Age-Related Neuromuscular Changes and Implications for Motor Performance

Introduction

Our nervous system and muscles work together to govern, direct, and facilitate the body's movement through the neuromuscular system. Motor neuron disease, Parkinson's disease, multiple sclerosis, Huntington's disease, muscular dystrophy, and polio are all movement-related illnesses (Kelley & Ferreira, 2017). The synapse between an alpha motor neuron and a skeletal muscle fiber is known as the neuromuscular junction. Aging is linked to neuromuscular junction remodeling and decreased neuromuscular transmission, which may increase the variability in motor unit activation in older people. Age-related changes in the basic functional unit of the neuromuscular system, the motor unit, and its neural inputs have a profound effect on motor function, especially among the expanding number of old (older than ∼60 yr) and very old (more aged than ∼80 yr) adults (Murphy et al., 2018).

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The loss of muscle mass and strength associated with aging has been connected to intracellular and extracellular abnormalities, namely sarcoplasmic reticulum-to-mitochondria faults and extracellular matrix metabolism. The need to lessen the burden of family care while maintaining the support of our medical institutions is a significant issue in today's super-aging society (Nishikawa et al., 2021). Sarcopenia, the devastating consequence of muscle loss and atrophy caused by age, is a fast-increasing significant health concern. This paper discusses the evidence that age-related changes in the nervous system can lead to impaired motor performance, such as 1) decreased maximal strength and power, slower contractile velocity, and increased fatigability; and 2) increased variability during and between motor tasks, such as decreased force steadiness and increased variability of contraction velocity and torque over repeat concentric circles.

The majority of data supporting age-related alterations in the neuromuscular junction comes from animal research, with some evidence from humans. Increased presynaptic branching, bigger and more dispersed postsynaptic endplate regions, and a reduction in the coupling of presynaptic vesicles and postsynaptic receptors have all been found in elderly animals (Clark, 2019). More significant mitochondrial dysfunction, oxidative stress, inflammation, and neurodegeneration are likely primary contributors behind these alterations and instability of the neuromuscular junction, all of which increase with age. Impaired neuromuscular transmission, which can result in total blocking of the action potential (impulse blocking) and inefficient and unpredictable muscle activation, are functional repercussions of these age-related alterations in the neuromuscular junction.

Falls in older persons are caused by neuromuscular aging, although the interconnected nature of these causes is not well understood (Roberts et al., 2018). Falls are a primary cause of morbidity and death in the elderly impacting one-third of individuals aged 65 and over and resulting in negative consequences such as serious injury, loss of independence, and institutionalization. Fall mortality rates rise rapidly with age in both sexes and across all racial and ethnic groupings, with falls accounting for 70% of all accidental deaths among people 75 and older (Clark, 2018). Falls are commonly connected with severe morbidity and can be indicators of poor health and critical function.

In the United Kingdom, 147 million injury-related visits to emergency departments were recorded between 1992 and 1995 (Boehm et al., 2020). 1 The most common cause of external damage was falls caused by neuromuscular aging, which accounted for 24% of all visits. 1 Child under the age of five and seniors 65 and older are more likely to attend the emergency room due to a fall. Older people who fall are ten times more likely to be hospitalized and eight times more likely to die due to a fall than children (Clark, 2018).

Alterations in skeletal muscle quantity and quality accompany aging, and these changes are a significant contributor to the increased prevalence of impairment among the elderly. Osteopenia and organogenic, in addition to sarcopenia, are signs of advancing age and may contribute to the development of disability. Sarcopenia was already identified as the age-related loss of muscle mass about two decades ago (Piasecki et al., 2021). We now understand that muscle mass and strength are causally connected, with changes in bulk causing changes in strength. It was discovered about three decades ago that muscle strength is not simply dependent on muscle mass. Muscle strength declines faster than muscle mass loss in the elderly, and muscle mass loss during disuse is only associated with a 10% loss of power. Experiments in which muscle mass is increased, but the age-related loss in muscle strength is not prevented support this viewpoint.

As a result, the previously stated viewpoint that muscle strength loss in senior persons is poorly correlated with loss of lean body mass reveals that muscular strength loss is primarily related to deficiencies in muscle neural activation. The loss of muscle mass, structure, and strength is linked to aging and inactivity or disuse (Roberts, 2018). Microcirculatory abnormalities, atrophy, protein loss, changes in contractile characteristics, and fiber-type switching occur in the skeletal muscle due to a sedentary lifestyle, bed rest, spaceflight, and hind limb suspension. Oxidative stress rises in both young and old skeletal muscles in response to unloading, suggesting that it may play a role in causing muscle atrophy. In skeletal muscle, unloading causes a decrease in the number of myonuclei and an increase in the number of apoptotic myonuclei.

Aging is a physiological process characterized by a steady loss of skeletal muscle mass, strength, endurance, and an inadequate response to tissue damage. The continued deterioration in numerous physiological capacities in the elderly is caused mainly by aging and a reduced physical level (Piasecki et al., 2021). The translational process in older human skeletal muscle affects protein synthesis rates, although the transcriptional process appears unaffected compared to those in younger males. Sarcopenia is caused by a decrease in myofibrillar protein synthesis and an increase in myofibrillar protein breakdown, which results in a slower turnover rate of muscle proteins, particularly contractile proteins, and a decrease in muscular strength.

Aging causes changes in posture and gait (walking pattern). Skin and hair changes are also very prevalent. The skeleton gives the body stability and structure. The places where bones meet are known as joints. They make it possible for the frame to move freely. Bones do not physically contact each other in a joint (Murphy et al., 2018). Instead, the cartilage in the joints, synovial membranes around the joint, and fluid cushion them. Muscles give the body the force and strength it needs to move. The brain controls coordination, although alterations in the muscles and joints have an impact. Power, joint, and bone changes impact posture and walk, resulting in weakness and decreased movement.

As people get older, they lose bone mass and density, especially women after menopause. Calcium and other minerals are lost from the bones. The vertebrae are the bones that make up the spine. A gel-like cushion sits between each bone (called a disk). The trunk (center of the body) gets shorter as the disks lose fluid and grow thinner with age (Pesonen et al., 2021). Vertebrae lose some of their mineral content as well, causing each bone to become lighter. The spinal column gets bent and crushed as a result of this condition (packed together). Bone spurs can grow on the vertebrae due to aging and the overall function of the spine. The foot arches become less prominent, resulting in a modest height decrease.

When compared to the reduced trunk, the limbs and legs appear longer. The joints stiffen and become less flexible. The fluid in your joints may diminish. The cartilage may start to rub together and wear away. Minerals can build up in and around joints (calcification). This is a regular occurrence in the area of the shoulder (Chugh et al., 2020). Cartilage loss in the hip and knee joints is a possibility (degenerative changes). The cartilage in the finger joints wears away, and the bones thicken slightly. Women are more likely than men to develop finger joint alterations, the most common of which are bone swellings known as osteophytes. These modifications could be passed down via the generations.

The amount of lean body mass diminishes. A loss of muscle tissue contributes to this decline (atrophy). Genes appear to be responsible for the speed and magnitude of muscle changes. Muscle changes commonly begin in men's 20s and women's 40s. In muscle tissue, lipofuscin (an age-related pigment) and fat are accumulated—muscle fibers contract (Pesonen et al., 2021). Muscle tissue regenerates at a slower rate. A tough fibrous tissue can replace muscle tissue that has been lost. This is especially apparent in the hands, which can appear thin and bony. Because of changes in muscle tissue and typical aging changes in the neurological system, muscles are less toned and less able to contract. Even with regular exercise, muscles can become inflexible and lose tone as they age.

Bones grow more fragile and are more likely to break—the trunk and spine shrink, resulting in a reduction in overall height. Inflammation, pain, stiffness, and deformity can all result from a joint breakdown. Almost everyone gets common problems as they become older. From modest discomfort to severe arthritis, these changes can occur (Chugh et al., 2020). The stooping posture may worsen (bent). Knees and hips may become more flexed as a result of this. The shoulders may narrow, and the neck may tilt while the pelvis expands. Movement becomes more complex and restricted. The gait (walking pattern) slows down and becomes shorter. Walking may become unsteady, and arms swinging is reduced. Older adults are more likely to become fatigued and have less energy. Strength and endurance levels fluctuate. Muscle mass loss reduces strength.

Osteoporosis is a common problem, particularly among women in their older years. Bones have a higher proclivity for shattering. Vertebral compression fractures are painful and restrict movement. Muscle weakness is characterized by fatigue, weakness, and lower exercise tolerance. Joint diseases range from minor aches and pains to severe arthritis (osteoarthritis) (Boehm et al., 2020). Falls can be caused by changes in gait, instability, or a loss of balance, all of which increase the risk of injury. Some older people's reflexes are compromised. The most prevalent causes are alterations in the muscles and tendons rather than abnormalities in the nerves. Knee and ankle jerk reflexes may be affected.

The elderly are more likely to experience involuntary movements (muscle tremors and small motions known as fasciculations). Inactive older individuals may experience weakness or strange sensations (paresthesias). Muscle contractures can occur in people who cannot move independently or who do not extend their muscles during exercise (Kelley & Ferreira, 2017). Training is one of the most effective ways to slow or prevent muscle, joint, and bone disorders. Moderate exercise can aid in the maintenance of strength, balance, and flexibility. Exercise aids in the care of solid bones. Before beginning a new workout program, consult with your doctor. It is critical to consume a well-balanced diet rich in calcium. Women, in particular, must be cautious about getting enough calcium and vitamin D as they grow older. Calcium intake for postmenopausal women and males over the age of 70 should be 1,200 mg per day.

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Vitamin D should be consumed in 800 international units (IU) per day by women and males over 70. Consult your doctor about prescription medications if you have osteoporosis. Diet and exercise habits can significantly impact a person's weight fluctuations over time (Nishikawa et al., 2021). Your lifestyle decisions affect how quickly you age. You can reduce age-related body changes by doing the following: Get some exercise regularly. Limit your alcohol consumption and stay away from tobacco and illicit drugs by eating a nutritious diet rich in fruits and vegetables, whole grains, and the correct quantity of healthy fats.

Conclusion

Motor performance deteriorates with age and is accelerated in old age (>65 years), with muscles that are weaker, slower, less strong, less stable, and more fatigable during high-velocity dynamic tasks. Reduced maximal power of lower-extremity forces predicts functional performance and disability, but little is known about the predictive strength of other components of motor performance, such as stability and fatigability, leaving room for high-impact research. Practice and increased physical activity tend to alleviate some of the disparities in motor unit performance and function commonly linked to aging (Kelley & Ferreira, 2017). Many studies that describe changes in motor performance and variability over time are cross-sectional. As a result, the future task will be to conduct sufficiently powered longitudinal studies to understand the processes underlying reduced motor performance and more significant variability and impact on functional performance and impairment in elderly and significantly older men and women.

References

Kelley, R. C., & Ferreira, L. F. (2017). Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology. Heart failure reviews, 22(2), 191-207.

Murphy, S., Zweyer, M., Mundegar, R. R., Swandulla, D., & Ohlendieck, K. (2018). Proteomic serum biomarkers for neuromuscular diseases. Expert review of proteomics, 15(3), 277-291.

Nishikawa, H., Fukunishi, S., Asai, A., Yokohama, K., Nishiguchi, S., & Higuchi, K. (2021). Pathophysiology and mechanisms of primary sarcopenia. International Journal of Molecular Medicine, 48(2), 1-8.

Clark, B. C. (2019). Neuromuscular changes with aging and sarcopenia. The Journal of frailty & aging, 8(1), 7-9.

Roberts, B. M., Lavin, K. M., Many, G. M., Thalacker-Mercer, A., Merritt, E. K., Bickel, C. S., ... & Bamman, M. M. (2018). Human neuromuscular aging: Sex differences revealed at the myocellular level. Experimental gerontology, 106, 116-124.

Boehm, I., Miller, J., Wishart, T. M., Wigmore, S. J., Skipworth, R. J., Jones, R. A., & Gillingwater, T. H. (2020). Neuromuscular junctions are stable in patients with cancer cachexia. The Journal of clinical investigation, 130(3), 1461-1465.

Piasecki, J., Inns, T. B., Bass, J. J., Scott, R., Stashuk, D. W., Phillips, B. E., ... & Piasecki, M. (2021). Influence of sex on the age‐related adaptations of neuromuscular function and motor unit properties in elite masters athletes. The Journal of Physiology, 599(1), 193-205.

Chugh, D., Iyer, C. C., Wang, X., Bobbili, P., Rich, M. M., & Arnold, W. D. (2020). Neuromuscular junction transmission failure is a late phenotype in aging mice. Neurobiology of Aging, 86, 182-190.

Pesonen, H., Laakkonen, E. K., Hautasaari, P., Aukee, P., Kovanen, V., Sipilä, S., ... & Tarkka, I. M. (2021). Perimenopausal women show modulation of excitatory and inhibitory neuromuscular mechanisms. BMC Women's Health, 21(1), 1-10.


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