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Your joints and muscles have a certain range of motion that the body allows. Flexibility is the ability of the body to move freely through this allowed range. Flexibility is also known as limberness. The parts engaged more while moving are usually more flexible than those that are not put to much use.
Some people are more flexible than others. Genetics play a role in determining how flexible your joints and muscles are. Exercise can also improve a person’s flexibility to a certain extent.
Dynamic flexibility - The ability to move joints to the maximum of their allowed range of motion (e.g., bending down to pick up an item or stretching to take something from a higher shelf).
Static flexibility - The ability to maintain a position for a longer time without any external support (e.g., lifting your leg and keeping it high without holding any support).
When you have higher flexibility, your body can handle physical stress much better. Hence, when you are exercising or doing a strenuous physical activity, the chances of getting hurt are lesser.
A study concluded that people who take up flexibility exercises and stretching two times a week for 12 weeks saw improved balance and lumbar strength.
A study that explored the effects of yoga on athletes reported that yoga improved flexibility in adult athletes. Flexibility, in turn, improved athletic performance.
When your body is more flexible, the muscles are better relaxed. This reduces general body pain in adults and children.
A 2009 article relates poor trunk flexibility to increased risks of arterial stiffening. Arterial stiffening is the stiffening and thickening of the artery walls that can lead to heart diseases.
The ACTN3 gene helps produce the Alpha-actinin protein. This protein gives structure to muscles in the body.
A 2014 study analyzed the effects of polymorphism of the ACTN3 gene in flexibility and injury risk in ballet dancers in Korea.
The result concluded that those ballerinas with the ACTN3 TT genotype of the rs1815739 SNP are less flexible than others and have higher risks for ankle-joint injuries. Ballerinas with the CT and CC genotype were more flexible and hence had lesser risks for injuries.
The COL5A1 gene is called the ‘flexibility gene.’ This helps produce the type V collagen. Collagen helps in strengthening your bones, muscles, skin, and tendons. It keeps your joints mobile and flexible. Lowered levels of collagen can result in stiffness and reduced flexibility.
rs12722 is an SNP of the COL5A1 gene. The T allele of this SNP causes quadricep stiffness and an increased risk of muscle injuries while the C allele is not associated with flexibility issues.
Ehlers-Danlos Syndrome (EDS) is a genetic disorder that results in loose joints, very stretchy skin, and overly flexible joints. People with the syndrome have extra ranges of joint movements, also called hypermobility. EDS can cause joint pain, frequent injuries, and bruises in the skin.
More than 100 different mutations in the COL5A1 gene are noted in people with EDS.
Age - Newborns are extremely flexible. Flexibility in the body reduces as you age. After 55 years of age, collagen production reduces, and tissues start losing water. This brings down flexibility levels.
Body Bulk - If you have more bulky, it may be difficult to stretch or move limbs and muscles.
Gender - Women are considered more flexible than men.
The temperature and time of the day - You might be surprised, but your body’s flexibility depends on what time of the day it is and the external temperature. Warmer climates improve flexibility, and people are more flexible in the afternoons than in the mornings.
Over-flexibility is a problem when your muscles, ligaments, and tendons stretch beyond what’s normal for them. It puts stress on your tendons and ligaments and results in injuries.
Ligaments are not to be stretched more than 6% of their length. Some people can be over flexible because of their genes, which increases their risks of injuries and ligament tear.
Yoga, stretching exercises, pilates, etc., are all different kinds of exercises that help improve your flexibility. All these exercises gently stretch muscles and improve mobility.
Static flexible exercises require you to hold a stretch or a position for 30 -60 seconds before relaxing. Static flexible exercises help improve flexibility.
Taking a warm water bath can instantly relax your muscles and improve your flexibility.
When done right, massages can help improve flexibility and your range of motion, keeping your joints stronger and agile.
Water is essential for the normal functioning of the body. Dehydration can cause inflexibility and limit your range of motion. Make sure you drink adequate water to improve flexibility.
Stress is known to tighten muscles and decrease physical flexibility. Working on mental stress levels can help the muscles relax and improve your flexibility levels.
https://www.frontiersin.org/articles/10.3389/fphys.2017.01080/full
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241924/
https://medlineplus.gov/genetics/gene/col5a1/#conditions
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4523805/
https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP085974
https://sites.psu.edu/kinescfw/health-education/exercise-articles/the-importance-of-flexibility-and-mobility/
https://www.sciencedirect.com/science/article/pii/S0002929707635290
Update on 16th January, 2021
ACTN3, popularly called the Speed Gene, is responsible for the production of α-actinin-3, a protein expressed in fast-firing skeletal muscle fibers. This protein is deficient in approximately 1.5 billion people worldwide.
Previous studies indicate that α-actinin-3 is associated with muscle function, and an α-actinin-3 deficiency adversely affects performance in speed and power activities. Recent research suggests that α-actinin-3 deficiency generates heat in the body (thermogenesis), and as a result, α-actinin-3 deficient humans adapt better to lower temperatures.
The α-actinin-3 protein was first identified during research into muscular dystrophy defects. Further studies showed that a deficiency of α-actinin-3 was common- roughly 18% of the world population has an ACTN3 deficiency mutation. This deficiency correlates with the following factors:
A previous study exploring the evolutionary implications of α-actinin-3 deficiency indicated that a version of the ACTN3 gene became more abundant as humans migrated out of Africa into the colder climates of Northern and Central Europe.
Studies also suggest that an X derivative of the ACTN3 gene is overexpressed among marathoners and endurance athletes but underexpressed in sprinters. The X derivative indicates an incomplete ACTN3 gene and is thereby associated with α-actinin-3 deficiency.
In general, an α-actinin-3 deficiency is detrimental for sprint and power activities. Evolutionary evidence also indicates a strong positive selection of the X derivative of the ACTN3 gene in European and East Asian populations. Positive selection is the process by which the "advantageous" changes or gene variants are passed on consistently in a population.
A study conducted by a team of researchers examined the mechanism responsible for the positive selection of the X derivative of the ACTN3 gene. It aimed to understand the thermogenic role of skeletal muscle during cold exposure in humans.
The study was conducted on the following two groups: Healthy males aged 18 to 40 years, residing in Kaunas, Lithuania. They followed moderate physical activity and had no exposure to an extreme temperature for at least three months prior to the study. Thirteen age-matched 3-month-old wild-type mice and mice with inactivated ACTN3 genes, housed in a specific-pathogen-free environment. They were maintained at a constant ambient temperature of 22°C and 50% humidity on a 12 h light-dark cycle, with limited access to food and water.
The following parameters were measured in humans:
Based on the above parameters, the following were calculated:
Coldwater exposure was conducted as follows:
The following parameters were examined in both humans and mice:
Apart from these, protein analyses in humans and RNA sequencing in mice were performed, and the data obtained were statistically analyzed.
The study observed that the percentage of individuals able to maintain their body temperature above 35.5°C during the cold-water exposure was higher in the ACTN3 deficient (XX) group than the ACTN3 efficient (RR) group. However, there was a significant overall increase in energy consumption induced by the cold irrespective of the ACTN3 gene status. This implies that α-actinin-3-deficient individuals exhibit superior protection of core body temperature during cold exposure without a corresponding increase in energy consumption.
Researchers suggest a physiological mechanism underlying the energy-efficient cold protection in XX individuals. Mammals regulate their body temperature when exposed to acute cold temperatures through involuntary muscle contraction. This is colloquially referred to as shivering - this activity was twice as high in RR individuals as in XX individuals. In individuals with the X derivative, these contractions most likely happen in slow twitch-type muscles with a heat-generating increase in muscle tone. This conserves more energy when compared to shivering.
The X derivative of the ACTN3 gene occurs more commonly in people living in colder climates, indicating an evolutionary survival advantage of α-actinin-3 deficiency as humans migrated to colder places.
In conclusion, α-actinin-3-deficient humans use a more energy-efficient mechanism of generating body heat, thereby exhibiting improved cold tolerance.
