We are less aware that lifetime health problems you may have or occur in future due to your genes and your strengths which you are gifted by your parents.Avastu Genetics help you to recognise them and also help you to cure your genetic health problems through counselling, diet and nutrition’s. It is a onetime Investment Program includes 105 Phenotypes tests which will guide to identify your Generic Strength and protect you from your Genetics Problem throughout your life.
ACTN3, the gene encoding for the synthesis of α-actinin-3 in skeletal muscle fibres, is the first structural skeletal-muscle gene associated with athletic performance α-actinin-3 is specifically expressed in fast-twitch my fibres responsible for generating force at high velocity.
It has been discovered for the first time a significant association between the ACTN3 genotype and athletic performance, reporting that the RR genotype was overrepresented in the elite sprint/power athletes. Since that time, the ACTN3 RR genotype has been correlated with elite sprint/power athletic performance in several replication studies. These findings suggest that ACTN3 RR genotype is associated with power performance in comparison with XX genotype, which might be postulated to contribute to endurance performance.
Certain gene variations or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). The release of IL6 has both pro and anti -inflammatory impacts and is an essential component for muscle repair, may contributes to hypertrophy, and could be involved in glucose and lipid metabolism.
Ankle injuries, including sprains, strains and other joint derangements and instability, are common, especially for athletes involved in indoor court or jumping sports.
Genetics plays an integral role in athletic performance and is increasingly becoming recognized as an important risk factor for injury. Ankle and knee injuries are the most common injuries sustained by soccer players. Often these injuries result in players missing training and matches, which can incur significant costs to clubs.
Four genes were assessed in relation to injury. Genotypes found to be associated with injury included the TT (nucleobase) genotype of the GDF5 gene, TT and CT (nucleobase) genotypes of AMPD1 gene, TT genotype of COL5A1 and GG (nucleobase) genotype of IGF2 gene. These genes were also associated with a decrease in the number of matches played.
Epidemiological studies have shown that regular physical activity improves health. The molecular mechanisms behind the beneficial effects have however not been completely elucidated. A number of factors such as individual genetic variability, different exercise protocols, the heterogeneous nature of exercise itself, and other lifestyle factors influence the effects observed. Furthermore, exercise exerts a number of effects on the body such as improving insulin sensitivity and lipid profile in addition to lowering blood pressure. All these factors influence each other making it hard to understand the complex interactions.
Exercise causes damage to the muscle resulting in disarrangement in fibre structures, loss of fibre integrity, and leakage of muscle protein. Trying to restore homeostasis, several repair processes starts, involving inflammation, resolution, muscle repair, and finally regeneration. The balance between pro- and anti-inflammatory cytokines and other signalling molecules seems to be important for the outcome of the repair and regenerating process.
Cardio-respiratory endurance is a key element of health and fitness. In sports, it is reflected in the ability to sustain exercise over an extended period of time. How well the body can take up oxygen, clear lactate, and move efficiently, determines your level of cardio-respiratory endurance, and these factors are largely influenced by age, physical training and genetics.
A large proportion of your ability to improve VO2max in response to training is influenced by your DNA. In fact, genetics can account for as much as 47% of the inter-individual variance in training responses10. Fitness Genes test for several genes that influence the trainability of your VO2max - the ACE, PGC1A, CKM, AMPD1, AKT1, HIF1A, VEGF and ADRB2 genes.
These genes impact cardio-respiratory endurance either via regulation and adaptation of the cardiovascular system, lactate clearance, mitochondrial function and many other biological processes. The Fitness Genes reports explains these processes in further detail, and identifies how your genetic variation relates to your VO2max and overall aerobic potential.
Important parameters that are closely related to the VO2max but give slightly more functional information for performance are:
1) Aerobic threshold – This occurs at an effort of around 60% of your aerobic capacity or around 80% of your lactate threshold, thus at a relatively low level of intensity that you can maintain for hours. It is measured by the point where lactate just begins to accumulate above the resting level.
2) Anaerobic threshold - This is the point where the amount of carbon dioxide exhaled becomes unaligned with the amount of oxygen consumed, indicating your body is starting to depend more on production of energy by the anaerobic system (glycolysis) than on the aerobic fat burning system (oxidative phosphorylation in the mitochondria). Well trained athletes can maintain performance at this level for approximately 1 hour.
3) Lactate threshold – This is often confused with the anaerobic threshold, but this is the point where the body can no longer clear lactate and thus lactate levels rapidly accumulate. Exercising at the lactate threshold can be maintained for a maximum of 1 hour.
Numerous biochemical and physiologic mechanisms are implicated in exercise training-induced improvements in insulin sensitivity; these include increased glucose transport via glucose transporter type 4 (GLUT4) genes and protein expression (25), improved mitochondrial function (23), and improved skeletal muscle lipid.
Recent studies provide further evidence to support the notion that regular physical activity (PA) reduces the risk of insulin resistance, metabolic syndrome and type 2 diabetes, and Insulin sensitivity (SI) improves when individuals comply with exercise and/or PA guidelines. Many studies indicate a dose response, with higher energy expenditures and higher exercise intensities, including high intensity interval training (HIIT), producing greater benefits on whole-body SI, although these findings are not unanimous. Aerobic exercise interventions can improve SI without an associated increase in cardio-respiratory fitness as measured by maximal or peak oxygen consumption. Both aerobic and resistance exercise can induce improvements in glycemic regulation, with some suggestions that exercise regimens including both may be more efficacious than either exercise mode alone.
At rest only about 20% of our total circulating blood is directed to skeletal muscle.
Over 60% of blood flow at rest is directed to the liver, kidneys and brain. This is illustrated on the adjacent graph.
As exercise commences and cardiac output increases, blood flow is shunted from the organs of the body to the working muscles.
Blood flow to the lungs also increases due to the increased activity of the right ventricle which pumps blood to the lungs.
Up to 87% of circulating blood can go to working muscles during prolonged vigorous exercise! Systolic blood pressure increases linearly with increases in exercise intensity. As a greater quantity of blood gets pumped from the heart the pressure rises in the blood vessels that transport the blood with each heart beat. In a healthy person with a ‘normal’ systolic pressure of 120 mmHg, vigorous aerobic fitness training can increase systolic pressure to 180 mmHg and take 10-20 minutes to return to resting levels.
The higher the intensity of exercise, the greater the rise in heart rate will be, and consequently the larger the increase in systolic blood pressure.
Frequent and regular physical activity has significant benefits for health, including improvement of body composition and help in weight control. Consequently, promoting training programs, particularly in those who are genetically predisposed, is a significant step towards controlling the presently increasing epidemic of obesity. Although the physiological responses of the human body to exercise are quite well described, the genetic background of these reactions still remains mostly unknown
The process of exercise-induced adaptation in the human body involves a number of signalling mechanisms, initiating replication of specific DNA sequences, enabling their subsequent translation, and finally generating new proteins. The physiological effects of these adaptations are determined by the volume, intensity and frequency of physical activity.
Osteoporosis is a common disease with a strong genetic component characterized by low bone mass, micro architectural deterioration of bone tissue and an increased risk of fracture. Studies have shown that genetic factors play an important role in regulating bone mineral density and other determinants of osteoporotic fracture risk, such as ultrasound properties of bone, skeletal geometry and bone turnover. Osteoporosis is a polygenic disorder, determined by the effects of several genes, each with relatively modest effects on bone mass and other determinants of fracture risk. It is only on rare occasions that osteoporosis occurs as the result of mutations in a single gene. Linkage studies in man and experimental animals have defined multiple loci which regulate bone mass but the genes responsible for these effects remain to be defined. Population-based studies and case-control studies have similarly identified polymorphisms in several candidate genes that have been associated with bone mass or osteoporotic fracture, including the vitamin D receptor, oestrogen receptor and collagen type IalphaI gene. The individual contribution of these genes to the pathogenesis of osteoporosis is small however, reflected by the fact that the relationship between individual candidate genes and osteoporosis has been inconsistent in different studies. An important aim of future work will be to define how the genes which regulate bone mass, bone turnover and other aspects of bone metabolism interact with each other and with environmental variables to cause osteoporosis in individual patients. If that aim can be achieved then there is every prospect that preventative therapy could be targeted to those at greatest risk of the osteoporosis, before fractures have occurred.
The following are factors that will increase the risk of developing osteoporosis:
• Female gender.
• Caucasian or Asian race.
• Thin and small body frame.
• Family history of osteoporosis (for example, having a mother with an osteoporotic hip fracture doubles your risk of hip fracture).
• Personal history of fracture as an adult.
• Cigarette smoking.
• Excessive alcohol consumption.
• Lack of exercise.
• Diet low in calcium.
• Poor nutrition and poor general health, especially associated with chronic inflammation or bowel disease.
• Malabsorption (nutrients are not properly absorbed from the gastrointestinal system) from bowel diseases, such as celiac sprue that can be associated with skin diseases, such as dermatitis herpetiformis.
• Low estrogen levels in women (which may occur in menopause or with early surgical removal of both ovaries).
• Low testosterone levels in men (hypogonadism).
• Chemotherapy that can cause early menopause due to its toxic effects on the ovaries.
• Amenorrhea (loss of the menstrual period) in young women is associated with low estrogen and osteoporosis; amenorrhea can occur in women who undergo extremely vigorous exercise training and in women with very low body fat (for example, women with anorexia nervosa).
• Chronic inflammation, due to chronic inflammatory arthritis or diseases, such as rheumatoid arthritis or liver diseases.
• Immobility, such as after a stroke, or from any condition that interferes with walking.
• Hyperthyroidism, a condition wherein too much thyroid hormone is produced by the thyroid gland (as in Grave's disease) or is ingested as thyroid hormone medication.
• Hyperparathyroidism is a disease wherein there is excessive parathyroid hormone production by the parathyroid gland, a small gland located near or within the thyroid gland. Normally, parathyroid hormone maintains blood calcium levels by, in part, removing calcium from the bone. In untreated hyperparathyroidism, excessive parathyroid hormone causes too much calcium to be removed from the bone, which can lead to osteoporosis.
• When vitamin D is lacking, the body cannot absorb adequate amounts of calcium from the diet to prevent osteoporosis. Vitamin D deficiency can result from dietary deficiency, lack of sunlight, or lack of intestinal absorption of the vitamin such as occurs in celiac sprue and primary biliary cirrhosis.
• Certain medications can cause osteoporosis. These medicines include long-term use of heparin (a blood thinner), antiseizure medicine such as phenytoin (Dilantin) and phenobarbital, and long-term use of oral corticosteroids (such as prednisone).
• Inherited disorders of connective tissue, including osteogenesis imperfecta, homocystinuria, osteoporosis-pseudoglioma syndrome and skin diseases, such as Marfan syndrome and Ehlers-Danlos syndrome (These causes of hereditary secondary osteoporosis each are treated differently.)