Hey everyone, have been really busy over the past week, so haven't spent much time through the forum. My brother in law, that is a plastic surgeon, and I discovered some pretty important info, on the exact healing process, of soft muscle tissue. Which as we all know, is in the penis. Now the recovery time regimens will vary, depending on your routine, and some of the information is intended for sports injuries.
However, there is plenty of info on just how the human body heals tissue, and how you can nurture the healing process. Depding on the amount of time you p.e throughout the week. But this should help out with understanding how to simplify, and hone in on the healing stages, and what needs to be done during these stages. Enjoy fellas, let me know if it was helpful. Hope everyone is doing well with the gains... SOFT TISSUE DAMAGE AND HEALING: THEORY AND TECHNIQUES
A. Mechanisms of Injury
B.
Many factors produce mechanical injuries or trauma in sports. Soft tissue damage occurs through direct or indirect trauma to muscles, ligaments, and joint capsules. Usually, direct trauma refers to an injury occurring from blunt trauma or a sudden overload, and is known as macro trauma, i.e., true muscle tear or ligament sprain. In contrast, indirect trauma results from repeated submaximal loading, leading to clinical signs and symptoms. Injury presents itself in three stages: acute, subacute/overuse, and acute/chronic.
The first, or acute, stage of direct trauma stems from sudden overloading, or macrotrauma (e.g. a 100 meter runner exploding out of the starting blocks). The subacute/overuse stage occurs when increased loads degenerate body tissues due to excessive cumulative loading, leading to micro trauma and an accompanying inflammatory response (e.g. Achilles tendinitis in the endurance athlete or runner, Figure 9-1). The last type, acute/chronic stage, integrates both cumulative loading and sudden overloading (e.g. chronic Achilles tendinitis that ruptures in a long jumper). Chronic tendinitis is a degenerative condition without inflammation. Macrotrauma Impact–Contact!
· Microtrauma
· Overuse–Cyclic Loading–Friction
· Structural Tissue Overload
· Mechanical Strain/Stress
· Specific
· Physiological
· Adaptation to
· Imposed Demand
· “Training Effect”
· Abusive Load
· without
· Major Structural
· Vascular Disruption
· Initial Cell-Matrix
· Stress Response
· Potentially Reversible
· Microtrauma
· Pain (?)
· Abusive Load with Major Structural
· and Vascular Disruption
· Spontaneous
· Resolution of
· Symptoms
· Degenerative
· Change
· Classical Inflammatory Reaction
· Irreversible Tissue Damage
· Cell Necrosis
· Optimal Load Continued Abusive Load
· Chronic Degenerative
· Response
· Regeneration
· Response
· Fibrotic
· Response
· Cell Atrophy
· Optimal
· Load
·
Figure 9-1. Schema demonstrating theoretical pathways of sports-induced tissue damagens! Whether muscle injury is caused by direct or indirect trauma, the end result is tissue dysfunction characterised by pain, inflammation, and altered internal tissue stress. The injury often results in functional disability, whereby an athlete may be able to carry on daily living routines, but is limited in his or her capacity to train and compete.
Any activity loads and deforms tissue, an effect known as a stress/strain, and described through a load and tissue elongation curve. As connective tissue is deformed it either stretches or tears, depending on the magnitude, rate, and intensity at which the loading occurs. Collagen deforms under low loading and fails at high loads. When the load is removed from normal tissue during the elastic phase, the material returns to its pre-stretch length. Injury occurs when the tissue is stretched into the plastic phase, causing tissue failure.
Of all the tissues involved, tendon is the least elastic. The most frequent site of injury in muscle strains is the myotendinal junction, because of increased collagen content at the transition zone of muscle sheath to tendon. This area has decreased local extensibility, as does scar tissue, and is frequently termed a stress riser. This transition in biologic tissues, which also appears at the tendoperiostial junction, is a point that is more susceptible to stress and injury. The relatively new term “tendinopathy” has been adopted as a general clinical descriptor of tendon injuries in sports. In overuse clinical conditions in
and around tendons, frank inflammation is infrequent and if seen, is associated mostly with tendon ruptures. Tendinosis implies tendon degeneration without clinical or histological signs of intratendinous inflammation, and is not necessarily symptomatic.
The term “tendonitis” is used in a clinical context and does not refer to specific histopathological entity. Tendonitis is commonly used for conditions that are truly tendinosis, however, and leads athletes and coaches to underestimate the proven chronicity of the condition. Paratendonitis is characterised by acute edema and hyperemia of the paratendon with infiltration and inflammatory cells, and possibly the production of a fibrinous exsudate with the tendon sheath causing a typical crepitus, which can be felt on clinical examination.
The term “partial tear of the tendon” should be used to describe the macroscopically evident partial tear of a tendon. This is an uncommon acute lesion. Most articles describing the surgical management of partial tears of a given tendon in reality deal with degenerative tendinopathies. The combination of pain, swelling, and impaired performance should be labeled tendinopathy. According to the tissues affected, the terms tendinopathy, paratendinopathy, or pantendinopathy (from both the tendon and the surrounding tissues involved) should be used Examination for injury in soft tissues such as muscle involves initial palpation with minimal force or compression (in the case of acute injuries), and progresses to firmer compression or higher loads if increased density has not been distinguished or pain has not been provoked at the site of the suspected lesion (see Table 9-1 for examination steps).
One can also have the athlete contract the muscle to increase the tension or passively stretch the myotendinal unit while palpating the area. The pain associated with palpation is secondary to the stimulation of free nerve endings with inflammation, decreased extensibility of tissue, or tissue insufficiency. While palpating muscle tissue, one should search carefully through various layers of tissue to find remnants of injuries and healing. Subtle tissue texture abnormalities may exist, and might be missed if the tissue were examined erratically. These abnormalities must be considered in formulating an assessment. However, the clinician must avoid going too deep or hard with palpation, using pain as a guideline.
The clinician needs to apply pressure and to sense the reactivity of the tissue. Since scar tissue heals three dimensionally, it does not fall into place like a brick. Instead, scar tissue reaches in the direction of the fascia and the neighbouring muscle sheaths, binding these tissues together. For example, when a runner strains a hamstring, the sheath tear heals and binds to neighbouring muscle sheath. The hamstring muscle group still functions to flex the knee, yet the athlete complains of dull ache or pain in
the posterior thigh. The reason may be that independent movement has been lost and the area of scar tissue has limited the extensibility of the myotendinal unit. Muscles do function and limbs do move, but the normal gliding that occurs between neighboring tissues is lost. As a result, there is a constant low-grade inflammatory process at the site of the decreased mobility. Scar tissue has a poor blood supply and is not as strong or resilient as the primary tissue it replaces. This area will likely be a site of re-injury
secondary to the transition zone of normal tissue to scar tissue.
Table 9-1. Examination of soft tissue injury.
1. History
• onset
• pain location
• mechanism of injury
• prior treatment and rehabilitation
• goals of athlete
2. Physical exam
• inspection
• AROM/PROM
• palpation
• neurological; myotome, dermatome, peripheral nerve tests,
deep tendon reflexes
• strength and motor control
• special tests
• functional exam
• gait analysis
3. Assessment
4. Treatment goals
5. Treatment plan
6. Treatment procedures
3. Stage 2: Regeneration and Repair—The Fibro-Elastic/Collagen-Forming Phase The second stage of an athletic injury is called the repair or fibroblastic phase. This phase lasts from 48 hours up to 6 weeks. During this time structures are rebuilt and regeneration occurs. Fibroblasts begin to synthesise scar tissue. The nature of the functional losses will determine the selection of therapeutic modalities and
exercises needed for this phase.
This is a risky period because the absence of pain may tempt the athlete (or the coach) to return to training and competition before the injured tissues are fully rehabilitated. 4. Management and Rehabilitation of Stage 2The rehabilitation goals in the second phase are to: 1) allow normal healing (similar to the first phase); 2) maintain function of uninjured parts; 3) minimise deconditioning of the athlete; 4) increase joint range of motion or flexibility; 5) improve muscle strength, local muscular endurance, and power; 6) increase aerobic capacity and power; and 7) improve proprioception, balance, and coordination.
These goals can be achieved by physical therapy and therapeutic exercise. stretching or flexibility exercises. Restoring flexibility should be a priority because later strength and aerobic conditioning may depend on first achieving full joint range of motion. As mentioned previously, stretching is more effective when tissues are warmed beforehand, which may require assistance from a therapist. A thorough stretching routine including all major parts of the body should be completed daily. Muscle strength can be developed using different types of muscle actions and equipment.
Muscle actions can be classified as static (isometric) or dynamic (isotonic and isokinetic). Both have been shown to induce adaptations in skeletal muscle function and can be useful in different clinical situations. Dynamic muscle actions can be further divided into concentric and eccentric groups, both useful for conditioning. Recent evidence suggests that eccentric actions may be more effective, but must be used with caution due to the common effect of muscle soreness.
Methods or equipment used for strength conditioning include maximal voluntary contractions at different joint angles with no joint movement (static training), electrical stimulation during voluntary contractions (see Part 3 of this chapter, Therapeutic Modalities), gravity, resistance of the therapist, free weights, “isotonic” equipment such as pulleys and benches, surgical tubing, isokinetic equipment, and
variable resistance equipment.
Rehabilitation strength conditioning requires a prescribed training plan outlining the type, intensity, duration, and frequency of exercise. Appropriate action and equipment depends on the clinical condition of the athlete (for example, if there is joint swelling, use static exercises with electrical stimulation). To induce significant gains in strength, exercise intensity should be above 60–80% of the one repetition maximum of the athlete. Usually, three sets of 8–10 repetitions are performed with each repetition including concentric and eccentric muscle actions. Free weight and machine weight lifting contain both concentric and eccentric muscle contractions.
Each muscle group is usually trained three times per week. Early strength gains are due to neurological factors, while muscle hypertrophy occurs only after several weeks of training. Restoration of optimal strength may require 3–6 months while maintenance training at a lower frequency (twice per week) should be a permanent component of the programme (see Stage 3: Remodelling Phase, below). Local muscular endurance can be developed using exercises and equipment similar to those used to develop strength. The classical approach to developing tolerance to fatigue is to use lighter loads (less than 60% of the athlete’s one repetition maximum) and higher repetitions (20 or more). Actually, strength conditioning contributes to muscular endurance. A stronger athlete can tolerate a higher absolute load for a longer period of time since that load represents a smaller percentage of his/her maximum strength. The relevance of local muscular endurance training depends on the particular demands of the event.
It is more important to the sprinter and middle-distance runner than the long-distance runner or discus thrower. Aerobic conditioning should be part of the rehabilitation program for all athletes at this stage. Cycling (stationary), swimming, and rowing improve aerobic capacity and promote recovery of full joint range of motion. The exercise
However, there is plenty of info on just how the human body heals tissue, and how you can nurture the healing process. Depding on the amount of time you p.e throughout the week. But this should help out with understanding how to simplify, and hone in on the healing stages, and what needs to be done during these stages. Enjoy fellas, let me know if it was helpful. Hope everyone is doing well with the gains... SOFT TISSUE DAMAGE AND HEALING: THEORY AND TECHNIQUES
A. Mechanisms of Injury
B.
Many factors produce mechanical injuries or trauma in sports. Soft tissue damage occurs through direct or indirect trauma to muscles, ligaments, and joint capsules. Usually, direct trauma refers to an injury occurring from blunt trauma or a sudden overload, and is known as macro trauma, i.e., true muscle tear or ligament sprain. In contrast, indirect trauma results from repeated submaximal loading, leading to clinical signs and symptoms. Injury presents itself in three stages: acute, subacute/overuse, and acute/chronic.
The first, or acute, stage of direct trauma stems from sudden overloading, or macrotrauma (e.g. a 100 meter runner exploding out of the starting blocks). The subacute/overuse stage occurs when increased loads degenerate body tissues due to excessive cumulative loading, leading to micro trauma and an accompanying inflammatory response (e.g. Achilles tendinitis in the endurance athlete or runner, Figure 9-1). The last type, acute/chronic stage, integrates both cumulative loading and sudden overloading (e.g. chronic Achilles tendinitis that ruptures in a long jumper). Chronic tendinitis is a degenerative condition without inflammation. Macrotrauma Impact–Contact!
· Microtrauma
· Overuse–Cyclic Loading–Friction
· Structural Tissue Overload
· Mechanical Strain/Stress
· Specific
· Physiological
· Adaptation to
· Imposed Demand
· “Training Effect”
· Abusive Load
· without
· Major Structural
· Vascular Disruption
· Initial Cell-Matrix
· Stress Response
· Potentially Reversible
· Microtrauma
· Pain (?)
· Abusive Load with Major Structural
· and Vascular Disruption
· Spontaneous
· Resolution of
· Symptoms
· Degenerative
· Change
· Classical Inflammatory Reaction
· Irreversible Tissue Damage
· Cell Necrosis
· Optimal Load Continued Abusive Load
· Chronic Degenerative
· Response
· Regeneration
· Response
· Fibrotic
· Response
· Cell Atrophy
· Optimal
· Load
·
Figure 9-1. Schema demonstrating theoretical pathways of sports-induced tissue damagens! Whether muscle injury is caused by direct or indirect trauma, the end result is tissue dysfunction characterised by pain, inflammation, and altered internal tissue stress. The injury often results in functional disability, whereby an athlete may be able to carry on daily living routines, but is limited in his or her capacity to train and compete.
Any activity loads and deforms tissue, an effect known as a stress/strain, and described through a load and tissue elongation curve. As connective tissue is deformed it either stretches or tears, depending on the magnitude, rate, and intensity at which the loading occurs. Collagen deforms under low loading and fails at high loads. When the load is removed from normal tissue during the elastic phase, the material returns to its pre-stretch length. Injury occurs when the tissue is stretched into the plastic phase, causing tissue failure.
Of all the tissues involved, tendon is the least elastic. The most frequent site of injury in muscle strains is the myotendinal junction, because of increased collagen content at the transition zone of muscle sheath to tendon. This area has decreased local extensibility, as does scar tissue, and is frequently termed a stress riser. This transition in biologic tissues, which also appears at the tendoperiostial junction, is a point that is more susceptible to stress and injury. The relatively new term “tendinopathy” has been adopted as a general clinical descriptor of tendon injuries in sports. In overuse clinical conditions in
and around tendons, frank inflammation is infrequent and if seen, is associated mostly with tendon ruptures. Tendinosis implies tendon degeneration without clinical or histological signs of intratendinous inflammation, and is not necessarily symptomatic.
The term “tendonitis” is used in a clinical context and does not refer to specific histopathological entity. Tendonitis is commonly used for conditions that are truly tendinosis, however, and leads athletes and coaches to underestimate the proven chronicity of the condition. Paratendonitis is characterised by acute edema and hyperemia of the paratendon with infiltration and inflammatory cells, and possibly the production of a fibrinous exsudate with the tendon sheath causing a typical crepitus, which can be felt on clinical examination.
The term “partial tear of the tendon” should be used to describe the macroscopically evident partial tear of a tendon. This is an uncommon acute lesion. Most articles describing the surgical management of partial tears of a given tendon in reality deal with degenerative tendinopathies. The combination of pain, swelling, and impaired performance should be labeled tendinopathy. According to the tissues affected, the terms tendinopathy, paratendinopathy, or pantendinopathy (from both the tendon and the surrounding tissues involved) should be used Examination for injury in soft tissues such as muscle involves initial palpation with minimal force or compression (in the case of acute injuries), and progresses to firmer compression or higher loads if increased density has not been distinguished or pain has not been provoked at the site of the suspected lesion (see Table 9-1 for examination steps).
One can also have the athlete contract the muscle to increase the tension or passively stretch the myotendinal unit while palpating the area. The pain associated with palpation is secondary to the stimulation of free nerve endings with inflammation, decreased extensibility of tissue, or tissue insufficiency. While palpating muscle tissue, one should search carefully through various layers of tissue to find remnants of injuries and healing. Subtle tissue texture abnormalities may exist, and might be missed if the tissue were examined erratically. These abnormalities must be considered in formulating an assessment. However, the clinician must avoid going too deep or hard with palpation, using pain as a guideline.
The clinician needs to apply pressure and to sense the reactivity of the tissue. Since scar tissue heals three dimensionally, it does not fall into place like a brick. Instead, scar tissue reaches in the direction of the fascia and the neighbouring muscle sheaths, binding these tissues together. For example, when a runner strains a hamstring, the sheath tear heals and binds to neighbouring muscle sheath. The hamstring muscle group still functions to flex the knee, yet the athlete complains of dull ache or pain in
the posterior thigh. The reason may be that independent movement has been lost and the area of scar tissue has limited the extensibility of the myotendinal unit. Muscles do function and limbs do move, but the normal gliding that occurs between neighboring tissues is lost. As a result, there is a constant low-grade inflammatory process at the site of the decreased mobility. Scar tissue has a poor blood supply and is not as strong or resilient as the primary tissue it replaces. This area will likely be a site of re-injury
secondary to the transition zone of normal tissue to scar tissue.
Table 9-1. Examination of soft tissue injury.
1. History
• onset
• pain location
• mechanism of injury
• prior treatment and rehabilitation
• goals of athlete
2. Physical exam
• inspection
• AROM/PROM
• palpation
• neurological; myotome, dermatome, peripheral nerve tests,
deep tendon reflexes
• strength and motor control
• special tests
• functional exam
• gait analysis
3. Assessment
4. Treatment goals
5. Treatment plan
6. Treatment procedures
3. Stage 2: Regeneration and Repair—The Fibro-Elastic/Collagen-Forming Phase The second stage of an athletic injury is called the repair or fibroblastic phase. This phase lasts from 48 hours up to 6 weeks. During this time structures are rebuilt and regeneration occurs. Fibroblasts begin to synthesise scar tissue. The nature of the functional losses will determine the selection of therapeutic modalities and
exercises needed for this phase.
This is a risky period because the absence of pain may tempt the athlete (or the coach) to return to training and competition before the injured tissues are fully rehabilitated. 4. Management and Rehabilitation of Stage 2The rehabilitation goals in the second phase are to: 1) allow normal healing (similar to the first phase); 2) maintain function of uninjured parts; 3) minimise deconditioning of the athlete; 4) increase joint range of motion or flexibility; 5) improve muscle strength, local muscular endurance, and power; 6) increase aerobic capacity and power; and 7) improve proprioception, balance, and coordination.
These goals can be achieved by physical therapy and therapeutic exercise. stretching or flexibility exercises. Restoring flexibility should be a priority because later strength and aerobic conditioning may depend on first achieving full joint range of motion. As mentioned previously, stretching is more effective when tissues are warmed beforehand, which may require assistance from a therapist. A thorough stretching routine including all major parts of the body should be completed daily. Muscle strength can be developed using different types of muscle actions and equipment.
Muscle actions can be classified as static (isometric) or dynamic (isotonic and isokinetic). Both have been shown to induce adaptations in skeletal muscle function and can be useful in different clinical situations. Dynamic muscle actions can be further divided into concentric and eccentric groups, both useful for conditioning. Recent evidence suggests that eccentric actions may be more effective, but must be used with caution due to the common effect of muscle soreness.
Methods or equipment used for strength conditioning include maximal voluntary contractions at different joint angles with no joint movement (static training), electrical stimulation during voluntary contractions (see Part 3 of this chapter, Therapeutic Modalities), gravity, resistance of the therapist, free weights, “isotonic” equipment such as pulleys and benches, surgical tubing, isokinetic equipment, and
variable resistance equipment.
Rehabilitation strength conditioning requires a prescribed training plan outlining the type, intensity, duration, and frequency of exercise. Appropriate action and equipment depends on the clinical condition of the athlete (for example, if there is joint swelling, use static exercises with electrical stimulation). To induce significant gains in strength, exercise intensity should be above 60–80% of the one repetition maximum of the athlete. Usually, three sets of 8–10 repetitions are performed with each repetition including concentric and eccentric muscle actions. Free weight and machine weight lifting contain both concentric and eccentric muscle contractions.
Each muscle group is usually trained three times per week. Early strength gains are due to neurological factors, while muscle hypertrophy occurs only after several weeks of training. Restoration of optimal strength may require 3–6 months while maintenance training at a lower frequency (twice per week) should be a permanent component of the programme (see Stage 3: Remodelling Phase, below). Local muscular endurance can be developed using exercises and equipment similar to those used to develop strength. The classical approach to developing tolerance to fatigue is to use lighter loads (less than 60% of the athlete’s one repetition maximum) and higher repetitions (20 or more). Actually, strength conditioning contributes to muscular endurance. A stronger athlete can tolerate a higher absolute load for a longer period of time since that load represents a smaller percentage of his/her maximum strength. The relevance of local muscular endurance training depends on the particular demands of the event.
It is more important to the sprinter and middle-distance runner than the long-distance runner or discus thrower. Aerobic conditioning should be part of the rehabilitation program for all athletes at this stage. Cycling (stationary), swimming, and rowing improve aerobic capacity and promote recovery of full joint range of motion. The exercise
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