Injury is a big part of sports and exercise.
The number of athletes injured in the course of training or during competition is staggering.
Over 10 million people are injured in the pursuit of fitness each year with one third of those injured requiring emergency room treatment.
Even passive sports, like bowling, have injured participants.
Injuries are an inherent risk of vigorous exercise.
Elite athletes can prevent or at lest minimize, the damage caused by injuries. Colorful foods and powerful extracts can help athletes stay injury-free.
The incidence of injuries in competitive athletes elite runners, jumpers, ballers as well as the world professional athletes, are higher than the incidence among noncompetitive performers.
Weekend warriors and recreational athletes have less incidence and this suggests that overuse increases stress on muscles and bones and causes fractures and tendonitis in joints.
Elite and professional athletes, despite world-class conditioning and training programs, have a higher incidence of sports related injuries.
Although each sport has different patterns of injuries, the type of movement executed in the sport determines the most injured body part.
For example, the ankle is the most often-injured body part in basketball, the fingers and hands in baseball, the legs in soccer, the back in golf while the face including the mouth, eyes, and ears are the most injured in cycling.
Overuse injuries are limited to specific sports (shin splints, tennis elbow, or jumper’s knee).
Exercise can cause two types of injuries. They can be of either of acute (traumatic) origin or of chronic overuse, in which small, repetitive, forces, are applied to the structural or contractile components of the body.
Injuries occur in almost any part of the musculoskeletal system. Bone, muscle, skin, cartilage, joints, ligaments, tendons, and spinal disks are all subject to wear, tear, strain, sprains, rupture or fracture.
The two most common traumatic injuries are sprains to ligaments and joints, and strains on muscles. Ligaments are bands of fibrous connective tissue that connects bones and cartilage.
The recovery time for injuries depends on many factors strarting with the severity of the injury. In addition, the inflammatory response that follows, amount of rest, nutritional fitness and blood supply to the affected area, all contribute to recovery time.
Blood supply is essential to healing because it delivers the nutrients, oxygen and inflammatory cells to the site of injury. In general, the greater the blood supply, the faster the body heals. For example, injuries to thw skin of the face heal within a 2 or 3 days, those to the arms and legs require 10 days to heal, while injuries to joints may never heal. The differences in recovery time are due to the excellent blood supply to the skin of the face and lack of a supply to joints.
The supply of blood to the skin regulates core body temperature and protects the musculoskeleatal system. The epidermis has a rich network of capillaries and is capable of receiving a great deal of blood. Injuries to the skin heal quickly. Muscles Muscle is a highly vascularized tissue. When ecercising, muscle requires oxygen and glucose in greater amounts than which upon straining causes capillaries to burst with the release of their contents. Black and blue marks (ecchymosis) are the result of capillary damage. Muscle strains typically heal in three weeks.
Despite a diminished blood supply, the strength of bones is dependent on the nutrition that it receives while growing. In addition, the forces that are transmitted to bone, such as those that are produced with intense exercise, causes bones to become stronger and requires an increase in calcium in the diet. This is particularly true for child athletes. Minimal Blood Delivery Ligaments and tendons. Ligaments and tendons are composed of collagen, a fibrous type of connective tissue with very few cells and a poor blood supply. Due to its lack of capillary support, collagen usually requires at least six weeks to properly heal.
Interverterbral disks are composed of an inner semifluid material (nucleus pulposus) and a strong outer ring of cartilage (annulus fibrosus). Injuries to the disks in the lower back and neck have a very poor blood supply and therefore require three months or more to heal.
Joints lack a blood supply of their own and depend upon collateral circulation for nutritional support. For example, the damaged cartilage of the knee or a torn meniscus of the knee can never fully heal. The knee due to its poor blood supply requires preventive action in the form of strengthening the ligaments around it and muscle supporting it. Nutritional factors can also help an athlete help resist injury.
Muscle injuries or strains are commonly referred to as “muscle pulls” and result from stretching or tearing of muscle. Strains usually result from a lack of coordination of muscle groups and from the excessive stretching of muscle fibers that occurs when athletes fail to sufficiently warm up. Strains occur in many different parts of the muscle. The most common sites include the body of the muscle, the junction of muscle to tendon and the tendon as it inserts on the bone.
Strains are classified by the severity of the strain.
Grade I strain produces a sensation of muscle tightness. Mild strains result from stretching a few muscle fibers with minimal tearing. Less than 10% of the fibers are damaged in Grade I strains.
Grade II strain is a more severe injury with partial tearing of the injured muscle. Fifty percent of a muscle’s fibers may be torn, with a physical defect that is palpated. Accompanying the pain in Grade II muscle strains is loss of function.
Grade III strain is an extensive tear or complete rupture. Between fifty and one hundred per cent of the muscle fibers are affected with a large palpable depression felt in the muscle unit. Grade III strains cause marked muscle disruption, severe pain and may require surgical intervention.
The hamstring, quadriceps and calf muscles frequently incur injuries. Moderate strains may take three weeks to several months to heal and often recur. Due to the inelastic scar tissue that forms at the site of strains, flexibility is hindered.
Proper rehabilitation must therefore restore the injured muscle’s flexibility as well as strength, before returning to the previous level of activity.
The extent or severity of an injury is dependent on the force generated within the muscle. A strain is usually related to sudden changes of tension in the muscle, not the amount of force applied. Five factors predispose an athlete to injury.
1. A previously injured muscle that has not completely healed.
2. A muscle that has healed using too much immature scar tissue.
3. Improper warming up and stretching techniques.
5. Cooling off followed by exertion without warming up. Inflammation is the response by the body to injury. The goal of treatment to an exercise related injury is to decrease pain, limit the swelling of the affected area and repress the inflammation responsible for the swelling. In acute injuries, a combination of Rest, Ice, Compression and Elevation (RICE) is recommended.
This program recommends a protocol that includes botanical antioxidants and natural anti-inflammatory agents to reduce the severity of injuries by limiting inflammation. Despite their use and advocacy by athlete’s medical teams, the use of steroids and non-steroidal painkillers to repress inflammation is not recommended. They are frequently prescribed to counter the chronic effects of degeneration emanating from the physical stress placed on joints. The anti-inflammatory agents recommended in this book are theorized to inhibit the excessive inflammatory response that occurs after injury and thereby minimize the damage to athletes.
The molecular mechanism that produces the earliest alteration in cell structures and function are initiated by free radicals.
Free radicals are very unstable and reactive compounds. Free radicals, reactive oxygen metabolites or reactive oxygen species are interchangeable terms that denote an unstable compound. This compound possesses an unpaired single electron in its outer orbit. This unpaired electron searches for an electronic partner in order to gain stability.
Free radicals attack other stable molecules to fill its need. The target is often a membrane-bound lipid. One electron from the lipid is thus transferred from the outer shell of a stable lipid producing a new unstable or oxidized one. This leads to the formation of altered receptors or oxidized lipoproteins. The original free radical is thus removed as an active radical but creates a new reactive species with an unpaired electron in its outer shell.The original free radical initiates a chain reaction that oxidizes target molecules and renders these compounds functionally altered.
The oxidative attack by free radicals produce structurally altered compounds. The accumulation of these altered compounds leads to a pattern of changes that is recognized as disease. In its ground state, the O2 molecule is very stable and does not react with organic substrates. During the functioning of various intracellular enzyme systems, activated O2 metabolites are formed. These metabolites further interact with each other forming hydroxyl radicals (OH-). Hydroxyl radicals have a high affinity for membrane lipids and thus cause the formation of highly unstable lipid peroxidation products.
More free radicals are produced as a result of exercise compared to an inactive or sedentary state. Lipid peroxidation is the universal mechanism of membrane damage. The damage modifies the permeability and alters the barrier, catalytic, and receptor functions in the affected membranes. Intense muscle activity is accompanied by oxidative stress in many body tissues. The amount of stress is proportional to the amount of free radical activity and the ability of antioxidant systems to cope with it.
Optimal physical performance is dependent upon optimum cellular function. Optimum performance always subjects cellular metabolism to the maximum limits of stress.
The regulation of lipid peroxidation in the body is by three main enzyme systems:
1. Superoxide dismutase
3. Glutathione peroxidase.
During high levels of exercise, oxygen consumption and its utilization dramatically increases. The resulting increased mitochondria activity produces more free radicals. Additionally, as blood flow is shunted away from many organs to supply working muscle, areas of hypoxia (oxygen deprivation) develop. After exercise, when these regions are re-oxygenated, a burst of free-radical production occurs and further membrane damage occurs.
This program anticipates the increase in free radical formation and recommends a diet of colorful carbohydrates and botanical supplements to meet that challenge. Since free radicals are the initiators of this biologic damage. Their neutralization prevents the accumulation of altered cell compounds.
Altered cell compounds become foci of inflammatory and immunological attack producing disease. Skeletal Muscle and Injury From Free Radical Attack Skeletal muscle contains a network of vesicles, tubules and cisterns that surround the myofibrils, a group of sarcomeres containing the contractile proteins actin and myosin. This network or sarcoplasmic reticulum transforms the nerve signal sent to the muscle into a response by the muscle’s contractile proteins. This function is accomplished by an alteration of calcium concentrations in the intracellular fluid.
A rise in calcium ion concentration causes muscle to contract, whereas a decrease allows muscle to relax. The sarcoplasmic reticulum membrane contains enzyme systems responsible for the transport of calcium.
Calcium dependent ATPase actively pumps calcium into the sarcoplasmic reticulum. The sarcoplasmic reticulum membrane is rich in phospholipids, which become the substrates for lipid peroxidation attack by free radicals. The resulting damaged membrane, inhibits calcium transport and increases its permeability to calcium thereby inducing muscle spasms. The formation of peroxide clusters within the membrane allows for the excessive accumulation of calcium ions within the sarcoplasm (cytoplasm of muscle). This prevents the sarcoplasmic reticulum from lowering calcium concentrations required for the relaxation of the muscle. This damages muscle and initates inflammation.