The specifics of low frequencies in a car: where to get the bass and how to set it up. Amyotrophic Lateral Sclerosis Female Singing Voices
Despite more than 100 years of study, amyotrophic lateral sclerosis (ALS) remains a fatal disease of the central nervous system. The disease is characterized by a steadily progressive course with selective damage to the upper and lower motor neurons, which leads to the development of amyotrophy, paralysis and spasticity. Until now, the issues of etiology and pathogenesis remain unclear, and therefore, specific methods for diagnosing and treating this disease have not been developed. A number of authors noted an increase in the incidence of the disease among young people (up to 40 years).
ICD-10 G12.2 Motor neuron disease
EPIDEMIOLOGY
amyotrophic lateral sclerosis debuts at the age of 40 - 60 years. Average age disease onset at age 56. ALS is a disease of adults, and is not observed in persons under 16 years of age. Men are slightly more affected(male-female ratio 1.6-3.0:1).
ALS is sporadic disease and occurs with a frequency of 1.5 - 5 cases per 100,000 population.
IN 90% of ALS cases are sporadic, and in 10% - family or hereditary character as with autosomal dominant(mostly) and autosomal recessive types of inheritance. The clinical and pathological characteristics of familial and sporadic ALS are almost identical.
Currently age is a major risk factor with ALS, which is confirmed by an increase in the incidence after 55 years, and in this age group there are no longer differences between men and women. Despite the significant association of ALS with age, aging is only one of the predisposing factors in the development of the pathological process. The variability of the disease in different age groups, and among people of the same age suggests the existence of certain risk factors: deficiency, or vice versa, the presence of certain neuroprotective factors, which currently include: neurosteroids or sex hormones; neurotrophic factors; antioxidants.
Some researchers note a particularly favorable course of the disease in young women, which confirms the undoubted role of sex hormones, especially estradiol and progestin, in the pathogenesis of amyotrophic lateral sclerosis. This is confirmed by: a high incidence of ALS in men under 55 years of age (at the same time, they have an earlier onset and rapid progression of the disease compared to women); with the onset of menopause, women get sick as often as men; isolated cases of amyotrophic lateral sclerosis during pregnancy. To date, there are single works on the study of the hormonal status of patients with amyotrophic lateral sclerosis, and none devoted to determining the concentrations of hormones in young patients.
ETIOLOGY
The etiology of the disease is not clear. The role of viruses, immunological and metabolic disorders is discussed.
The role of mutations in the gene has been shown in the development of the familial form of ALS superoxide dismutase-1(Cu/Zn-superoxide dismutase, SOD1), chromosome 21q22-1, ALS associated with chromosome 2q33-q35 was also identified.
Syndromes that are clinically indistinguishable from classic ALS may result from:
Structural lesions:
parasagittal tumors
foramen magnum tumors
spondylosis of the cervical spine
Arnold-Chiari syndrome
hydromyelia
arteriovenous anomaly of the spinal cord
Infections:
bacterial - tetanus, Lyme disease
viral - poliomyelitis, shingles
retroviral myelopathy
Intoxications, physical agents:
toxins - lead, aluminum, other metals.
medicines - strychnine, phenytoin
electric shock
x-rays
Immunological mechanisms:
plasmocyte dyscrasia
autoimmune polyradiculoneuropathy
Paraneoplastic processes:
paracarcinomatous
paralymphomatous
Metabolic disorders:
hypoglycemia
hyperparathyroidism
thyrotoxicosis
folate deficiency,
vitamins B12, E
malabsorption
Hereditary biochemical disorders:
androgen receptor defect - Kennedy's disease
hexosaminidase deficiency
a-glucosidase deficiency - Pompe disease
hyperlipidemia
hyperglycinuria
methylcrotonylglycinuria
All of these conditions can cause the symptoms seen in ALS and should be considered in the differential diagnosis.
PATHOGENESIS
To date, there is no generally accepted hypothesis of the pathogenesis of amyotrophic lateral sclerosis. According to modern ideas , the development of ALS is due to the interaction of hereditary and exogenous provoking factors. Many pathological changes in neurons lead to the assumption of a multivariate etiological factor.
The disorders at the cellular level in motor neuron disease are extensive and include:
changes in the cytoskeleton: structural disorganization of neurofilaments, which leads to impaired axonal transport
toxic effect of intracellular protein aggregates affecting the functioning of the mitochondrial apparatus and disruption of the secondary assembly of cytoplasmic proteins
microglial activation and changes in free radical and glutamate metabolism.
Normally, SOD-1 inhibits the IL-1b-converting enzyme. Under the action of the latter, IL-1b is formed, which initiates the death of neurons after binding to its membrane receptor. The product of the defective SOD-1 gene is not capable of inhibiting the IL-1b-converting enzyme; the resulting IL-b induces the death of motor neurons at various levels of the nervous system.
Modern views on the pathogenesis of amyotrophic lateral sclerosis include understanding of the great role of oxidative stress in the development of this pathology.
Supposed that hydrogen peroxide could serve as an abnormal substrate for the conformed SOD1 molecule. As a result, there is an increase in peroxidant reactions and an increase in the production of toxic hydroxyl radicals. The significant role of oxidative stress in the pathogenesis of ALS is confirmed by biochemical studies, which revealed the presence in patients of deficiency of a number of antioxidant defense systems, mitochondrial dysfunction, dysmetabolism of glutathione, glutamate excitotoxin, and mechanisms of glutamate transport. It is possible that oxidative damage to protein targets (SOD1, neurofilament proteins, alpha-synuclein, etc.) can facilitate and accelerate their joint aggregation, the formation of cytoplasmic inclusions, which serve as a substrate for further pathochemical oxidative reactions.
CLASSIFICATION
According to the predominant localization of the lesion of various muscle groups, the following forms of amyotrophic lateral sclerosis are distinguished:
cervicothoracic form(50% of cases)
bulbar form(25% of cases)
lumbosacral shape(20 - 25% of cases)
high (cerebral) form(1 – 2%)
ALS-plus syndromes are distinguished as a separate variant of ALS, which include:
ALS associated with frontotemporal dementia. It is most often familial and accounts for 5-10% of cases.
ALS, combined with frontal dementia and parkinsonism, and associated with a mutation of the 17th chromosome.
North American classification of ALS (Hudson A.J. 1990)
Sporadic ALS
1. Classic ALS
Debuts:
bulbar
cervical
chest
lumbar
diffuse
respiratory
2. Progressive bulbar palsy
3. Progressive Muscular Atrophy
4. Primary lateral sclerosis
Family ALS
1. Autosomal dominant
no SOD-1 mutation (mutations of other genes, no known genetic defect)
2. Autosomal recessive
associated with SOD-1 mutations
other forms (total 10 linkage loci are known)
3. Western Pacific ALS-parkinsonism-dementia complex
ALS classification O.A. Hondkariana (1978)
Forms of ALS:
bulbar
cervicothoracic
lumbosacral
primary generalized
high
Options:
mixed (classic)– uniform lesion of CMN and PMN
segmental-nuclear- preemptive PMN lesion
pyramidal (high form of ALS)- Presumptive lesion of CMN
PATHOMORPHOLOGY
Pathological examination reveals:
selective atrophy of the anterior motor roots and cells of the anterior horns of the spinal cord, the most pronounced changes occur in the cervical and lumbar segments
posterior sensory roots remain normal
in the nerve fibers of the lateral corticospinal tracts of the spinal cord, demyelination, uneven swelling is observed, followed by disintegration and death of the axial cylinders, which usually extends to peripheral nerves
in some cases, atrophy of the precerebral gyrus of the large brain is noted, sometimes atrophy captures the VIII, X and XII pairs of cranial nerves, the most pronounced changes occur in the nucleus of the hypoglossal nerve
atrophy or absence of motor neurons, accompanied by moderate gliosis without signs of inflammation
loss of giant pyramidal cells (Betz cells) of the motor cortex
degeneration of the lateral pyramidal tracts of the spinal cord
atrophy of muscle fiber groups (as part of motor units)
CLINIC
Initial manifestations of the disease:
weakness in the distal arms, clumsiness with fine finger movements, weight loss in the hands, and fasciculations (muscle twitches)
less commonly, the disease debuts with weakness in the proximal arms and shoulder girdle, atrophy in the muscles of the legs in combination with lower spastic paraparesis
it is also possible the onset of the disease with bulbar disorders - dysarthria and dysphagia (25% of cases)
cramps (painful contractions, muscle spasms), often generalized, occur in almost all patients with ALS, and are often the first sign of the disease
Characteristic clinical manifestations of ALS
Amyotrophic lateral sclerosis is characterized by a combined lesion of the lower motor neuron (peripheral) and a lesion of the upper motor neuron (pytamide pathways and / or pyramidal cells of the motor cortex of the brain.
Signs of damage to the lower motor neuron:
muscle weakness (paresis)
hyporeflexia (decreased reflexes)
muscular atrophy
fasciculations (spontaneous, fast, non-rhythmic contractions of bundles of muscle fibers)
Signs of damage to the upper motor neuron:
muscle weakness (paresis).
spasticity (increased muscle tone)
hyperreflexia (increased reflexes)
pathological foot and hand signs
For ALS in most cases asymmetry of symptoms.
In atrophied or even outwardly intact muscles, fasciculations(muscle twitches), which may be in a local muscle group or be widespread.
In a typical case, the onset of the disease with weight loss of thenar muscles one of the hands with the development of weakness of adduction (adduction) and opposition of the thumb, (usually asymmetrically), which makes it difficult to grip the thumb and forefinger and leads to impaired fine motor control in the muscles of the hand. The patient feels difficulty when picking up small objects, when fastening buttons, when writing.
Then, as the disease progresses, the muscles of the forearm are involved in the process, and the hand takes on the appearance of a “clawed paw”. A few months later, a similar lesion of the other hand develops. Atrophy, gradually spreading, captures the muscles of the shoulder and shoulder girdle.
At the same time or later damage to the bulbar muscles often develops: fasciculations and atrophy of the tongue, paresis of the soft palate, atrophy of the muscles of the larynx and pharynx, which manifests itself in the form of dysarthria (speech disorders), dysphagia (swallowing disorders), salivation.
Mimic and masticatory muscles are usually affected later than other muscle groups.. As the disease develops, it becomes impossible to protrude the tongue, puff out the cheeks, and stretch the lips into a tube.
Sometimes weakness of the extensors of the head develops due to which the patient cannot keep his head straight.
When involved in the process of the diaphragm paradoxical breathing is observed (on inspiration, the stomach sinks, on exhalation it protrudes).
Legs usually atrophy first anterior and lateral muscle groups, which is manifested by a “hanging foot” and a steppage-type gait (the patient raises his leg high and throws it forward, sharply lowering it).
!!! Characteristically, muscle atrophy is selective.
Atrophy is observed on the hands:
tenara
hypothenar
interosseous muscles
deltoid muscles
Muscles involved in the legs performing dorsiflexion of the foot.
in the bulbar muscles the muscles of the tongue and soft palate are affected.
pyramidal syndrome develops, as a rule, at an early stage of ALS and is manifested by the revival of tendon reflexes. Following this, lower spastic paraparesis often develops. In the hands, an increase in reflexes is combined with muscle atrophy, i.e. there is a combined, simultaneous lesion of the central (pyramidal) pathways and peripheral motor neuron, which is characteristic of ALS. Superficial abdominal reflexes disappear as the process progresses. Babinsky's symptom (with dashed irritation of the sole, the big toe unbends, the other fingers fan-shaped diverge and unbend) is observed in half of the cases of the disease.
There may be sensory disturbances. In 10% of patients, paresthesias are observed in the distal parts of the arms and legs. Pain, sometimes severe, usually nocturnal, may be associated with joint stiffness, prolonged immobility, spasms due to high spasticity, with cramps (painful muscle spasms), depression. Loss of sensitivity is not typical.
Oculomotor disorders are not characteristic and occur in the terminal stages of the disease.
!!! Dysfunction of the pelvic organs is not typical, but in advanced stages, urinary retention or incontinence may occur.
Moderate cognitive impairment(decrease in memory and mental performance) are manifested in half of the patients. 5% of patients develop dementia of the frontal type, which can be combined with Parkinson's syndrome.
!!! A feature of ALS is the absence of bedsores even in paralyzed bedridden patients.
Clinic of the main forms of the disease
cervicothoracic form(50% of cases):
atrophic and spastic-atrophic paresis of the arms and spastic paresis of the legs are characteristic
bulbar form:
occurs in 25% of ALS cases
Bulbar disorders predominate (paralysis of the soft palate, tongue, weakness of the masticatory muscles, speech and swallowing disorders, continuous saliva flow, respiratory disorders in the later stages), it is possible to attach pseudobulbar manifestations in the form of violent laughter and crying, revitalization of the mandibular reflex
later signs of damage to the limbs join
with this form, the shortest life expectancy: patients die from bulbar disorders (due to aspiration pneumonia, respiratory failure), while often remaining able to move independently
lumbosacral shape(20 - 25% of cases):
atrophic paresis of the legs develops with mild pyramidal symptoms
on late stages arm muscles and cranial musculature are involved
High (cerebral) form(1 – 2%):
manifested by spastic tetraparesis (or lower paraparesis), pseudobulbar syndrome (violent laughter and crying, revival of the mandibular reflex) with minimal signs of damage to peripheral motor neurons
Complications of ALS
paresis and paralysis of the limbs, neck muscles (inability to hold the head)
swallowing disorders
respiratory failure, respiratory failure
aspiration pneumonia
limb contractures
urosepsis
depression
multiple cramps (painful muscle spasms)
cachexia
Progression of movement disorders ends in death in a few (2-6) years. Sometimes the disease has an acute course.
DIAGNOSTICS
Diagnosis of amyotrophic lateral sclerosis primarily based on careful analysis of the clinical picture of the disease. An EMG study (electromyography) confirms the diagnosis of motor neuron disease.
Amyotrophic lateral sclerosis should be suspected:
with the development of weakness and atrophy, and possibly fasciculations (muscle twitches) in the muscles of the hand
with weight loss of the thenar muscles of one of the hands with the development of weakness of adduction (adduction) and opposition of the thumb (usually asymmetrically)
at the same time, there is difficulty in grasping with the thumb and forefinger, difficulty in picking up small objects, in fastening buttons, in writing
with the development of weakness in the proximal arms and shoulder girdle, atrophy in the muscles of the legs in combination with lower spastic paraparesis
when a patient develops dysarthria (speech disorders) and dysphagia (swallowing disorders)
when a patient develops cramps (painful muscle contractions)
Diagnostic criteria for ALS of the world organization of neurologists (1998):
defeat (degeneration) of the lower motor neuron, proven clinically, electrophysiologically or morphologically
lesion (degeneration) of the upper motor neuron according to the clinical picture
progressive development of subjective and objective signs of the disease at one level of damage to the central nervous system or their spread to other levels, determined according to the anamnesis or examination
!!! At the same time, other possible reasons degeneration of the lower and upper motor neurons.
Diagnostic criteria for ALS:
Clinically significant ALS is diagnosed:
in the presence of clinical signs of damage to the upper motor neuron (for example, spastic paraparesis) and lower motor neuron at the bulbar and at least two spinal levels (damage to the arms, legs)
or
in the presence of clinical signs of damage to the upper motor neuron at two spinal levels and the lower motor neuron at three spinal levels
Clinically probable ALS is diagnosed by:
with damage to the upper and lower motor neurons at least at two levels of the central nervous system
And
if there are symptoms of an upper motor neuron lesion above the levels of a lower motor neuron lesion
Clinically possible ALS:
lower motor neuron symptoms plus upper motor neuron symptoms in 1 region of the body
or
upper motor neuron symptoms in 2 or 3 regions of the body, such as monomelic ALS (ALS manifestations in one limb), progressive bulbar palsy
Suspicion of ALS:
if there are symptoms of lower motor neuron involvement in 2 or 3 regions, such as progressive muscle atrophy or other motor symptoms
NB!!! The regions of the body are divided into:
oral-facial
brachial
crural
thoracic
trunk
ALS confirmation criteria:
fasciculations in one or more areas
a combination of signs of bulbar and pseudobulbar palsy
rapid progression with the development of a lethal outcome within a few years
absence of oculomotor, pelvic, visual disturbances, loss of sensitivity
non-myotomous distribution of muscle weakness (eg, simultaneous development of weakness in the biceps brachii and deltoid muscles; both are innervated by the same spinal segment, albeit by different motor nerves)
no signs of simultaneous damage to the upper and lower motor neurons in one spinal segment
non-regional distribution of muscle weakness (for example, if paresis first developed in right hand, usually the right leg or left arm is later involved in the process, but not left leg)
unusual course of the disease over time (ALS is not characterized by onset before age 35, duration more than 5 years, absence of bulbar disorders after one year of illness, indications of remission)
ALS exclusion criteria
For the diagnosis of amyotrophic lateral sclerosis, the absence of:
sensory disorders, primarily loss of sensitivity (possible paresthesia and pain)
pelvic disorders - disorders of urination and defecation (their attachment is possible in the final stages of the disease)
visual disturbances
autonomic disorders
parkinson's disease
dementia of the Alzheimer's type
ALS-like syndromes
EMG(electromyography) helps in confirming clinical findings and findings.
Characteristic changes and findings on EMG in ALS:
fibrillation and fasciculations in the muscles of the upper and lower extremities, or in the extremities and head region
a decrease in the number of motor units and an increase in the amplitude and duration of the action potential of motor units
normal conduction velocity in nerves innervating slightly affected muscles, and a decrease in conduction velocity in nerves innervating severely affected muscles (the speed should be at least 70% of the normal value)
normal electrical excitability and speed of impulse conduction along the fibers of sensory nerves
Differential diagnosis of ALS (syndromes similar to ALS):
Spondylogenic cervical myelopathy.
Tumors of the craniovertebral region and spinal cord.
Craniovertebral anomalies.
Syringomyelia.
Subacute combined degeneration of the spinal cord with vitamin B12 deficiency.
Strümpel's familial spastic paraparesis.
Progressive spinal amyotrophies.
Post-polio syndrome.
Intoxication with lead, mercury, manganese.
Hexosaminidase type A deficiency in adults with GM2 gangliosidosis.
diabetic amyotrophy.
Multifocal motor neuropathy with conduction blocks.
Creutzfeldt-Jakob disease.
Paraneoplastic syndrome, in particular with lymphogranulomatosis and malignant lymphoma.
ALS syndrome with paraproteinemia.
Axonal neuropathy in Lyme disease (Lyme borreliosis).
radiation myopathy.
Guillain-Barré syndrome.
Myasthenia.
Multiple sclerosis.
ONMK.
Endocrinopathy (thyrotoxicosis, hyperparathyroidism, diabetic amyotrophy).
Malabsorption syndrome.
Benign fasciculations, i.e. fasciculations lasting for years without signs of damage to the motor system.
Neuroinfections (poliomyelitis, brucellosis, epidemic encephalitis, tick-borne encephalitis, neurosyphilis, Lyme disease).
Primary lateral sclerosis.
TREATMENT
There is no effective treatment for the disease. The only drug, the glutamate release inhibitor riluzole (Rilutek), delays death by 2 to 4 months. It is prescribed 50 mg twice a day.
The basis of treatment is symptomatic therapy:
Physiotherapy.
Physical activity. The patient should be physically active as much as possible. As the disease progresses, a wheelchair and other special devices are needed.
Diet. Dysphagia poses a risk of food entering the respiratory tract Sometimes there is a need for feeding through a tube or in a gastrostomy.
The use of orthopedic devices: cervical collar, various splints, devices for gripping objects.
For cramps (painful muscle spasms): quinine sulfate 200 mg twice a day, or phenytoin (Difenin) 200–300 mg/day, or carbamazepine (Finlepsin, Tegretol) 200–400 mg/day, and/or vitamin E 400 mg twice a day, as well as magnesium preparations, verapamil (Isoptin).
With spasticity: baclofen (Baclosan) 10 - 80 mg / day, or tizanidine (Sirdalud) 6 - 24 mg / day, as well as clonazepam 1 - 4 mg / day, or memantine 10 - 60 mg / day.
When drooling atropine 0.25-0.75 mg three times a day, or hyoscine (Buscopan) 10 mg three times a day.
When unable to eat due to a violation of swallowing, a gastrostomy is imposed or a nasogastric tube is inserted. Early percutaneous endoscopic gastrostomy prolongs the life of patients by an average of 6 months.
For pain syndromes use the entire arsenal of analgesics. Including narcotic analgesics in the final stages.
Sometimes some temporary improvement bring anticholinesterase drugs (neostigmine methyl sulfate - neostigmine).
Cerebrolysin in high doses(10-30 ml IV drip for 10 days in repeated courses). There are a number of small studies showing the neuroprotective efficacy of cerebrolysin in ALS.
Antidepressants: Sertalin 50 mg/day or Paxil 20 mg/day or Amitriptyline 75-150 mg/day
When respiratory problems occur: artificial ventilation of the lungs in hospitals, as a rule, is not carried out, but some patients purchase portable ventilators and carry out ventilators at home.
Developments are underway for the use of growth hormone, neurotrophic factors in ALS.
Stem cell therapy has been actively developed in recent years.. This method promises to be promising, but is still at the stage scientific experiments.
FORECAST
amyotrophic lateral sclerosis is a fatal disease. The average life expectancy of ALS patients is 3-5 years, however, 30% of patients live 5 years, and about 10-20% live more than 10 years from the onset of the disease.
Unfavorable prognostic signs- old age and bulbar disorders (after the appearance of the latter, patients live no more than 1 - 3 years).
PREVENTION
There is no specific prophylaxis.
Bass is the lowest male singing voice. The range of the bass is from the F of a large octave to the F (G) of the first. True, the range of the central bass and profundo bass can capture lower notes. The brightest note in the high bass is up to the first octave, the working middle is the B flat of the big octave - D of the first octave. Bass is a very expressive and rich voice, but unfortunately there are very few singers with such a voice, and opera parts little is written for bass. The range distinguishes between high (bass cantato), medium (central) bass and low (bass profundo). According to the nature of the sound, baritone bass, characteristic bass or comic bass (bass buffo) are distinguished.
high bass - this is a melodious bass, timbre is the brightest and brightest voice. It sounds like a baritone, especially in the upper tessitura. Its operating range is from the salt of a large octave to the salt of the first.
central bass – it is a bass that has a wider range of possibilities. It has a solid, sonorous and formidable timbre color. The working middle of such voices is the salt of a large octave - up to the first octave. The entire range of such a voice sounds good only in the chest resonator; in the head resonator, the bass loses its timbre color greatly.
Low bass, profundo bass – another name for this extremely rare male voice is the bass octave. Vocalists with these voice characteristics can sing the lowest notes (counter-octave F-sol). It even seems that the human voice cannot produce such sounds. Bass profundos often perform parts in opera or church choir. A low deep sound, reminiscent of a roar or seething, is mesmerizing. Such a phenomenon, according to critics and connoisseurs of vocals, can only be found in Russia, they are called " Russian miracle”, awarding such a voice with the title of a unique natural phenomenon.
baritone bass— it is a voice that has features of both bass and baritone. It has a good high and low, but without profundus notes. Bass-baritones often have a very rich timbre and powerful sound, and are able to sing the baritone repertoire.
bass buffo— this O usually the bass-buffo performs the supporting parts. Often these are comic parties or the parties of old people. From the owner of such a voice, first of all, acting skills are required, and they might not have any singing features or beauty of timbre at all. In the opera seria of the 18th century, basses were rarely used, and recognition came to them only with the advent of opera buff, where a significant place was given to basses.
By its nature, the bass singing voice is less common than other male voices, often it does not appear immediately, and for a long time the singer may consider himself a baritone, but as a result of training, over time, a baritone can develop into a bass. The fact is that the signs by which this or that voice is determined may be blurred or not yet developed among beginners. An exception can only be voices set by nature. The exercises for the bass voice are the same as for other singing voices only in their tessitura. So if you have a bass, then you are the representative of very rare singing voices.
in our catalogue.
Source: Car Tuning Magazine (featuring Car&Music), April 2012
A lot has already been said about car subwoofers in our magazine - both how to choose the right speaker, and how to make the right case for it. But one important question mentioned only in passing - this is a setting. We often receive letters like "I did everything, but it still doesn't play as it should." So, let's figure out what needs to be switched and tweaked so that the sub plays as it should.
What is bass anyway?
But before you immediately rush to turn the knobs and flip the switches, let's clarify a little, but what exactly is a bass as such. The speaker with its oscillating cone creates an alternation of compression and rarefaction of the air. It is generally accepted that the average person perceives such air vibrations precisely as sound if they occur at frequencies from 16-20 times per second to 14-18 thousand times per second. That is, from 16-20 hertz to 14-18 kilohertz. So, the bass is considered the lowest range of these sound vibrations - from about 20 to 150 Hz. It is with such frequencies that the diffusers of subwoofers and mid-bass speakers oscillate. It is usually said that oscillations up to 50 Hz - low bass, 50-100 is the middle bass, and 100-150 is the upper bass (although this division is very conditional and approximate).
REMEMBER THAT THE PURPOSE OF A SUBWOOFER IS NOT TO SING WITH A VOICE, BUT ONLY TO PLAY THE LOWEST FREQUENCIES. MUSIC SHOULD BE PLAYED BY THE MAIN ACOUSTIC SYSTEMS (FRONT OR TOGETHER WITH REAR), AND THE SUB SHOULD ONLY GIVE THE SOUND THE NECESSARY MASSIVENESS AND SOLIDITY
BY THE WAY
When tuning the bass, it's helpful to know which frequency region in the sound is responsible for what. For take an example drum set: the frequency range around 40 Hz determines the depth and softness of the impact, around 63 Hz - the heaviness, severity of the impact, the area around 80 Hz - the hardness of the impact. In the sound of a bass guitar or double bass, frequencies in the region of 40–50 Hz determine the massiveness of the instrument, and in the region of 100 Hz, the density and elasticity of the bass.
What are we listening to?
But the physics of the process, let's now look at the whole thing from the musical side. Let's start with rap, hip-hop or dubstep. Black guys especially love the low, uterine bass on the verge of infrasound, which makes all the giblets vibrate. So, such a “gut shaker” is sounds with frequencies in the region of 30-50 Hz. You may be surprised, but these are perhaps the only genres that require the full reproduction of such low frequencies, in all other musical genres such a deep bass does not carry any serious information content.
For example, if we take music with "live" instruments, then in it almost all the informative component and energy of the bass is concentrated in the frequency range above 40 Hz. For example, the bass guitar. The sound of its strings consists not only of fundamental tones, but also of overtones - harmonics from the fundamental tone, which have higher frequencies. would try to play the same melody in the same key.It is the overtones that have the highest information content in the sound of most instruments.Or take, for example, a dynamic electronic music- peppy tuber. The classics of house and trance is the sound of the Roland TR-909 and TR-808 drum machines, and their frequency spectrum also lies not in the deepest bass region - 40-100 Hz.
IF THE SUBWOOFER IS POORLY AGREED WITH THE MIDBASS, THE BASS WILL BE STRETCHED, THE SOUND WILL LOSE AND DRIVE, Juiciness, EMOTIONALITY. IN ELECTRONIC MUSIC, WE WILL GET NOT A DENSE BASS RHYTHM, BUT OR A SLOW HOOT, OR ON THE CONTRAST - A BOOMING BEAT, FROM WHICH AFTER 10 MINUTES THE HEAD BEGINS. IN THE WORST CASE, THE SUB WILL BE PERCEIVED AT ALL PLAYING SEPARATELY, AS IF BY ITSELF.
First step: turn on the low-pass filter
So, we need to attenuate the mids and highs in the subwoofer signal, and leave only the lows. A frequency filter can do this, in this case a low-pass filter (LPF, also known as Low Pass Filter, denoted as LPF or simply LP). It passes everything below the tuning frequency and attenuates everything above. Such a filter can be equipped, for example, with a head unit, an amplifier, or it can be both there and there at the same time.
Now find the knob responsible for the frequency of the filter settings. In the amplifier, this is the usual “twist”, denoted as Frequency or something like that. Set it for now to a frequency of 80 Hz. With this setting, only low frequencies will pass to the subwoofer unhindered, and everything above 80 Hz will be noticeably attenuated. Do not overdo it with the level, the sub should not shout over everything else!
IF THE SUB LEVEL IS TOO HIGH, THE BASS WILL LOSE IN ITS NATURALITY (IMPORTANT FOR "LIVE" MUSIC GENRES), CLARITY AND RESISTANCE (IMPORTANT FOR ANY MUSIC). DOESN'T DIE YOUR FEEL, A LOT OF BAD BASS IS WORSE THAN ANY GOOD.
Fourth stage: adjusting the subsonic
Many bass amplifiers are equipped with a so-called “sub-tone filter”, a subsonic. This is actually a regular high-pass filter that attenuates everything in the signal that is below its tuning frequency, that is, it removes the very, very low frequencies. Here, for sure, the question may arise - why is it needed, isn’t the sub designed to reproduce lower frequencies?
It's just that the lower the frequency, the higher the speaker travel, and at ultra-low frequencies it can be so large that it's not far from a torn suspension, a broken cone or a jammed voice coil. I often had to observe a situation where the subwoofer cone shakes, and the bass is sluggish and booming. And on the contrary, a really loud, juicy and elastic bass can often be emitted by a subwoofer, the cone of which seems to be barely moving. But we have already said that in real music there are practically no frequencies below 30 Hz, and even in the most downhole gangsta rap. Therefore, we can attenuate uninformative ultra-low frequencies without any damage to the music. Being freed from them, the subwoofer will play much better - it will bass clearer and more elastic, the maximum volume limit will increase. Tune the subsonic to a frequency of about 20 Hz. If you like very loud bass, you can turn it up to 30, and in extreme cases even up to 40 Hz. Don't worry, you won't lose any of the richness and fleshiness of the bass, but keep the speaker intact. By the way, if you have a subwoofer in a case with a phase inverter, then the subsonic is generally from the category must have. The fact is that in a closed case, the volume of air enclosed inside holds the speaker and does not allow it to become too loose. But in a phase inverter, this happens only above the port tuning frequency, and at lower frequencies the cone dangles almost unrestrained, and very quickly reaches its physical travel limits with all the consequences, as they say.
Fifth stage: "splicing" the sound of the subwoofer with the sound of the mid-bass speakers more carefully
At this stage of tuning, you have to find the optimal tuning frequency of the low-pass filter (LPF, LPF, LP) and the volume of the subwoofer. These two adjustments should always be set in combination. The principle is something like this:
- If we decrease the cutoff frequency of the LP and increase the volume at the same time, the bass becomes softer and deeper. But if you overdo it, you can get the effect when the front of the bass impact is separated from the low-frequency filling - the sub will sound as if by itself.
- If we increase the cutoff frequency of the LP, then the bass becomes harder, acquires more impact. At the same time, the volume must be turned down, otherwise you can get excessive "clatter", and it will no longer be bass, but a hollowing booming sound like a stick on empty barrel We don't need this either. In a well-tuned system, the subwoofer should not be perceived as playing alone. It should merge with the sound of the main acoustics as if it were bass. Try to make the instruments sound as natural as possible. And then you can say with confidence: “Yes, I have a very good quality bass in my car.”
WHAT GIVES TURNING ON THE HIGH PASS FILTER IN THE MAIN CHANNELS?
If you're just adding a subwoofer to your stock system, then all you have to tweak is the adjustments on the subwoofer itself (more precisely, on the subwoofer amplifier). If you have a more developed system in which the main channels also work from the amplifier, then there are probably some adjustments in it.
In this case, we need a high-pass filter (HPF, Low Pass Filter, LPF, LP). It works, as you probably already understood, in the exact opposite of a low-pass filter - it passes everything that is higher than the tuning frequency and attenuates everything that is lower.
If you turn it on, then attenuate the lowest bass in the signal for the main speakers. And it doesn’t matter that small 6.5-inch midbasses (or whatever you have there) don’t really reproduce low bass, being freed from low-frequency signals, the speakers will play much easier, elasticity and clarity will appear in the sound, the buzz and overtones of the door will go away, it will become much easier to merge the sound of midbass with a subwoofer.
If the HPF setting is available to you in the main channels, then first adjust this filter without turning on the subwoofer. Too high a tuning frequency deprives the sound of solidity, weight, and with too low a cone stroke, it can be too large. Find a compromise where the speaker cones have little travel but still don't lose bass. After that, proceed to setting up the subwoofer.
IF THE DIFFUSER WALKS WALKING, ALMOST JUMPING OUT OF THE SPEAKER, THEN THIS IS NOT A SIGN OF COOLITY, IN GENERAL. OFTEN EXACTLY TO THE REVERSE.
Many amplifiers are equipped with a phase shifter. It is needed to more accurately match the sound of the subwoofer and midbass speakers. At step number 3, we selected the best switching polarity by simply throwing wires at the subwoofer speaker terminals. This essentially corresponds extreme provisions phase shifter, which are designated as "0" and "180 degrees". The phase shifter itself also allows you to set intermediate values. You can use it when finalizing the system.
FREQUENT ERROR
Many put oval speakers and a subwoofer at the back at the same time, naively believing that, they say, the more the better. This is an erroneous judgment. The ovals, if correctly installed, are bass enough in themselves, so it turns out that they will reproduce the same part of the sound spectrum simultaneously with the subwoofer. But they will do it in different ways (we will not go into details now, the reason for this is the difference in phase, impulse characteristics), and in the end it will turn out like in that saying: who is in the forest, who is for firewood. Will you get normal bass with this? Of course not.
THIS IS INTERESTING
| Of the real, non-electronic percussion instruments, the deepest bass comes from Japanese Taiko drums. Taiko in Japanese means "a big drum that fills the air with blows similar to thunder and the gentle murmur of a stream at the same time." Not without romanticism, however. | The deepest bass of all real instruments can be produced by an organ. This instrument can sound not only in the audible range, but even in infrasound. |
WHAT MUSIC CAN I USE TO SET THE SUBWOOFER?
For tuning, pick up music with a well-recorded bass. But it should not be electronic bass, but some kind of “live” instruments. When you listen to them, it will be easier for you to imagine them, which means that you can tune the system more precisely. One of the most tricky and difficult instruments for any audio system is the double bass. Good example- Superbass and Superbass II discs, recorded by Telarc studio.
amyotrophic lateral sclerosis(ALS, or Charcot's disease, or Gehrig's disease, or motor neuron disease) is an idiopathic neurodegenerative progressive disease of unknown etiology, caused by selective damage to peripheral motor neurons of the anterior horns of the spinal cord and motor nuclei of the brainstem, as well as cortical (central) motor neurons and lateral columns of the spinal cord.
The disease is manifested by steadily increasing paresis (weakness), muscle atrophy, fasciculations (rapid, irregular contractions of muscle fiber bundles) and pyramidal syndrome (hyperreflexia, spasticity, pathological signs) in the bulbar muscles and muscles of the extremities. The predominance of the bulbar form of the disease with atrophy and fasciculations in the muscles of the tongue and speech and swallowing disorders usually leads to a more rapid increase in symptoms and death. In the extremities, atrophic paresis in the distal sections predominates, in particular, atrophic paresis of the muscles of the hand is characteristic. Weakness in the hands increases and spreads with the involvement of the muscles of the forearms, shoulder girdle and legs, and the development of both peripheral and central spastic paresis is characteristic. In most cases, progression of the disease is observed within 2-3 years with the involvement of all limbs and bulbar muscles.
Diagnosis of amyotrophic lateral sclerosis is based on a thorough analysis of the clinical picture of the disease and is confirmed by an electromyographic study.
There is no effective treatment for the disease. Its basis is symptomatic therapy.
The progression of movement disorders ends in death after a few (2-6) years. Sometimes the disease has an acute course.
ALS-plus syndromes are distinguished as a separate variant of ALS, which include:
- ALS associated with frontotemporal dementia. It is most often familial and accounts for 5-10% of cases.
- ALS, combined with frontal dementia and parkinsonism, and associated with a mutation of the 17th chromosome.
- Epidemiology
Amyotrophic lateral sclerosis makes its debut at the age of 40-60 years. The mean age of onset was 56 years. ALS is a disease of adults and does not occur in persons under 16 years of age. Men get sick a little more often (the relation of the man-woman 1,6-3.0: 1).
ALS is a sporadic disease with an incidence of 1.5-5 cases per 100,000 population. In 5-10% of cases, amyotrophic lateral sclerosis has a family character (it is transmitted in an autosomal dominant manner).
- Classification
According to the predominant localization of the lesion of various muscle groups, the following forms of amyotrophic lateral sclerosis are distinguished:
- Cervical-thoracic form (50% of cases).
- Bulbar form (25% of cases).
- Lumbosacral form (20 - 25% of cases).
- High (cerebral) form (1 - 2%).
- ICD code G12.2 Motor neuron disease.
Diagnostics
Diagnosis of amyotrophic lateral sclerosis is primarily based on a thorough analysis of the clinical picture of the disease. An EMG study (electromyography) confirms the diagnosis of motor neuron disease.
- When to Suspect ALS
- Amyotrophic lateral sclerosis should be suspected in the development of weakness and atrophy, and possibly fasciculations (muscle twitches) in the muscles of the hand, in particular, when the thenar muscles of one of the hands are thinning with the development of weakness of adduction (adduction) and opposition of the thumb (usually asymmetrically). At the same time, there is difficulty in grasping with the thumb and forefinger, difficulty in picking up small objects, in fastening buttons, and in writing.
- With the development of weakness in the proximal arms and shoulder girdle, atrophy in the muscles of the legs in combination with lower spastic paraparesis.
- With the development of the patient's dysarthria (speech disorders) and dysphagia (swallowing disorders).
- When a patient develops cramps (painful muscle contractions).
- ALS Diagnosis Criteria of the World Federation of Neurologists (1998)
- Defeat (degeneration) of the lower motor neuron, proven clinically, electrophysiologically or morphologically.
- Damage (degeneration) of the upper motor neuron according to the clinical picture.
- The progressive development of subjective and objective signs of the disease at one level of damage to the central nervous system or their spread to other levels, determined according to the anamnesis or examination.
At the same time, it is necessary to exclude other possible causes of degeneration of the lower and upper motor neurons.
- ALS diagnostic categories
- Clinically significant ALS is diagnosed:
- If there are clinical signs of damage to the upper motor neuron (for example, spastic paraparesis) and lower motor neuron at the bulbar and at least two spinal levels (damage to the arms, legs), or
- In the presence of clinical signs of damage to the upper motor neuron at two spinal levels and the lower motor neuron at three spinal levels.
- Clinically probable ALS is diagnosed by:
- When the upper and lower motor neurons are affected at least at two levels of the central nervous system, and
- If there are symptoms of an upper motor neuron lesion above the levels of a lower motor neuron lesion.
- Possible ALS:
- Lower motor neuron symptoms plus upper motor neuron symptoms in 1 region of the body, or
- Upper motor neuron symptoms in 2 or 3 regions of the body, such as monomelic ALS (ALS manifestations in one limb), progressive bulbar palsy.
- Suspicion of ALS:
- If there are symptoms of damage to the lower motor neuron in 2 or 3 regions, such as progressive muscle atrophy or other motor symptoms.
In this case, the regions of the body are divided into oral-facial, brachial, crural, thoracic and trunk.
- Clinically significant ALS is diagnosed:
- Diagnosis of ALS is Confirmed by Signs (ALS Confirmation Criteria)
- Fasciculations in one or more areas.
- A combination of signs of bulbar and pseudobulbar paralysis.
- Rapid progression with the development of death within a few years.
- The absence of oculomotor, pelvic, visual disturbances, loss of sensitivity.
- Non-myotomous distribution of muscle weakness. For example, the simultaneous development of weakness in the biceps of the shoulder and the deltoid muscle. Both are innervated by the same spinal segment, albeit by different motor nerves.
- The absence of signs of simultaneous damage to the upper and lower motor neurons in one spinal segment.
- Non-regional distribution of muscle weakness. For example, if paresis first develops in the right arm, usually the right leg or left arm is later involved in the process, but not the left leg.
- Unusual course of the disease over time. ALS is not characterized by an onset before the age of 35, a duration of more than 5 years, the absence of bulbar disorders after one year of illness, and indications of remission.
- ALS exclusion criteria
For the diagnosis of amyotrophic lateral sclerosis, the absence of:
- Sensory disorders, primarily loss of sensitivity. Paresthesia and pain are possible.
- Pelvic disorders (impaired urination and defecation). Their accession is possible at the final stages of the disease.
- visual disturbances.
- Vegetative disorders.
- Parkinson's disease.
- Dementia of the Alzheimer's type.
- ALS-like syndromes.
- Electromyographic study (EMG)
EMG helps in confirming clinical data and findings. Characteristic changes and findings on EMG in ALS:
- Fibrillations and fasciculations in the muscles of the upper and lower limbs, or in the limbs and head region.
- Reducing the number of motor units and increasing the amplitude and duration of the action potential of motor units.
- Normal conduction velocity in nerves innervating slightly affected muscles, and a decrease in conduction velocity in nerves innervating severely affected muscles (the velocity should be at least 70% of the normal value).
- Normal electrical excitability and speed of impulse conduction along the fibers of sensory nerves.
- Differential diagnosis (ALS-like syndromes)
- Spondylogenic cervical myelopathy.
- Tumors of the craniovertebral region and spinal cord.
- Craniovertebral anomalies.
- Syringomyelia.
- Subacute combined degeneration of the spinal cord with vitamin B12 deficiency.
- Strümpel's familial spastic paraparesis.
- Progressive spinal amyotrophies.
- Post-polio syndrome.
- Intoxication with lead, mercury, manganese.
- Hexosaminidase type A deficiency in adults with GM2 gangliosidosis.
- diabetic amyotrophy.
- Multifocal motor neuropathy with conduction blocks.
- Creutzfeldt-Jakob disease.
- Paraneoplastic syndrome, in particular with lymphogranulomatosis and malignant lymphoma.
- ALS syndrome with paraproteinemia.
- Axonal neuropathy in Lyme disease (Lyme borreliosis).
- radiation myopathy.
- Guillain-Barré syndrome.
- Myasthenia.
- Multiple sclerosis.
- ONMK.
- Endocrinopathy (thyrotoxicosis, hyperparathyroidism, diabetic amyotrophy).
- Malabsorption syndrome.
- Benign fasciculations, i.e. fasciculations lasting for years without signs of damage to the motor system.
- Neuroinfections (poliomyelitis, brucellosis, epidemic encephalitis, tick-borne encephalitis, neurosyphilis, Lyme disease).
- Primary lateral sclerosis.
This question is by no means idle. A car audio system is built quite differently than a home audio system. Here the limited space of the cabin plays a role, and especially the installation of acoustic systems. Therefore, the approach to solving the problem looks unusual for many.
The reason why I would like to start with this topic is very simple. As practice shows, not every motorist wants to completely rebuild the standard audio system. Therefore, many are limited to only its slight upgrade for a more confident low-frequency sound. In most regular systems, bass is really one of the weakest points. The acoustic design of the speakers often leaves much to be desired, and the standard subwoofer, if any, rarely boasts a decent sound in any system.
Regular subwoofers, as a rule, are built on small speakers and have plastic cases. I must warn you right away that we are talking about a normal musical system, in which the bass is a solid foundation that gives the sound fullness regardless of the genre. Unfortunately, many today associate the phrase “car subwoofer” with incomprehensible structures in trunks that make humming and rattling sounds and have nothing to do with music. Let's leave these "50 Shades of Bass" and other car audio perversions overboard, and take a good home system as a guideline.
Acoustic conditions
The first noticeable difference between car conditions and home conditions is that the interior space is limited. Many skeptics operate on this very argument, believing that building a high-end audio system in a car is pointless. In such cases, I usually counter that this is indeed the case with the home approach. But if you correctly use the specifics of "small volumes", then you can achieve impressive results, which has been repeatedly proven in practice.
Actually, one of the main features of the acoustic properties of the car interior is "help" in reproducing low frequencies. It is clear that as the frequency decreases, the length of the sound wave increases. For example, at a frequency of 1000 Hz, the wavelength is about 30 cm, and at 300 Hz it is already more than a meter. With an even greater decrease, it becomes completely commensurate with the size of the cabin.
At this moment, sound waves in the usual representation cease to exist, and the speaker cone begins to create a uniform alternation of compression-discharge of the air mass throughout the volume. Like a piston in a cylinder. And here, last but not least, much will depend on the amplitude of the diffuser oscillations. Lower frequency - higher amplitude. In the closed volume of the car interior, this creates the effect of acoustic amplification of low frequencies: lower frequency - more diffuser stroke - higher acoustic amplification.
Acoustic gain in car interior (dB/Hz) In theory, the “help” of the cabin starts from 50-100 Hz, depending on the size of the car. The smaller the car, the higher frequencies this effect begins to manifest itself. Moreover, with a decrease in frequency for each octave, the increase in gain will be 12 dB. In practice, of course, everything is not so rosy - air leaks, loss of sound energy through vibrations, etc. will affect. In addition, this mathematical model does not take into account the individual characteristics of different salons. And it's not just the geometric dimensions, even the material of the upholstery can matter.
Different acoustic conditions at the closed and open top make convertibles and roadsters one of the most difficult when building audio systems. high level It is very easy to feel the effect of the “help” of the cabin at low frequencies. Turn on any song with accented bass. Pay attention to how the low frequency range sounds. Now open the doors and trunk lid. I am sure you will feel the difference right away - as if the low frequencies were turned down with a tone control.
Do you need a subwoofer?
Knowing this feature of a closed cabin, it is logical to assume that there is no need for a separate subwoofer link in a car at all. It may be so, but let's compare car acoustics with home ones. In both cases, loudspeakers of similar calibers are used - from 5 to 8 inches. 6.5 inches is the "golden mean" and classic car speakers.
The home speaker is a one-piece complete assembly, designed and manufactured to give the speakers the best possible acoustic performance. And most importantly - a durable case, devoid of vibrations. In the car, unfortunately, this is most often only a dream. Cases for speakers in most cases are doors or some niches and spaces in the body elements. Get in such conditions the normal reproduction of low frequencies? Oh, don't laugh.
This is how the speakers are installed in the Burmester 3D High End Sound System for 8000 Euros. To put it mildly, not the best acoustic design:
So it turns out that in most cases, acoustics are able to more or less effectively "hold out" only up to 80-100 Hz, no matter what the manufacturers say. What is the solidity of the sound here.
The situation can be corrected either by seriously strengthening the doors, turning it into a heavy "reinforced concrete" structure, or by manufacturing separate cases for the speakers. Well, or even hit some exotic:
In any case, attempts to create a low-playing speaker system come down to radical intervention in the design of the car, and for this you need to be quite a fanatic. And therefore it turns out that the subwoofer is the most rational way to solve the car's low-frequency problem. Another thing is exactly how it should be and how to seamlessly merge it with the rest of the acoustics so that it does not mumble in the trunk on its own, but is a full-fledged part of the sound system.
Making enclosures in the doors is not so exotic, but also a very radical and costly way to create the desired acoustic design for the speaker. In the photo - the work of Alexander Lysenko Selecting a subwoofer link
I think it makes no sense to dwell on the choice of a specific subwoofer concept for a person familiar with home appliances, many things are obvious. But in some ways, automotive specificity is still different from home.
For home appliances, the volume of the case, although it plays a certain role, is not as significant as in a car. Here it is desirable to fit the entire structure in as small volumes as possible. This task is very contradictory, and its solution is full of compromises. As soon as you clamp the speaker into a tight volume, the lower cut-off frequency immediately increases and the subwoofer turns into just a woofer. To restore the status quo, manufacturers have to make the moving system heavier, and this entails a decrease in sensitivity, which means that a more powerful amplifier is required. So don't be surprised by car bass monoblocks with hundreds of watts of power - they usually have to pull fairly tight drivers.
So when choosing a speaker, you have to prioritize - either give preference to "lightweights" with soft suspensions and low weight of the movement, with good impulse response and not exorbitant requirements for the amplifier, but which will require large cases, or "heavyweights" that fit in compact cases, but require high-power amplifiers.
The subwoofer does not have to be large and take up half the trunk. It can be a small neat design that does not eat up useful space in the trunk. Now a little about the size of the speakers. The fact that large loudspeakers, all other things being equal, require large enclosures, I believe, is already obvious. But there is also another factor. The size of the subwoofer also directly determines how well it can be spliced with speaker systems. For example, if the bass potential of the latter is completely bad, then choosing some heavyweight 15-inch subwoofer is at least stupid - it is unlikely to work normally above 50-60 Hz. But, for example, "tens", all other things being equal, can easily reach from below to the acoustics and dock well with it.
Perhaps these are the two main points that you should pay attention to when building a low-frequency link for a car audio system. Everything else is a matter of specific speaker implementations. There can be light subwoofers of large sizes, and small "slow-movers". Each of them, of course, requires its own approach to the choice of acoustic design. But this is a separate topic and now there is no need to delve into it.
By the way, as for the design, I consider it necessary to mention subwoofer speakers for free-air installation. They usually stand a little apart. These do not require separate buildings. Rather, the cases for them will be the volume of the trunk - they are placed in the rear shelf or partition between the trunk and the passenger compartment. Despite the apparent simplicity, it is rather difficult to ensure proper design for them, if only because of the fact that it is necessary to radically strengthen the seats for the speakers to stone rigidity, and this is due to the high laboriousness of such work. Throwing a case into the trunk is much easier, so there are very few “free-air” subs on the market. Although, in my opinion, this is still one of the best subwoofers, which provide the most accurate sound of the low-frequency range.
Back bass problems
Continuing the topic of merging the sound of a subwoofer with speakers, I should touch on another important issue - the localization of the subwoofer. It would seem that our ears do not determine the position of the sound source in the frequency spectrum in which the subwoofer operates. That is why no one is particularly keen to place it in the front of the cabin, and installation in the trunk is considered a classic.
Don't want to put a sub in the trunk? Yes, please, at least embed it in the dashboard ... You can also in literally However, in practice, in very many cases, the bass is still perceived as coming from behind, when the main sound picture is formed in front of the listener, and low frequencies live their own lives. There may be several reasons for this.
Reason one: vibration
Powerful bass chords can resonate adjacent panels and elements. And these sounds, as you understand, are far from low-frequency. They blend in so well with the subwoofer that we can't always identify them, but they do spoil the overall picture.
Treated by processing body elements vibration-damping materials, fitting plastic upholstery on sealing “anti-creak” materials, reliable fastening of the subwoofer case and, in the end, elementary tidying up in the trunk.
Reason two: bad case
Try with the subwoofer turned on, just touch it with your palm. A good case should not have vibrations. If they are, then here is the second reason for you - in addition to the speaker cone, the walls of the case themselves emit sound. And also not at the lowest frequencies. This is mainly the fault of cheap subwoofers with flat walls, most of them are made of chipboard with a thickness of 18-20 mm at best.
The way out is to make a normal body with thick walls, reinforce it with internal braces or use a multilayer structure using vibration-damping materials as intermediate layers. The disadvantage is that it is laborious, and the case is too heavy. Lightweight construction with sufficient rigidity is combined in fiberglass hulls. A centimeter thickness for fiberglass walls of complex shape is enough to make the structure sufficiently monolithic.
The curved surfaces of the fiberglass body, even with a thickness of about 1 cm, have sufficient rigidity Reason three: air turbulence
At low frequencies, the cone travel is often quite significant, especially if you turn up the heat. At the same time, if the speaker itself is covered with a too dense protective grill, then at large amplitudes air turbulences may appear, which will be clearly audible.
If a bass-reflex enclosure is used, the port itself is another potential source. Especially if it has a too small section or sharp edges.
Reason Four: Incorrect amplifier filter settings
It is very important in the subwoofer channel to correctly limit the frequency range from above. You can choose the cutoff of the low-pass filter only empirically, starting, again, from the potential of the front acoustics. In the simplest case, such a possibility is usually found in a subwoofer amplifier, for more complex systems with processors, you can choose not only the cutoff frequency, but also, for example, the steepness of the filter, and sometimes even its quality factor. In top-level custom systems, such processor capabilities are in demand. Naturally, if the tuner has sufficient experience and has an idea of what exactly he is tuning.
Digital processors provide almost unlimited possibilities for customizing the audio system. Configuration, as a rule, is carried out from a computer through special software. Unlike home systems, in cars, the low-pass frequency in the subwoofer channel usually lies in the range of 50-100 Hz. As for the slope of the filter, it is generally accepted that the higher it is, the better, but I would argue with this statement. Customization is a creative and purely individual matter, template approach does not always bring the desired result.
It is important to understand that it is necessary to match the subwoofer with speaker systems not only in terms of their frequency response, but also in phase. Many specialized subwoofer amplifiers have so-called "phase shifters" for this. It's easier if you have a system with a digital processor, where you can operate with delays, as a rule, by virtually pushing the front channels away with them.
If you have already tried everything, but the subwoofer still sounds separate from everything else and is localized in the back, just flip the "+" and "-" on the speaker. In other words, reverse the phase and try the setting again.
Finishing this material, I would like to note the following. When making any decision - whether it's a simple upgrade of a stock system or building a complex custom system on top components, always keep in mind what exactly you want to achieve. Car audio is a means to increase the comfort of your personal space, specifically your car. The sound should be accurate, precise and, most importantly, enjoyable.
