Inflammatory response and injury – Certain genes control the aggressiveness of the immune system and may lead to a higher risk of injury.
During excessive exercise, the tissues are slightly damaged in many places. The immune system normally recognizes this as a normal process and there is no inflammation or swelling. Certain genes control the aggressiveness of the immune system. In case of errors, there is a problem and a strong inflammatory reaction.
COL1A1 and COL5A1 are the genetic codes for the proteins that make up collagen fibers, the basic building blocks of tendons, ligaments and skin. Collagen is actually the human body’s glue that keeps connective tissue in the right shape. Variations in collagen genes influence both flexibility and an individual’s risk of connective tissue injury (such as Achilles tendon rupture).
The only thing we can say about athletes with a certain genetic profile is that they are at a higher risk of injury based on our current knowledge. You can modify any workouts you’re currently doing to minimize the risk, or you can do “pre-rehab” workouts to strengthen the risk area.
Oxidative stress and sports
Athletes produce far more free radicals (which can damage tissue) because they consume more energy during intensive exercise. These molecules affect your health and athletic performance so negatively. Your body has certain genes that can recognize and neutralize these molecules. Many people have genetic variations in these genes that interfere with function and protection.
Certain micronutrients – antioxidants – can compensate for the lack of protection (if they are at the right dose). It is therefore possible to test the appropriate genes and compensate for any genetic weaknesses with the right dose of micronutrients, regardless of the result. Results include oxidative stress in cells, recommended dose and substance of antioxidants, etc.
Perception of pain in sport
Genes affect how we perceive pain. Tolerating and managing pain is essential for most elite athletes. Some people’s bodies sort of “slack off” and no longer let them perform at their best. Due to genetic differences between individuals, none of us can truly recognize another person’s physical pain. COMT – is the most commonly studied gene as a participant in pain relief. It is part of the metabolism of neurotransmitters in the brain, including dopamine. The enzyme catechol-O-methyltransferase (COMT) can deactivate various substances (adrenaline, noradrenaline, dopamine, estrogen) and direct them towards degradation. Additionally, COMT can block the effect of various drugs.
Two common versions of COMT depend on whether a particular part of the DNA sequence of this gene codes for the amino acid valine or methionine. Based on cognitive testing and brain imaging studies, it was found that people with two versions of methionine tended to perform better and consume less metabolic effort in cognitive and memory tasks, but were simultaneously more sensitive to anxiety and more sensitive to pain. Carriers of two Valin are somewhat less successful at cognitive tasks that require rapid mental elasticity, but they may be more resistant to stress and pain.
In acute stressful situations, the brain blocks out pain (stress-induced analgesia) to fight or flight without having to think about a broken bone. The system for blocking pain in extreme situations has developed in the genes and also manifests itself in sports. A sports match can trigger a “flight or fight” mechanism. When you engage in a battle you care about, you activate this system. An athlete’s ability to cope with pain is a complex combination of innate and learned.
The role of genes in head trauma
The APOE (Apolipoprotein E) gene plays a central role in human metabolism. Comes in three common variants called E2, E3 and E4. E4 is associated with an increased risk of heart disease and Alzheimer’s disease. The significance of this gene also determines the ability to recover from brain injury. For example, ApoE4 carriers who suffer head injuries in traffic accidents are in a coma longer, suffer more bleeding and bruising, have more frequent seizures after injury, have less success in rehabilitation and are more likely to suffer permanent consequences or die.
The ApoE gene is involved in inflammation of the brain following trauma, and in people with the ApoE4 variant, it takes longer. Several studies have shown that athletes with the ApoE4 variant who sustain a blow to the head take longer to recover and are at risk of developing dementia later in life. You can’t stop athletes from playing sports, but you can at least help them by watching them closely. ApoE4 probably does not increase the risk of concussion, but it may affect recovery.
Genes and sudden death in sport
Nitric oxide synthase 1 (NOS1AP) adapter protein is an adapter protein and allows interaction with other molecules. Its variants are associated with a prolonged QT interval on the ECG and an increased risk of sudden cardiac death. The following risk factors contribute to the development of QT interval prolongation in the ECG and arrhythmias: congenital predisposition to QT interval prolongation, simultaneous administration of multiple QT interval-prolonging drugs, hypokalemia and other electrolyte and acid-base disorders, organic heart disease and certain other factors. The QT interval is hereditary to some degree, and women are more at risk than men of prolonging the QT interval.
People with left ventricular hypertrophy, heart failure, impaired internal environment, and other factors are at higher risk for QT interval prolongation. It seems that one of the most common causes of QT interval prolongation is taking medication. Examples of drugs that prolong the QT interval: ZOFRAN (ondansetron), TENSAMIN (dopamine), ADRENALIN (epinephrine), KLACID (clarithromycin), SUMAMED (azithromycin), NIZORAL (ketocenazole), SEREVENT, SERETIDE (salmeterol), PROTAZIN (promethazine ) . When two or more drugs are administered that can individually prolong the QT interval, side effects in the form of QT interval prolongation are added
Sometimes it is enough to receive one of the drugs that can prolong the QT interval while another substance is administered which, although it does not itself prolong the QT interval, increases the plasma concentrations of the first drug, potentiating its side effects, including prolongation of the QT interval. The other substance may not even be a drug, like grapefruit juice.