WHY DO WE RAISE OUR VOICE WHEN WE'RE ANGRY?

WHY DO WE RAISE OUR VOICE WHEN WE'RE ANGRY?

Surely, this must have had an intimidating effect on predators back in the Stone Age, and on human enemies upon every battlefield in history.
But nowadays, this reaction can prove a relevant disturbance. We're no longer fending off a sabertooth in a cave, or Leaguers at Breitenfeld, or anything like that, but we still get incensed after all. And we raise our voices, perchance convinced that this will scare the other away and bring him/her over to our side.
Yet we can't control this volume shift. For it is actually literally beyond reason. To be more precise, tension is part of the somatic-affective modality of anger. Somatic means physical/bodily. This makes it an instinctive response, one that can't be regulated by the cortex because its origin can be traced back to our reptilian ancestors.

 The rapid, minimal, and evaluative processing of the emotional significance of the sensory data is done when the data passes through the amygdala in its travel from the sensory organs along certain neural pathways towards the limbic forebrain.

Noradrenaline, or norepinephrine, is the hormone that triggers the fight response. And we can trace it to the postganglionic neurons of the sympathetic nervous system:

There are two kinds of neurons involved in the transmission of any signal through the sympathetic system: pre-ganglionic and post-ganglionic^]

At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons. In response to this stimulus postganglionic neurons—with two important exceptions—release norepinephrine, which activates adrenergic receptors on the peripheral target tissues. The activation of target tissue receptors causes the effects associated with the sympathetic system.

 α1-receptors (adrenergic) primarily mediate smooth muscle contraction, but have important functions elsewhere as well. The hormone noradrenaline has higher affinity for the α1 receptor than does adrenaline.

Increased muscle tension in order to provide the body with extra speed and strength.

• Muscles Tense

In order to give us extra speed and strength the muscles of our body tense.

One may see this as a reflex, an unconscious reaction with the purpose of intimidating and/or subjugating our opponents.

The fight response, these alpha-1 receptors... the intercostal muscles between the ribs tense (it's like wearing an invisible corset that restrains how much your chest can expand), and so do those in the throat, around the larynx and trachea, constraining the amount of air that can get through and the position of the vocal cords.

There is greater muscle tension in the larynx, coupled with higher subglottal pressure (Subglottic pressure is pressure of air in the trachea below the glottis when the glottis is closed).

Vocal loudness is the consequence of subglottal pressure. 

This is also the reason why, as you have certainly heard or read, that a person with a deep wound in the chest, upper back, or upper side will always speak softly. The injury causing this is a punctured lung: the lungs can't fill properly because of a wound that has opened a hole into the intercostals and interferes with respiration. Also, there is often a ruptured blood vessel and the airways fill up with blood (coughed up, seen on lips), which also will affect speech.

It has been stated that respiration is an indicator in certain emotional situations, including conflict.  An increase in respiration rate would result in an increased subglottal pressure during speech. Anger is manifested in a higher subglottal pressure and a narrower glottal pulse.

Anger and hatred are characterised by heightened activity of the expiratory muscles (inner intercostal muscles) and of the intrinsic adductor muscles of the glottis. The considerable effort of the expiratory muscles causes high subglottal pressure.

Lateral cricoarytenoid muscles adduct and internally rotate the arytenoid cartilages, increase medial compression.

These can, ironically, save lives by temporarily shutting the glottis (for seconds) before expelling a foreign object. In this context, however, a high subglottal pressure is life-saving.

These muscles receive their innervation from the Recurrent laryngeal nerve which is a branch of the Vagus nerve (CN X).

Subglottal pressure is the pressure of the airflow in the trachea below the glottis. This is the main factor used by speakers to control phonation when producing speech. Subglottal pressure affects the amplitude of speech signals and fundamental frequency. Higher subglottal pressure causes higher airflow velocity, thus, it has an impact on glottal flow. It can therefore be considered as one of the feature parameters for classifying stressed speech.

The subglottal cavity consists of the trachea and the lungs. 

Pistons are initiators. The term initiator refers to the fact that they are used to initiate a change in the volumes of air cavities, and, by Boyle's Law, the corresponding air pressure of the cavity. The term initiation refers to the change. Since changes in air pressures between connected cavities lead to airflow between the cavities, initiation is also referred to as an airstream mechanism. Some of the pistons present in the articulatory system are the larynx, and the physiological structures used to manipulate lung volume (in particular, the floor and the walls of the chest). The lung pistons are used to initiate a pulmonic airstream (found in all human languages). The larynx is used to initiate the glottalic airstream mechanism by changing the volume of the supraglottal and subglottal cavities via vertical movement of the larynx (with a closed glottis).

The air pressure from the lungs (subglottal pressure) pushes the vocal folds open and the air begins to flow through the glottis. The velocity of the flow is highest in the narrowest parts, with the consequence that air pressure decreases between the vocal folds and sucks them together again.

Raising your voice" in this sense involves more subglottal pressure, more vocal effort, higher amplitude, and also higher pitch.

subglottal pressure coming from the lungs. 

(e.g., the standard value of subglottal pressure for phonation is 2-8 cmH2O, but 10-12 cmH2O for loud speech)

Such linguistic and pragmatic changes to F0 are mediated by coordinated adjustments to vocal fold tension, vertical larynx position and subglottal pressure. The effects of emotion on F0 variation are difficult to predict. Emotional changes to muscle tone are likely to be tonic, and thus affect F0 level as described above, rather than F0 variation. It is possible that the major physiological mediator of emotional changes to F0 range and F0 variance is expiratory force. An example is the case of angry utterances, in which powerful expiration will lead to an eventual drop in subglottal pressure (due to exhaustion of the air supply in the lungs), causing a corresponding drop in F0. 

Under difficult obstructive conditions, the vocal folds remain closed for a greater proportion of the glottal cycle, at the “expense” of the period during which the folds are open. This pattern of results corresponds to the description of the effects of increased laryngeal muscle tension given by Sundberg (1994) according to which the vocal folds are held in a closed position with greater force. A higher subglottal pressure is therefore required to build up so as to force open the vocal folds. When the vocal folds do eventually open, the rush of air through the glottis causes a sudden drop in pressure due to the Bernoulli effect. The vocal folds are thus rapidly drawn back together again,

both under the influence of elastic forces of the increased muscle tension, and the pressure drop between them. The result, termed “tense voice”, is a more skewed glottal pulse, with longer closed phase and shorter open phase. 

Any change in the air pressure directly below the larynx (e.g. due to a change in respiratory function), or the tension and position of the vocal folds, will affect how the vocal folds open and close, thus producing variations in the intensity, f0 and the harmonic energy distribution of the sound. For example, when the vocal folds are under heightened tension and subglottal pressure is high due to heavy expiratory effort, the vocal folds will close more suddenly, leading to an increase not only in overall intensity, but also in f0 and the energy in the higher harmonics (Iwarsson, Thomasson and Sundberg, 1998; Hixon, 1987; Ladefoged, 1968). Such a vocal configuration might be expected for certain high arousal emotions, such as anger.

At the segmental level, quickened respiration leads to increases in subglottal air pressure which, in turn, puts more strain on the vocal cords. This impacts how the cords vibrate. In response, muscular tension on the cords tends to spontaneously increase and this raises F0. 

This implies that angry and loud conditions are manifested in a higher subglottal pressure and a narrower glottal pulse. 

Intensity is described in terms of strength of subglottal pressure; its acoustic correlate is loudness.

Emotions change physiological parameters such as heart rate, blood flow, and muscle tension, which in turn alter vocal production. Emotional arousal, for example, increases laryngeal tension and subglottal pressure, resulting in increased intensity. 

◦Increased subglottal pressure/airflow = increased loudness

Respiration is frequently a sensitive indicator in certain emotional situations. When an individual experiences a stressful situation, his/her respiration rate increases. This presumably will increase subglottal pressure during speech, which 

is known to increase fundamental frequency (or pitch) during voiced section.

For instance, anger yields increased tension in the laryngeal musculature coupled with increased subglottal air pressure. This changes the production of sound at the glottis and hence changes the timbre of the voice (Johnstone & Scherer, 2000).

Long story short:

The reason why is due to the tension in respiratory muscles, which make respiration more shallow (the system takes up a higher gear and requires more oxygen, hence the reason why), and thus force air out of the lungs and raise the pressure below the larynx. This physiological activity is called high subglottal/subglottic pressure, and it is the reason why angry people raise their voices.

Well, whenever I feel from disappointed to furious, I feel like a lump in my throat or a noose around it. It will disappear whenever I release my feelings out loud (never better said), but remain there if I do not voice these feelings. I did not know what this "lump" or "noose" was until now, when I have finally discovered what it is.

Interestingly, neurotoxins like strychnine also affect the respiratory muscles in a similar way, the internal intercostals tightening the ribcage as the lateral cricoarytenoids shut the glottis. But these tensions are not reversible. The poisoned person is suffocated, "strangled from within".

In other words, thus died Joffrey "Baratheon".

Our own case of rage is, on the other hand, temporary, and it wears off pretty quickly (as soon as we are not aroused). However, it leaves persistent effects on others.