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5.6: Age Related Changes to the Skeletal System - Biology

5.6: Age Related Changes to the Skeletal System - Biology


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Age Related Changes to Bone

The major age related change in the skeletal system is the loss of calcium in the bone. Most men don’t begin to the lose calcium until they reach the age of 60.

In addition to the lose of calcium as one ages protein synthesis also slows. As a result there is little to no new formation of collagen fibers. These fibers are what give the bones strength and flexibility. Without them bones become brittle resulting in a higher rate of fracture.

Finally bone reabsorption continues without the continued formation of new bone. This results in larger centrally located medullary cavities of the long bones and thinner walls of compact bone.

All of these changes result in a decrease of bone mass. While the causes of these changes are not well understood, it is thought that hormonal imbalances and changes in activity level may be factors.

Age Related Changes to Cartilage

One of the main roles of the skeletal system is the smooth functioning of the various movable joints of the body. Articular cartilage covers the ends of bone involved in a joint. As the joint moves articular cartilage rubs against articular cartilage, as opposed to bone on bone contact. This cartilage reduces friction and produces smooth movements in the joints. As you age this cartilage becomes thinner and deteriorates. The resulting bone on bone contact makes movement of the joint painful.

Costal cartilage has the specific function of connecting the ribs to the sternum. This cartilage make it possible for the rib cage to expand and contract with respiration. As one ages the cartilage calcifies resulting in a loss of flexibility. This restricts breathing.

Fibrocartilage makes up the intervertebral discs which specifically provides cushioning between the vertebrae which make up the spinal column. After the age of about 40 years of age, the cartilage experiences a gradual loss of cells and water. This results in a decreased level of cushioning provided by these discs.


Aging changes in the bones - muscles - joints

Changes in posture and gait (walking pattern) are common with aging. Changes in the skin and hair are also common.

The skeleton provides support and structure to the body. Joints are the areas where bones come together. They allow the skeleton to be flexible for movement. In a joint, bones do not directly contact each other. Instead, they are cushioned by cartilage in the joint, synovial membranes around the joint, and fluid.

Muscles provide the force and strength to move the body. Coordination is directed by the brain, but is affected by changes in the muscles and joints. Changes in the muscles, joints, and bones affect the posture and walk, and lead to weakness and slowed movement.

People lose bone mass or density as they age, especially women after menopause. The bones lose calcium and other minerals.

The spine is made up of bones called vertebrae. Between each bone is a gel-like cushion (called a disk). With aging, the middle of the body (trunk) becomes shorter as the disks gradually lose fluid and become thinner.

Vertebrae also lose some of their mineral content, making each bone thinner. The spinal column becomes curved and compressed (packed together). Bone spurs caused by aging and overall use of the spine may also form on the vertebrae.

The foot arches become less pronounced, contributing to a slight loss of height.

The long bones of the arms and legs are more brittle because of mineral loss, but they do not change length. This makes the arms and legs look longer when compared with the shortened trunk.

The joints become stiffer and less flexible. Fluid in the joints may decrease. The cartilage may begin to rub together and wear away. Minerals may deposit in and around some joints (calcification). This is common around the shoulder.

Hip and knee joints may begin to lose cartilage (degenerative changes). The finger joints lose cartilage and the bones thicken slightly. Finger joint changes, most often bony swelling called osteophytes, are more common in women. These changes may be inherited.

Lean body mass decreases. This decrease is partly caused by a loss of muscle tissue (atrophy). The speed and amount of muscle changes seem to be caused by genes. Muscle changes often begin in the 20s in men and in the 40s in women.

Lipofuscin (an age-related pigment) and fat are deposited in muscle tissue. The muscle fibers shrink. Muscle tissue is replaced more slowly. Lost muscle tissue may be replaced with a tough fibrous tissue. This is most noticeable in the hands, which may look thin and bony.

Muscles are less toned and less able to contract because of changes in the muscle tissue and normal aging changes in the nervous system. Muscles may become rigid with age and may lose tone, even with regular exercise.

Bones become more brittle and may break more easily. Overall height decreases, mainly because the trunk and spine shorten.

Breakdown of the joints may lead to inflammation, pain, stiffness, and deformity. Joint changes affect almost all older people. These changes range from minor stiffness to severe arthritis.

The posture may become more stooped (bent). The knees and hips may become more flexed. The neck may tilt, and the shoulders may narrow while the pelvis becomes wider.

Movement slows and may become limited. The walking pattern (gait) becomes slower and shorter. Walking may become unsteady, and there is less arm swinging. Older people get tired more easily and have less energy.

Strength and endurance change. Loss of muscle mass reduces strength.

Osteoporosis is a common problem, especially for older women. Bones break more easily. Compression fractures of the vertebrae can cause pain and reduce mobility.

Muscle weakness contributes to fatigue, weakness, and reduced activity tolerance. Joint problems ranging from mild stiffness to debilitating arthritis (osteoarthritis) are very common.

The risk of injury increases because gait changes, instability, and loss of balance may lead to falls.

Some older people have reduced reflexes. This is most often caused by changes in the muscles and tendons, rather than changes in the nerves. Decreased knee jerk or ankle jerk reflexes can occur. Some changes, such as a positive Babinski reflex, are not a normal part of aging.

Involuntary movements (muscle tremors and fine movements called fasciculations) are more common in the older people. Older people who are not active may have weakness or abnormal sensations (paresthesias).

People who are unable to move on their own, or who do not stretch their muscles with exercise, may get muscle contractures.

Exercise is one of the best ways to slow or prevent problems with the muscles, joints, and bones. A moderate exercise program can help you maintain strength, balance, and flexibility. Exercise helps the bones stay strong.

Talk to your health care provider before starting a new exercise program.

It is important to eat a well-balanced diet with plenty of calcium. Women need to be particularly careful to get enough calcium and vitamin D as they age. Postmenopausal women and men over age 70 should take in 1,200 mg of calcium per day. Women and men over age 70 should get 800 international units (IU) of vitamin D daily. If you have osteoporosis, talk to your provider about prescription treatments.


[Aging, basal metabolic rate, and nutrition]

Age is one of the most important factor of changes in energy metabolism. The basal metabolic rate decreases almost linearly with age. Skeletal musculature is a fundamental organ that consumes the largest part of energy in the normal human body. The total volume of skeletal muscle can be estimated by 24-hours creatinine excretion. The volume of skeletal musculature decreases and the percentage of fat tissue increases with age. It is shown that the decrease in muscle mass relative to total body may be wholly responsible for the age-related decreases in basal metabolic rate. Energy consumption by physical activity also decreases with atrophic changes of skeletal muscle. Thus, energy requirement in the elderly decreases. With decrease of energy intake, intake of essential nutrients also decreases. If energy intake, on the other hand, exceeds individual energy needs, fat accumulates in the body. Body fat tends to accumulate in the abdomen in the elderly. Fat tissue in the abdominal cavity is connected directly with the liver through portal vein. Accumulation of abdominal fat causes disturbance in glucose and lipid metabolism. It is shown that glucose tolerance decreases with age. Although age contributes independently to the deterioration in glucose tolerance, the decrease in glucose tolerance may be partly prevented through changes of life-style variables, energy metabolism is essential for the physiological functions. It may also be possible to delay the aging process of various physiological functions by change of dietary habits, stopping smoking, and physical activity.


Effects of Aging on the Musculoskeletal System

From about age 30, the density of bones begins to diminish in men and women. This loss of bone density accelerates in women after menopause. As a result, bones become more fragile and are more likely to break (see Osteoporosis), especially in old age.

As people age, their joints are affected by changes in cartilage and in connective tissue. The cartilage inside a joint becomes thinner, and components of the cartilage (the proteoglycans—substances that help provide the cartilage's resilience) become altered, which may make the joint less resilient and more susceptible to damage. Thus, in some people, the surfaces of the joint do not slide as well over each other as they used to. This process may lead to osteoarthritis. Additionally, joints become stiffer because the connective tissue within ligaments and tendons becomes more rigid and brittle. This change also limits the range of motion of joints.

Loss of muscle (sarcopenia) is a process that starts around age 30 and progresses throughout life. In this process, the amount of muscle tissue and the number and size of muscle fibers gradually decrease. The result of sarcopenia is a gradual loss of muscle mass and muscle strength. This mild loss of muscle strength places increased stress on certain joints (such as the knees) and may predispose a person to arthritis or falling. Fortunately, the loss in muscle mass and strength can partially be overcome or at least significantly delayed by a program of regular exercise.

The types of muscle fibers are affected by aging as well. The numbers of muscle fibers that contract faster decrease much more than the numbers of muscle fibers that contract slower. Thus, muscles are not able to contract as quickly in old age.


2 ECM AND AGING

ECM is the noncellular component of tissues and organs that provides a scaffold for tissues as well as critical cellular cues that support biological function. 17 Notably, the composition, biomechanics, and supramolecular structure of the ECM are specific to support the function of each tissue. Generally, the components of the ECM are composed of two classes: fibrous proteins and proteoglycans (or nonfiber forming proteins). 18 Due to the insoluble nature of many ECM components, it is challenging to form a complete component list for all organ-specific ECMs. Generally speaking, the core components required for any ECM are collagens, proteoglycans, glycoproteins, growth factors, and ECM modifiers. 12, 19 However, over 1000 ECM proteins have been identified within “the matrisome” and are catalogued at http://matrisomedb.pepchem.org/ where one can search by species, tissue, and disease. 20 Among all organ-specific ECMs, the ECM of the dermis has been the most extensively described due to ease of organ collection, especially in the context of molecular and cellular aging. These changes over time encompass the accumulation of mutations over many years, including changes in secretory functions as well as the loss or gain of molecules involved in both signaling and biophysical cues. The loss or gain of ECM molecules in particular can directly impact tumor cells through altered signaling. For example, in the case of the skin ECM, young skin presents a highly organized matrix that is rich in collagen and aged skin presents a degraded ECM with fewer fibrillar components and less structural integrity. 21 Our laboratory has found that HAPLN1, a proteoglycan linker protein, is lost during aging and renders the ECM less tightly organized with lower integrity. 21 This affects not only the way tumor cells move in this ECM, but also the integrity of lymphatic vessels and immune cell motility. 21, 22 Aged skin is thus characterized primarily by alterations in the dermal ECM that lead to aberrancies in skin biomechanics such as increased stiffness and decreased elasticity. 23 This is largely due to alterations in the secretomes of dermal fibroblasts, which produce the ECM. Aged fibroblasts decrease production of both ECM components, such as collagen, as well as ECM modifiers. 21, 24, 25 The resulting degradation of the ECM is known to be a critical determinant for progression of the skin cancer, melanoma. In addition to altered secretomes, dermal fibroblasts become less dense with age and have disrupted homeostasis. 26 These sorts of changes, in addition to the accumulation of chronic genetic damage, changes in adaptive immunity, and other insults, may explain why aging has long been considered an independent prognostic factor in melanoma whereby older patients have poorer prognoses. 27-29

The complex and dynamic meshwork produced by the matrisome provides mechanical integrity and cellular regulation at an organ-specific level. 15 This concept has been dubbed “dynamic reciprocity,” or where ECM/cell crosstalk potentiates function. The ECM exerts physical and chemical influence on the cell, which in turn alters the cell's interaction with the ECM. 30 This give-and-take phenomenon is also referred to as “mechanotransduction,” which is necessary for the proper biomechanical function of organs and tissues to support whole-body health. 31 However, as we age, these complex networks begin to break down. This breakdown largely occurs due to irreversible modifications of existing ECM proteins such as oxidation, deamidation, carbonylation, glycation, succination, and carbamylation. 32 Because many ECM proteins, particularly collagen, have very long half-lives (on the order decades), they are particularly susceptible to buildup of these pathogenic modifications as we age. 33 The best-studied of these are the formation of advanced glycation end-products, or AGEs. These occur via a nonenzymatic reaction between reducing sugars and proteins, lipids, or nucleic acids. 34 AGEs modify binding domains and alter the mechanical function of ECM proteins, particularly collagens, which lead to overall aberrant ECM topography. This stiffens the tissue, reducing critical viscoelastic function, which confers age-related pathologies. 35 Similarly, matrix metalloproteinases (MMPs) are normally responsible for ECM breakdown to maintain homeostasis and ensure proper tissue remodeling. 36 However, MMP activity becomes elevated as we age, resulting in aberrant ECM organization via accumulation of fragmented, heavily cross-linked collagen and loss of critical ECM ligands. 37 In the context of cancer, these changes create an environment that is permissible for cancer cell attachment and outgrowth. In particular, it has been well-documented that primary tumors modify their ECM to form a stiffer, more permissive stroma that promotes cancer cell endothelial to mesenchymal transition, 38 endothelium interaction, 39 and migration. 21, 40 Thus, age-related biomechanical changes that occur in the ECM throughout the body potentiate cancer permissive niches that, when cancer cells reach the organ site, are primed for metastatic outgrowth.


Physical activity can help


Exercise can prevent many age-related changes to muscles, bones and joints – and reverse these changes as well. It’s never too late to start living an active lifestyle and enjoying the benefits.

  • Exercise can make bones stronger and help slow the rate of bone loss.
  • Older people can increase muscle mass and strength through muscle-strengthening activities.
  • Balance and coordination exercises, such as tai chi, can help reduce the risk of falls.
  • Physical activity in later life may delay the progression of osteoporosis as it slows down the rate at which bone mineral density is reduced.
  • Weight-bearing exercise, such as walking or weight training, is the best type of exercise for maintenance of bone mass. There is a suggestion that twisting or rotational movements, where the muscle attachments pull on the bone, are also beneficial.
  • Older people who exercise in water (which is not weight bearing) may still experience increases in bone and muscle mass compared to sedentary older people.
  • Stretching is another excellent way to help maintain joint flexibility.

See your doctor before you start any new physical activity program. If you haven’t exercised for a long time, are elderly or have a chronic disease (such as arthritis), your doctor, physiotherapist or exercise physiologist can help tailor an appropriate and safe exercise program for you. If you suffer from osteoporosis, you may also be advised to take more calcium. Sometimes, medications are needed to treat osteoporosis.


5.6: Age Related Changes to the Skeletal System - Biology

All systems in the body accumulate subtle and some not-so-subtle changes as a person ages. Among these changes are reductions in cell division, metabolic activity, blood circulation, hormonal levels, and muscle strength (Figure 4.17). In the skin, these changes are reflected in decreased mitosis in the stratum basale, leading to a thinner epidermis. The dermis, which is responsible for the elasticity and resilience of the skin, exhibits a reduced ability to regenerate, which leads to slower wound healing. The hypodermis, with its fat stores, loses structure due to the reduction and redistribution of fat, which in turn contributes to the thinning and sagging of skin.

The accessory structures also have lowered activity, generating thinner hair and nails, and reduced amounts of sebum and sweat. A reduced sweating ability can cause some elderly to be intolerant to extreme heat. Other cells in the skin, such as melanocytes and dendritic cells, also become less active, leading to a paler skin tone and lowered immunity. Wrinkling of the skin occurs due to breakdown of its structure, which results from decreased collagen and elastin production in the dermis, weakening of muscles lying under the skin, and the inability of the skin to retain adequate moisture.

Many anti-aging products can be found in stores today. In general, these products try to rehydrate the skin and thereby fill out the wrinkles, and some stimulate skin growth using hormones and growth factors. Additionally, invasive techniques include collagen injections to plump the tissue and injections of BOTOX ® (the name brand of the botulinum neurotoxin) that paralyze the muscles that crease the skin and cause wrinkling.


Effects of Exercise and Aging on Skeletal Muscle

A substantial loss of muscle mass and strength (sarcopenia), a decreased regenerative capacity, and a compromised physical performance are hallmarks of aging skeletal muscle. These changes are typically accompanied by impaired muscle metabolism, including mitochondrial dysfunction and insulin resistance. A challenge in the field of muscle aging is to dissociate the effects of chronological aging per se on muscle characteristics from the secondary influence of lifestyle and disease processes. Remarkably, physical activity and exercise are well-established countermeasures against muscle aging, and have been shown to attenuate age-related decreases in muscle mass, strength, and regenerative capacity, and slow or prevent impairments in muscle metabolism. We posit that exercise and physical activity can influence many of the changes in muscle during aging, and thus should be emphasized as part of a lifestyle essential to healthy aging.

Copyright © 2018 Cold Spring Harbor Laboratory Press all rights reserved.

Figures

Sedentary lifestyle contributes to an…

Sedentary lifestyle contributes to an “unhealthy aging.” ( A ) In this scenario,…


Anatomy and physiology of ageing 10: the musculoskeletal system

With advancing age, the skeletal muscles lose strength and mass while the bones lose density and undergo decalcification and demineralisation. Consequently, older people often experience a loss of strength, become more prone to falls, fractures and frailty, develop a stooping curvature of the spine, and have conditions such as sarcopenia, osteoporosis and osteoarthritis. As all our body systems, the musculoskeletal system benefits from moderate exercise as keeping active in old age helps to maintain both muscle strength and bone density. This is the penultimate article in our series on the anatomy and physiology of ageing.

Citation: Knight J et al (2017) Anatomy and physiology of ageing 10: the musculoskeletal system. Nursing Times [online] 113: 11, 60-63.

Authors: John Knight is senior lecturer in biomedical science Yamni Nigam is associate professor in biomedical science Neil Hore is senior lecturer in paramedic science all at the College of Human Health and Science, Swansea University.

  • This article has been double-blind peer reviewed
  • Scroll down to read the article or download a print-friendly PDF here to see other articles in this series

Introduction

Skeletal muscles allow the body to move and maintain posture by contracting, they also aid the venous return of blood to the heart and generate heat that helps maintain body temperature. Bones support the body, protect vulnerable regions and allow physical movement via a system of levers and joints they also store fat and minerals, and house the red bone marrow responsible for blood cell production. With age, these components of the musculoskeletal system progressively degenerate, which contributes to frailty and increases the risk of falls and fractures. Part 10 in our series on the anatomy and physiology of ageing explores the age-related changes that occur in skeletal muscles and bones.

Changes in skeletal muscles

Older people often experience a loss of strength that can be directly attributed to anatomical and physiological changes in skeletal muscles (Papa et al, 2017 Freemont and Hoyland, 2007) (Box 1).

Box 1. Age-related changes in skeletal muscles

  • Reduction in protein synthesis
  • Reduction in size and number of muscle fibres, particularly in the lower limbs
  • Decrease in the number of progenitor (satellite) cells
  • Reduction in muscle growth
  • Reduction in the ability of muscles to repair themselves
  • Replacement of active muscle fibres by collagen-rich, non-contractile fibrous tissue
  • Reduction in the number of motor neurons and deterioration of neuromuscular junctions
  • Increase in fat deposition at the expense of lean muscle tissue
  • Accumulation of lipofuscin (an age-related pigment)
  • Reduction in the number of mitochondria (although not all studies are in agreement)
  • Less-efficient metabolism, particularly in fast-twitch muscle fibres
  • Reduction in blood flow to the major muscle groups

With age, skeletal muscles atrophy and decrease in mass (Fig 1), and the speed and force of their contraction reduce (Choi, 2016). This phenomenon, known as senile sarcopenia, is accompanied by a decrease in physical strength. Sarcopenia can impair the ability to perform everyday tasks such as rising from a chair, doing housework or washing oneself (Papa et al, 2017).

Maximal muscle mass and strength are reached in the 20s and 30s. This is followed by a gradual decline through middle age. From the age of 60, the loss of muscle tissue accelerates. In late old age, the limbs may lose so much muscle tissue that people with reduced mobility appear to be little more than skin and bone. Deep furrows may develop between the ribs because of intercostal muscle atrophy, while the loss of facial muscle tissue contributes to a general loosening of the features.

This considerable loss of muscle tissue often seen in later years (senile sarcopenia), is associated with increasing frailty. While frailty is multifactorial, musculoskeletal deterioration and sarcopenia are central to it, and are both associated with increased weakness, fatigue and risk of adverse events such as falls, which can all increase morbidity (Fragala et al, 2015).

Skeletal muscles are composed of two main types of fibres:

  • Slow-twitch fibres (type 1), used for endurance activities, such as walking long distances
  • Fast-twitch fibres (type 2), used in short ‘explosive’ activities such as sprinting.

Sarcopenia is associated with changes in the number and physiology of fast-twitch fibres, while slow-twitch fibres are relatively unaffected by age (Bougea et al, 2016). Indeed, recent studies show that slow-twitch fibres maintain and even increase the concentrations of some metabolic enzymes, perhaps to counteract the decrease in fast-twitch muscle fibre activity (Murgia et al, 2017).

Sarcopenia is also thought to be driven by the loss of motor neuron fibres (denervation) and loss and degeneration of neuromuscular junctions (the synapses connecting motor neurons to skeletal muscles) as a consequence, muscles are less stimulated and lose mass (Stokinger et al, 2017 Power et al, 2013).

Sarcopenia is exacerbated by the reduction in the levels of circulating anabolic hormones – such as somatotropin (growth hormone), testosterone and testosterone-like hormones – which decline from middle age onwards. As skeletal muscles are metabolically very active, sarcopenia is a major factor contributing to the age-related reduction in metabolic rate. On average, we lose 3-8% of lean muscle mass per decade from the age of 30, which compounds the decline in basal metabolic rate that starts from around the age of 20. If calorific intake stays the same as in younger years, there is a much greater risk that excess calories will be stored in the form of fat. This may be exacerbated in older people who are insulin-resistant, as their skeletal muscles are less able to take up glucose and the amino acids used to generate new muscle fibres (Cleasby et al, 2016 Fragala et al, 2015).

The loss of skeletal muscle mass leads to a progressive reduction in the support afforded to the bones and joints, which in turn contributes to the postural changes observed in older age (Fig 2). It also increases the risk of joint pathologies, particularly osteoarthritis, as well as the risk of falls and fractures.

Aged muscles are more prone to injury and take longer to repair and recover. This slower recovery may be due to a reduction in the number of progenitor (satellite) cells – undifferentiated stem cells that can develop into new muscle cells or myocytes – combined with progressive cellular senescence (Bougea et al, 2016).

Changes in bones

  • The inorganic component calcium phosphate (hydroxyapatite)
  • The organic component type 1 collagen.

Calcium phosphate crystals form the bone matrix and give bones their rigidity. The skeleton acts as a calcium reservoir: it stores around 99% of all the calcium in the body (Lau and Adachi, 2011). Insufficient levels of calcium or vitamin D (essential for calcium absorption) can lead to a reduction in bone density and increase predisposition to osteoporosis and fractures. In older people, the gut absorbs less calcium and vitamin D levels tend to decrease, which reduces the amount of calcium available for the bones.

Collagen provides anchorage for the calcium phosphate crystals, knitting the bone together to prevent fractures. Some people have genes leading to faulty collagen production, which results in brittle bone disease (osteogenesis imperfecta).

Like muscle, bone is a dynamic tissue continuously being deposited and broken down. This state of flux is mediated by the two major bone cell types:

  • Osteoblasts, which deposit bone
  • Osteoclasts, which digest bone, releasing ionic calcium into the blood.

Osteoblasts are more active when the bones are under the stress imposed by the weight of an upright, active body. In young mobile adults, osteoblasts and osteoclasts work at a similar rate and bone density is maintained. Inactivity means a decrease in osteoblast activity that ultimately results in reduced bone density (Nigam et al, 2009). The age-related loss of skeletal muscle mass contributes to the reductions in load (both weight and contractile force) on the bones, which compounds decalcification. It is therefore essential that older people keep as mobile and active as possible.

Changes to bone density

Studies (predominantly in the US) show that around 90% of peak bone mass is achieved in men by age 20 and women by age 18. Increases continue in both sexes until around the age of 30 when peak bone strength and density is achieved (National Institutes of Health, 2015). Bone density decreases as middle age approaches.

Women are at particular risk of bone demineralisation and osteoporosis as they gradually lose the osteo-protective effects of oestrogen pre and post menopause. In a 10-year study, women lost 1.5-2 times more bone mass per year from their forearms than men (Daly et al, 2013). Bone loss in both sexes continues into old age, and 80-year-olds have approximately half the bone mass they had at its peak in young adulthood (Lau and Adachi, 2011 Kloss and Gassner, 2006).

Osteoporosis

The age-related loss of calcium from the skeleton commonly leads to the bones taking on the porous, sponge-like appearance indicative of osteoporosis. There are two recognised forms of this (Lau and Adachi, 2011):

  • Type I, seen in menopausal and post-menopausal women and thought to occur as a result of falling oestrogen levels
  • Type II, referred to as senile osteo-porosis, which affects both men and women and appears to be caused by reductions in the number and activity of osteoblasts. Additionally, some pro-inflammatory cytokines (whose numbers increase with age) such as interleukin 6 stimulate osteoclasts, leading to bone demineralisation.

The vertebrae are particularly vulnerable to osteoporosis and may develop micro-fractures resulting in them collapsing under the weight of the body and becoming compressed and deformed. This contributes to the stooping curvature of the spine often seen in older age (Fig 2).

Many factors contribute to age-related bone loss and senile osteoporosis (Box 2).

Box 2. Factors contributing to age-related bone loss and senile osteoporosis

  • Reduction in testosterone levels in men and osetrogen levels in women
  • Reduction in growth hormone levels (somatopause)
  • Reduction in body weight
  • Reduction in levels of physical activity
  • Reduction in calcium absorption and vitamin D levels
  • Increase in the levels of parathyroid hormone
  • Smoking

Risk of fracture

The age-related decrease in bone density is associated with an increased risk of fracture in many bones including the femur, ribs, vertebrae and bones of the upper arm and forearm. Osteoporosis is linked not only to a loss of inorganic mineral content, but also with a loss of collagen and changes to its structure. As collagen helps to hold bones together, this further increases the risk of fracture (Boskey and Coleman, 2010 Bailey, 2002).

The risk of fracture is compounded by a lack of mobility, for example, due to a prolonged stay in hospital (Nigam et al, 2009). Not only are fractures more common in old age, but healing takes much longer (Lau and Adachi, 2011).

Population studies in the US show that around 5% of adults over the age of 50 have osteoporosis affecting the femoral neck (neck of the femur) (Looker et al, 2012). This region is particularly vulnerable to fracture, as the two femoral necks support the weight of the upright body. Costache and Costache (2014) found that femoral neck fractures – which are serious and potentially life-threatening injuries – become more frequent after the age of 60 years and that women are more affected than men.

Joint changes

The articular cartilages in synovial joints play the role of shock absorbers, as well as ensuring the correct spacing and smooth gliding of bones during joint movement. The number and activity of chondrocytes, the cartilage-forming cells, decrease with age (Freemont and Hoyland, 2007), which can result in a reduction in the amount of cartilage in important joints, such as the knees (Hanna et al, 2005). A lack of cartilage results in aged joints becoming more susceptible to mechanical damage and increases the risk of painful bone-to-bone contact that is commonly seen in osteoarthritis.

Osteoarthritis

Osteoarthritis is the most common arthropathy (joint pathology) in the world. Large-scale studies in the US have shown that around 10% of men and 13% of women over the age of 60 are affected by symptomatic osteoarthritis of the knee (Zhang and Jordan, 2010). In the UK, around 8.5 million people have joint pain due to osteoarthritis (National Institute for Health and Care Excellence, 2015). This places a great burden on health services as many patients will require expensive joint surgery, particularly to the knee, hip and lumbar spine.

The outer portion of a joint capsule is composed of elastic ligaments that bind the joint together, preventing dislocation while allowing free movement. With age, changes to the collagen and elastin components of ligaments decrease their elasticity (Freemont and Hoyland, 2007), resulting in stiffness and reduced mobility. Certain joints are particularly susceptible for example, between the ages 55 and 85 years, women lose up to 50% of flexibility and range of motion in their ankles (Vandervoort et al, 1992). Although there are many risk factors associated with the disease (including genetic predisposition, gender, obesity and previous joint injury), age is by far the greatest.

Healthy musculoskeletal ageing

Many factors influence how our bones and skeletal muscles age genetics, environmental factors and lifestyle all play a role, so there is much individual variation. Preserving the structural and functional integrity of the musculoskeletal system is essential to maintain good health and slow down the progression to frailty.

Calorific restriction

Programmed cell death (apoptosis) plays a role in bone loss and sarcopenia. The apoptotic pathways involved may be attenuated by exercise, calorific restriction and anti-oxidants such as carotenoids and oleic acid (Musumeci et al, 2015). Recent studies have shown that calorific restriction can slow down, and sometimes even reverse, age-related changes in neuromuscular junctions, thereby providing a potential mechanism for reducing sarcopenia.

Drugs that mimic the effects of calorific restriction and exercise – such as metformin (an oral hypoglycaemic used to treat diabetes) and resveratrol (an anti-inflammatory and anti-oxidant) – could be used instead of reducing food intake. Stokinger et al (2017) have reported some success with these drugs, particularly resveratrol, in animal models.

Dietary supplementation

Increasing the intake of calcium, vitamin D and lean protein can increase bone density and provide amino acids for muscle growth. This may offset the reduction in the efficiency of nutrient absorption seen in older age. We know that, in younger adults, increasing protein intake can enhance protein synthesis in skeletal muscles, but this seems to work less well in older people. Fragala et al (2015) found that dietary supplementation with creatinine can increase muscle strength and performance, while the intake of protein drinks supplemented with the amino acid β-alanine increases muscle-working capacity and quality in older men and women.

Hormone replacement therapy

Hormone replacement therapy (HRT) improves bone health in older people: oestrogen HRT and testosterone replacement therapy (TRT) are proven to increase bone density in women and men, respectively, thereby reducing the risk of fracture.

The effects of HRT on muscle physiology are less well investigated. TRT has been shown to increase lean muscle mass in men and appears to negate some of the effects of ageing on muscles occurring during the andropause however, in women, HRT (with either oestrogen or oestrogen plus progesterone) does not have the same anabolic effect (Fragala et al, 2015). Women can use TRT, but they may be reluctant to do so because of unwanted effects such as facial and body hair growth and deepening of the voice.

Exercise

Unless regularly used and placed under load, muscle fibres and neuromuscular junctions degenerate, resulting in disuse atrophy (Kwan, 2013). Moderate exercise helps to maintain lean muscle mass, increase bone density and reduce fat accumulation. Exercise also increases the number of mitochondria in muscle fibres, enhancing energy release, metabolism and muscle power. In people who remain physically active, the efficiency of mitochondria in releasing energy appears to be maintained until at least the age of 75 (Cartee et al, 2016).

Progressive resistance training is considered to be the most effective method to increase bone density and promote muscle growth in older people with sarcopenia. Older people attending a single exercise class per week and doing some exercise at home can improve muscle strength by 27%, effectively reversing age-related decline (Skelton and McLaughlin, 1996). When it comes to keeping the musculoskeletal system healthy, the bottom line is the common colloquialism: use it or lose it.

Key points

  • The age-related degeneration of the musculoskeletal system makes older people prone to frailty, falls and fractures
  • Sarcopenia is produced by the atrophy and shrinkage of skeletal muscles, coupled with a reduction in the speed and force of their contraction
  • Osteoporosis and osteoarthritis commonly occur in old age as a result of bone changes
  • To have a healthy musculoskeletal system, it is essential that older people keep as physically active as possible

Also in the series

Bailey AJ (2002) Changes in bone collagen with age and disease. Journal of Musculoskeletal and Neuronal Interactions 2: 6, 529-531.

Boskey AL, Coleman R (2010) Aging and bone. Journal of Dental Research 89: 12, 1333-1348.

Bougea et al (2016) An age-related morphometric profile of skeletal muscle in healthy untrained women. Journal of Clinical Medicine 5: pii, E97.

Cartee GD et al (2016) Exercise promotes healthy aging of skeletal muscle. Cell Metabolism 23: 6, 1034-1047.

Choi SJ (2016) Age-related functional changes and susceptibility to eccentric contraction-induced damage in skeletal muscle cell. Integrative Medicine Research 5: 3, 171-175.

Cleasby ME et al (2016) Insulin resistance and sarcopenia: mechanistic links between common co-morbidities. Journal of Endocrinology 229: 2, R67-R81.

Costache C, Costache D (2014) Femoral neck fractures. Bulletin of the Transilvania University of Brasov, Series VI: Medical Sciences 7(56): 1, 103-110.

Daly RM et al (2013) Gender specific age-related changes in bone density, muscle strength and functional performance in the elderly: a-10 year prospective population-based study. BMC Geriatrics 13: 71.

Fragala MS et al (2015) Muscle quality in aging: a multi-dimensional approach to muscle functioning with applications for treatment. Sports Medicine 45: 5, 641-658.

Freemont AJ, Hoyland JA (2007) Morphology, mechanisms and pathology of musculoskeletal ageing. Journal of Pathology 211: 2, 252-259.

Hanna F et al (2005) Factors influencing longitudinal change in knee cartilage volume measured from magnetic resonance imaging in healthy men. Annals of the Rheumatic Diseases 64: 7, 1038-1042.

Kloss FR, Gassner R (2006) Bone and aging: effects on the maxillofacial skeleton. Experimental Gerontology 41: 2, 123-129.

Kwan P (2013) Sarcopenia, a neurogenic syndrome? Journal of Aging Research 2013: 791679.

Lau AN, Adachi JD (2011) Bone aging. In: Nakasato Y, Yung RL (eds) Geriatric Rheumatology: A Comprehensive Approach. New York: Springer.

Looker AC et al (2012) Osteoporosis or low bone mass at the femur neck or lumbar spine in older adults: United States, 2005-2008. National Center for Health Statistics Data Brief 93: 1-8.

Murgia M et al (2017) Single muscle fiber proteomics reveals fiber-type-specific features of human muscle aging. Cell Reports 19: 11, 2396-2409.

Musumeci G et al (2015) Apoptosis and skeletal muscle in aging. Open Journal of Apoptosis 4: 41-46.

National Institute for Health and Care Excellence (2015) Osteoarthritis.

National Institutes of Health (2015) Osteoporosis: Peak Bone Mass in Women.

Nigam Y et al (2009) Effects of bedrest 3: musculoskeletal and immune systems, skin and self-perception. Nursing Times 105: 23, 18-22.

Papa EV et al (2017) Skeletal muscle function deficits in the elderly: current perspectives on resistance training. Journal of Nature and Science 3: 1, e272.

Power GA et al (2013) Human neuromuscular structure and function in old age: a brief review. Journal of Sport and Health Science 2: 4, 215-226.

Skelton DA, McLaughlin AW (1996) Training functional ability in old age. Physiotherapy 82: 3, 159-167.

Stokinger J et al (2017) Caloric restriction mimetics slow aging of neuromuscular synapses and muscle fibers. The Journals of Gerontology. Series A glx023.

Vandervoort AA et al (1992) Age and sex effects on mobility of the human ankle. Journal of Gerontology 47: 1, M17-M21.

Zhang Y, Jordan JM (2010) Epidemiology of osteoarthritis. Clinics in Geriatric Medicine 26: 3, 355-369.


HABITUAL LEVEL AND TYPE OF PHYSICAL ACTIVITY

For the past 25 years, differences of opinion have existed regarding the relative roles in the development of frailty of immutable age-related changes in the structure and function of skeletal muscles 15, 42, 49 and those attributable to a sedentary, low physical activity lifestyle. 17, 50 For adult men and women, the ‘master athletes’ typify the most physically active in any age group. Throughout their lifespan, barring injury or illness, the master athlete maintains a high level of fitness and competes in his or her sport or specialized individual event of running, throwing or weight-lifting. Even among these men and women, performance declines after approximately 40 years of age. By age 80, the decrease in peak performance is from 35 to 65% for different events (Fig. 3). The variability between events is dependent largely on whether an event involves moving the body mass, as in running, or moving a fixed mass, as in weight-lifting, shot-put or discus throwing. Performance in all events and at all ages has been improved by the advent of ‘plyometric training’. 56 ‘Plyometric training’ includes vigorous movements that involve each of the three types of contractions, shortening, isometric and lengthening, as described in the first section. Significant improvements in muscle mass, strength, power and endurance have also been achieved in previously sedentary men and women over 75 years of age through participation in conditioning programmes that include: (i) participation three times per week on alternative days (ii) muscle contractions involving each of the three types of contractions (iii) continuous increments in loading based on improvements in strength and (iv) a duration of 12 weeks or more. 32, 33, 35, 56, 57 The improvements in such training programmes have been increased considerably by the inclusion of lengthening contractions at > 80% of one execution maximum strength, but such programmes require the supervision of professional trainers and great care must be taken not to cause ‘contraction-induced injury’ to participants. 6, 7, 56, 57 The success of the master athletes and of previously sedentary elderly who have undertaken well-designed, carefully administered training programmes indicate that the atrophy, weakness and fatigability usually associated with advancing years can be slowed. Although the loss in the number of fibres within muscles appears immutable, 15 the magnitude of the loss in muscle mass can be ameliorated to some degree by hypertrophy of the fibres that remain. 32, 35

Performance of masters athlete for the marathon run () and weight-lifting (○). Data for the marathon run are taken from the Alan L Jones website (http://home.stny.rr.com/alanjones/AgeGrade.html) data for Masters weight-lifting are from IWF Masters Records December 2006 (men's weight class 85 kg, clean and jerk), available from http://www.iwfmasters.net/records/iwf.men.pdf.

In summary, clearly both immutable changes in skeletal muscle structure and function, as well as an increasingly sedentary lifestyle, contribute to increasing frailty among the elderly. Young people and even adults appear able to extricate themselves without difficulty from the temporary conditions of frailty induced by physical inactivity, injury, starvation or illness, whether voluntarily or involuntarily induced. 23, 50 Although significant gains have been realised in the quality and in the scientific bases for physical conditioning programmes specifically for the frail elderly, 23, 24, 58 the phenomenon of the ‘failure to thrive’ for many of the participants continues to be an incomprehensible aspect of even well-designed physical activity programmes. 8, 58 In the US, the estimated cost of physical frailty among elderly people is in the millions of dollars per year and, with the ever increasing numbers of frail elderly, the doubling time is estimated to be 40 years. 59 Despite the enormity of the increasing cost and the seriousness of the problem, 59 few new insights have been gained and only modest progress has been made towards the provision of successful programmes to resolve the conditions of physical frailty 23 or failure to thrive. 8, 58


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