the threshold of tactile detection on the face compared to the index finger.

Fig. 2.11 – The area of the face where a mask or nose clip is worn is sensitive to an applied force, a) areas of skin supplied by the three major trigeminal nerve divisions

[107]; b) Tactile detection threshold of areas on the face compared to the index finger (weights in milligrams) [108].

The use of a mouthpiece can stimulate the lips, gingiva and teeth [109]. Perez and Tobin noted that these stimuli had a lesser effect on the breathing pattern than changes to the respiratory route, from wearing a nose clip while breathing through a mouthpiece [110]. Contrary to Perez and Tobin, Wester and Patrick noted that the awareness of breathing being monitored is the major cause of respiratory alternations (changes in the respiratory route were said to have a less profound effect) [111]. This finding is in agreement with Shea et al. [112], where the need to control ‘behavioural and environment variables when making measurements of breathing at rest’ was highlighted. If these variables were not sufficiently controlled, there was increased risk of dramatic changes in breathing rate and tidal volume. An article by Mador and Tobin supported these statements and demonstrated that audio-visual stimulation tended to increase the variability of tidal volume, whereas mental arithmetic had no effect [113].

Gilbert et al. proposed an experiment to determine if the changes in breathing were caused by the stimulation of using a mouthpiece and nose-clip or by the dead volume in the instrument used to measure tidal volume [106]. Before the experiment, patients were left to breathe quietly for 1 hour prior to a mouthpiece and nose-clip being fitted. Electromagnetic sensors were used to unobtrusively monitor respiratory rate without the need to capture breath (by detecting chest movement). A total of 14 subjects

participated in the experiment (6 without respiratory disease and 8 with). With only the mouthpiece and nose-clip worn (without other apparatus, no dead volume added) the tidal volumes measured across the subject group increased by an average of 98 ml, and respiratory rate decreased by 25 % on average. With a pneumograph connected the tidal volume of the group increased by 124 ml/min on average and the respiratory rate fell by 6 breaths per minute. It was concluded the irritation and stimulation of the nasal mucosa was the most likely cause of depressing the respiratory frequency in humans and the fall in respiratory rate was repeated to the apparatus (mouthpiece and nose-clip). If the theory is correct, the rise in tidal volume could be a secondary effect, in response to maintaining adequate ventilation.

2.3.2.2 Automatic or Conscious Respiratory System

Automatic breathing originates in the ponto-medullary respiratory oscillator [114]. The respiratory muscles, which dictate regular breathing are controlled by a bulb- signal projection from synapses with the anterior horn cells in the cervical and thoracic spinal cord [114]. Cope et al. justify a notable respiratory effect when a mouthpiece is used, as being a sign that the control of breathing has been shifted from the automatic respiratory centres to the cerebral cortex, causing the breathing rate to alter [104]. John noted that voluntary breathing control is dependent on the functions of the cerebral cortex, while automatic ventilation is regulated by the mechanisms of the pons and medulla [115].

Further reports suggest that vagal nerve stimulation (in the nucleus of the tractus solitarius) can effect respiratory oscillations [116]. It was stated however, it is unlikely to affect the rate of breathing during normal ventilation [116]. It is noted that in affecting breathing this phenomenon has a greater effect, where vagal input becomes significant [114]. The risk of a face mask stimulating the vagal nerve has been noticed by Mostafa-Gharehbaghi et al., where it is advised face masks be fitted to infant’s faces with care [117]. They should be tight enough the prevent leaks, but not apply too much pressure, else risk inducing a vagal response. The Vagus nerve is effected by breathing, regardless of whether the breathing is automatic or consciously controlled. The alternating effect of breathing on heart rate is known as ‘respiratory sinus arrhythmia’ [118]. The Vagus nerve innervates the heart causing a parasympathetic response in the nerve, perceived by a decrease in heart rate.

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