“People think that once you got to a certain age, your muscles didn’t grow any more – that in fact muscles waste with age,” Yarosheski.
Aging is associated with alterations in body composition. There appears to be a loss of muscle mass with aging and a concomitant increase in the percentage of fat in the muscle. Also, it has been noted that total body water decreases from maturity to senescence. Cohn and co-workers determined that skeletal muscle protein is reduced and non-muscle protein is maintained with advancing age.
Lexell et al. , in a study of cadavers ages 20 to 80 years old, demonstrated that girth measurements were inadequate for accurately determining the cross sectional area of muscle, as fat and connective tissue replaced muscle tissue with increasing age. There was a decline of muscle mass beginning around age 30, with a 10%, decrease by age 50, and a 40 to 50% decline by age 80. Another study, using subjects from 30-70 years of age demonstrated a decline in muscle mass of 23% in men and 22% in women.
Total body nitrogen losses are closely related to losses in total body calcium, and suggest the loss of skeletal muscle is related to the reduced bone density seen in the elderly
The subjects show changes concomitantly and relate all these changes to the aging cycle.
Increased fat and connective tissue in the muscle
Decreased muscle mass (decreased nitrogen)
Decreased bone density (decreased calcium)
But are these the result of aging? Past beliefs tell us they are. The metabolic rate of the body is believed to decline with age. The Baltimore Longitudinal Study of Aging (BLSA) “found that resting metabolic rate evidenced no decline up to age 45 years, but with each succeeding decade the resting metabolic rate decreased significantly”. The authors of the study measured 24-hour urinary creatine excretion as a means to correlate metabolic rate with total muscle mass. From this they concluded that “the loss of muscle mass with aging accounts for most of the age-related decrease in resting metabolic rate”.
All movement is the result of centrally processed commands being carried out by a peripheral organ system, skeletal muscle. The commands are translated into force and the forces applied by means of an intricate system of links and levers to produce purposeful movement.
The final common pathway of both central and peripheral motor commands is the motor unit. Therefore, the demonstration of maximal muscular strength should be thought of as a specific motor skill, dependent not only on the individual’s complement of motor units, but also his or her ability to activate them in the most optimal pattern.
Most studies show a decline in strength with age. Strength losses appear to vary with muscle groups and age, but most studies show consistent trends in both men and women. Frontera et al., concluded that the loss of muscle mass is the main factor associated with the age-related loss of muscular strength, rather than a deterioration in the contractile capacity of the muscle. Young et al. also found the decrease in muscle size associated with aging accounts for some of the reduction in muscle strength. These studies do not support the idea that aging skeletal muscle becomes intrinsically weaker.
Table I, from Vandervoort , reports the results of studies comparing young and elderly men and women using voluntary isometric strength in specific muscle groups as the dependent variable. The table demonstrates the decline in voluntary isometric strength found in 18 strength studies using four different muscle groups (knee extensors, ankle plantarflexors, elbow flexors, and handgrip (wrist,
carpal, metacarpal, and phalangeal flexors)). The ages represented in the studies cover the last four decades of normal human life expectancy (6th to the 10th decades). As can be seen from the table, the average decline in strength by the eighth decade was 30% in males and 59% in females. From the eighth to the tenth decade, males experienced a further decline to 44% of a young adult’s strength; while females experienced an additional 24% decrease in voluntary isometric strength to an average of 50% of a young adult’s strength levels.
Booth concludes that strength is maintained through 50 years of age. After 50 years of age the following losses are documented:
50-60 years 15% decline in strength
60-70 years 15% decline in strength
70-80 years 30% decline in strength
80-90 years 30% decline in strength
These declines are similar to the declines demonstrated by Vandervoort in Table I.
Larson et al. studied 114 males aged 11 to 70 years, finding quadriceps strength increased to age 30 and stayed relatively constant to age 50. Between the ages of 50-70, dynamic strength decreased 24% and speed of movement declined 36%. Vandervoort reports similar findings in his own strength studies. Healthy people in their 70s demonstrate a 20% decline in strength; by their 80s a 40% decline compared to young adults is evident. Vandervoort states that the very old (over 85 years) show an even greater decline in strength of 50% or more
Table I :
Voluntary Isometric Strength of Elderly Men and Women Compared to Young Adults
|Source (grouped by muscle)||Age (by decade)||Sex||% of Young Adult*||% Decline|
|Larsson et al. (1979)||70||male||75||25|
|Murray et al. (1980)||80-90||male||55||45|
|Clarkson et al. (1981)||60-80||male||61||39|
|Young et al. (1984)||80||female||65||35|
|Murray et. al. (1985)||80-90||female||63||37|
|Young et al. (1985)||80||male||61||39|
|Davies et al. (1986)||70-80||female||72||28|
|Davies et al. (1986)||70-80||male||62||38|
|Vandervoort & McComas (1986)||90-100||female||45||55|
|Vandervoort & McComas (1986)||90-100||male||55||45|
|Petrella et al. (1989)||70-80||male||57||43|
|Fisher & Birren (1947)||60-70||male||83||17|
|Mathlowetz et al. (1985)||80-100||female||41||59|
|Mathlowetz et al. (1985)||80-100||male||47||53|
|Kaliman et al. (1990)||90||male||66||34|
|McDonagh et al. (1984)||70-80||male||80||20|
|Clarkson & Dedrick (1988)||70-80||female||85||15|
|Mean of elderly groups divided by mean of young adult groups*|
Muscle Fiber Types
Over the years, various classification systems have been developed to describe the differing capabilities of skeletal muscle. The oldest and simplest was the fast twitch/slow twitch – red/white classification. As chemical, biologic, electromyographic, and histologic capabilities became more precise other systems with up to six or seven subclassifications have been used. The most common classification system identifies three fiber types (I, IIa, IIb) based on the work of Brooke and Kaiser. Another system with three types of fibers was developed in 1972 by Peter et al. (Slow Oxidative, Fast Oxidative Glycolytic, Fast Glycolytic) and the tendency exists to equate the two classification systems although considerable overlap in oxidative capability exists among Type IIa and IIb fibers, more overlap than is inherent in the SO, FOG, FG system.
This paper will generally use the classification system of Brooke and Kaiser since most of
the literature referenced uses the Type I, Type IIa, Type IIb, Type IIc system to discuss fiber
types. The following discussion is intended as a review and is not an exhaustive treatment of the
subject. It is only intended to refresh the reader’s memory with regards to the
physiological characteristics of the various muscle fiber types.
Type I muscle fibers are innervated by small diameter, slow conducting motor nerves (30 – 45 m/s). They have slow contraction speeds (90 – 110 ms) and minimum discharge frequencies in the range of 7 – 15 contractions per second (32). They have a low activation threshold and are usually the first fibers activated in voluntary muscular contractions. They are active throughout a strength performance and are the “first on and last off” muscle
The Type I fibers are small diameter fibers; and have a low level of myosin ATPase activity and a slow reacting isoform of myosin. A poorly developed sarcoplasmic reticulum and a poor troponin affinity for calcium provides evidence of the fiber’s poor glycolytic and phosphogen system capacity. Low levels of phosphocreatine and glycogen, but high levels of triglyceride stores and myoglobin, combined with high levels of mitochondrial enzyme activity point to the fiber types’ high capacity for oxidative metabolism.
When these fibers contract, they produce very low twitch tensions, but the amount of force produced per unit of energy expended is high; resulting in a very efficient force producing capability. They are basically fatigue resistant and have many mitochondria. A large number of capillaries in relation to muscle fibers (capillary density) limits the need for glycogen storage. The elastic capacity of Type I fibers is low, providing a physiologic and biologic explanation for the better power performances of individuals with low percentages of Type I fibers. Normal subjects generally have approximately 45% Type I fibers in their leg muscles, while sprinters may have as little as 23% of this fiber type, and elite distance runners may have 80% Type I fibers.
Type II fibers are divided into three subtypes – a, b, and c. Type Ila and Ilb fibers are large diameter fibers, served by large diameter, fast conducting motor nerves (40 – 55 m/s). They have fast contraction times (40 – 84 ms) and discharge frequencies of 16 – 35 Hz or more. Type II fibers are more difficult to activate due to higher recruitment thresholds. Type IIb fibers are sometimes considered very difficult to activate under voluntary conditions for untrained individuals and are generally considered “last on and first off” in terms of recruitment during voluntary muscular contractions.
Type II fibers generally have high myosin ATPase activity, fast reacting myosin, a highly developed sarcoplasmic reticulum, high troponin affinity for calcium, and high levels of phosphocreatine and glycogen storage. Type IIa fibers also have a large number of mitochondria, high mitochondrial enzyme activity, and high levels of oxidative enzyme activity. Type IIa fibers have moderate levels of triglyceride storage, an intermediate number of capillaries per muscle fiber (capillary density), and moderate levels of myoglobin. Type IIb fibers have few mitochondria and very low levels of mitochondrial enzyme activity. Low capillary density, triglyceride stores, myoglobin content, and oxidative enzyme activity support the hypothesis that these fibers make up the highly fatigable, hard to recruit, high force motor units sometimes referred to as Fast Glycolytic.
Type II fibers are highly elastic. This capability leads to the increased force/power potential of elite strength athletes. Normals have about 50% of the fibers in their leg muscles made up of Type II fibers. Elite distance runners may have as little as 5% of their total leg musculature as Type IIb fibers and only 20% as Type II. Sprinters may have as much as 75% of their leg musculature made up of Type II fibers, with an approximate 60/40 split between Type IIa and IIb respectively.
The percentage of the various fiber types in a person’s muscles are predominately determined by genetic factors, though training may play some role in the ultimate fiber composition of specific muscles. Type IIc, or undifferentiated muscle fibers are present in most muscles.
In humans, infants are born with a approximately 40% Type I fibers, 30% Type IIa fibers, 10% Type IIb fibers, and 20% Type IIc or unclassified fibers. In the neonate, these fibers (IIc) are believed to have the ability to enter the fiber pool as either I, IIa, or IIb fibers. For comparison, the amount of IIc fibers in an adult is negligible, 2 – 3% or less in the literature. Some research points to the theory that, depending on the training stimulus the muscle is exposed to, they may ultimately enter the fiber pool as either Type I or Type II fibers (53). Other research seems to suggest that training will result in their ultimate expression as either Type IIa or IIb fibers.
Where they (Type IIc fibers) come from or what specific purpose they serve is unknown. One author goes so far as to suggest that they are merely an anatomical anomaly that provides academics fodder for the publication mill. The percentage of fibers of this type appears to be fairly constant in the literature on training adaptations, possibly due to the consistency of the training stimulus.
For our purposes it is necessary to keep in mind that all human skeletal muscle possesses all of the various subtypes of muscle fibers. The fiber type is determined by the nerve supplying the motor unit. The motor unit is composed of only one type of muscle fiber type, even though the whole muscle is composed of all fiber types.
The performance characteristics of intact skeletal muscle are the result of the fiber composition of the whole muscle (percentages of the various fiber types) and the type of training or lack of training the muscle has been exposed to over time. It is accepted that each of the various fiber types have specific performance and physiologic characteristics. It has also been shown that muscle fiber type recruitment patterns are fairly static and are determined by what Henneman called the Size Principle Simply stated the Size Principle postulates that the size of the motor nerve determines the velocity of conduction of the neural impulse. The faster the conduction velocity of the nerve the higher the threshold for the propagation of the impulse. The size of the motor nerve also determines the characteristics of the muscle fibers in the nerve’s motor unit. Small diameter, slow conduction velocity, low threshold nerves activate small diameter, slow contracting, low force, low threshold, fatigue resistant muscle fibers. Large diameter, fast conduction velocity, high threshold nerves activate large diameter, fast contracting, high force, high threshold, fatigable muscle fibers.
The nerve supplying the fiber is the ultimate determinant of the fiber type, due to the trophic effect of the motor nerve. Animal studies involving cross innervation have supplied information on the effects of the nerve in determining the physiologic characteristics of the fiber types. Laboratory rats whose muscle fibers were cross innervated appeared to experience muscle fiber type transformation from slow to fast and vice versa.
Training and Fiber Types
In humans, training appears to affect the percentage of Type IIa and IIb fibers, as well as the cross sectional area of the various fiber types. A 1995 study by Kraemer et al. measured the percentages of Type I, IIa, IIb, and IIc fibers; as well as the cross sectional areas of the various fiber types in the vastus lateralis. Training was performed four days per week for three months using the principle of periodized training (two heavy days and two moderate days of training per week). Physically fit males (n=40) were assigned to one of five groups, strength training (n=9), combined strength training and high intensity endurance training (n=9), high intensity endurance training (n=8), upper body strength training and high intensity endurance training (n=9), and a nonexercising control group.
Total body strength training, using 5 RM loads two days per week and 10 RM loads two days per week, resulted in significant increases in the fiber cross sectional area of all fiber types, except Type IIb (which increased, however it was not a statistically significant increase). A significant increase in Type IIa fiber type percentage and a significant decrease in Type IIb fiber type percentage was also observed.
High intensity endurance training, which included 2 days of interval training and two long duration runs per week, resulted in significant decreases in fiber type cross sectional area for Type I and IIc fibers and a trend toward reduced cross sectional area for Types IIa and IIb. Endurance training also resulted in significant increases in the percentage of Type IIa and IIc fibers; and a significant decrease in the percentage of Type IIb fibers.
Combined total body strength training and high intensity endurance training resulted in a significant increase in the percentage of Type IIa fibers and a significant decrease in the percentage of Type IIb fibers. Fiber cross sectional area was reduced for Type I and Type IIb fibers, and increased for Type IIa and IIc fibers; although only the increase for Type IIa fiber areas was statistically significant.
The combination of upper extremity strength training and high intensity endurance training lead to significant increases in the percentage of Type IIa and IIc fibers and a significant decrease in the percentage of Type IIb fibers. The changes in fiber cross sectional areas were not significant for any fiber type but displayed a slight trend toward reduced fiber area for all fiber types with Type IIc and IIa showing the least effect.
Muscle Strength Loss and Fiber Type in Aging
The decline in strength we have seen demonstrated in the literature is related to the decline in muscle mass. But is there a selective decline among the different fiber types? According to Rogers & Evans Lexell et al. found, “There is no significant alteration in mean fiber type percentage or preferential loss of either Type I or Type II muscle fibers with age.”
Larsson et al., found a decline in muscle mass, but also demonstrated a decline of Type II fiber areas of 36% between ages 40 and 60 years. Further studies by Lexell found there was no significant change in Type I muscle fiber size with age when studying 20 to 80 year olds. However, there was a 59% reduction in Type II fiber size between the ages of 20 and 80 years. Klitgaard et al. hypothesized that changes in skeletal muscle with aging appear to be mainly related to a larger relative area of Type I fibers, as a result of a selective atrophy of Type II fibers. Coggan et al. found a preferential atrophy of Type II fibers when comparing young and old subjects. In this study, males demonstrated a 13% decline in Type IIa and a 22% decline in Type IIb fiber area; while females had a 24% decline in Type IIa and a 30% decline in Type IIb fiber area. Table 2 is adapted from Vandervoort, information on the percentages of the various fiber types and additional studies were added when the information was available.
As Table 2 illustrates, most of the decline in muscle strength with age appears to be related to a decline in Type II muscle fiber area. Type II or fast twitch fibers possess a low aerobic capacity They are activated by high threshold, high velocity motor nerves and are seldom used under the stress of most people’s activities of daily life. The study of Klitgaard et al. comparing young sedentary males with elderly sedentary controls, elderly strength trainers, elderly runners, and elderly swimmers makes a strong case for this interpretation of the data.
In the study by Klitgaard et al. , the performances of the elderly strength trainers were similar to the young controls; while the performances of the elderly swimmers and runners were indicative of a statistically significant difference between the young controls and the elderly exercisers. The fiber type areas were similar when comparing the elderly controls and the elderly swimmers and runners. These results were significantly different from the fiber type areas of the young controls and the elderly strength trainers. The elderly strength trainers demonstrated cross sectional areas similar to the young controls and the greatest percentage of Type II fibers of all groups studied. The authors state that, “these results seem to suggest that strength training can counteract the age-related changes in function and morphology of the aging human skeletal muscle”.
Table 2 : Muscle Fiber Size and Number in Elderly Humans
|Aniansson et aL (1986)||73 – 83||Decreases in Type IIa 14%,
IIb 25% fiber areas
|Clarkson et al (1981)||55 – 73||Decreases in Type II fiber areas|
|Essen-Gustavsson & Borges (1986)||78 – 80||Decreases in Type I &. II fiber areas|
|Grimby et al (1982)||78 – 82||Decreases in Type II fiber areas|
|Larsson et al. (1978)||40 – 60||Decreases in Type II fiber areas,
36% in males
|Larsson et al. (1979)||60 – 65||Decreases in Types I &. II fiber areas|
|Lexell et al. (1988)*||80-83||Types I & II fiber number reduced 50%|
|Lexell et al. (1988)||20 – 80||Type II fiber atrophy 59%|
|Oertel (1986)*||70 – 80||Type II fiber atrophy|
|Coggan et al. (1992)||25 – 65||Type II fiber atrophy
IIa 13% male, 24% female,
IIb 22% male, 30% female
|*Involved analysis of tissue obtained at autopsy. Other studies used the needle biopsy technique on elderly volunteers.|
Motor Unit And Aging
Studies show that anterior horn cells decline after age 60. “Lexell and Downham
state that segregative fibers were common in young muscle, a random mosaic-like pattern
predominated in men between ages 30 and 50 years, and over 60 years an excess of enclosed
fibers were evident. This fiber-type grouping implies that the fiber population is continually in a state of transition throughout life and that denervation and reinnervation occur in normal muscle during aging.” Booth also discusses Lexell’s work reporting that,
As a result of the loss of motor units, it is inferred, some of the muscle fibers from the lost motor unitbecome reinnervated by the other remaining motor units. The reason for this inference is based upona) the enlargement of motor unit size with aging, and b) muscle fibers within a given area of themuscle becoming more homogeneous in fiber type, i.e., fiber type grouping. The changes in fiber type arrangement with aging have been interpreted by Lexell to mean that a neurogenic process is likely tobe one of the major contributors to the age related reduction in muscle volume. Remodeling of motor nerve terminals appears to be a lifelong process in animals.
Astrand reports similar findings. With age there is a decrease in muscle strength with a concomitant reduction in muscle mass – the age related loss of muscle fibers is related to a loss of motor neurons.
The force generating capacity of the muscle is unchanged and no signs of denervation in aging muscle is evident. However, the muscle fibers per motor unit have been reported to increase, which corresponds with the loss of some of the motor neurons, compensated for by peripheral sprouting from healthy nerve terminals and thereby reinnervation of muscle fibers that lost their original motor neurons.
We have begun using this information at our facility, with good result in a 43-year-old stroke victim. The patient had a stroke 15 years ago that resulted in his becoming a left hemiplegic. Approximately one year ago he began training with his effected arm doing eccentric elbow extension, three one minute to one and a half minute repetitions, three times per week. Within one month he was able to abduct his shoulder to 90° without demonstrating his characteristic flexor pattern. He can currently flex his elbow to 90° and abduct his shoulder to 90° without the flexor pattern being initiated. His exercise load has increased by over 100% since the program was started. The patient’s doctor recently discovered a palpable increase in grip strength and documented a decreased need for hypertensive agents as a result of the strength training program.
Aging Or Lack Of Exercise
The studies thus far were mainly undertaken with less active, often sedentary individuals. Marie Fiatarone, M.D., states, “Older people probably lose more strength than they need to, even if they remain healthy and have no disease, simply because they decrease their activity level. What we have in the past called aging is probably aging, plus disuse, plus malnutrition, plus disease. Only a moderate amount of muscle dysfunction is due to aging”. Along this same line Astrand quotes Rowe and Kahn stating,
Research in aging has emphasized average age related losses and neglected the substantial heterogeneity of older persons. The effect of the aging process itself hasbeen exaggerated, and the modifying effects of diet, exercise, personal habits, and psychosocial factors underestimated. Within the category of normal aging; a distinctioncan be made between usual aging, in which extrinsic factors play a neutral or positiverole. Research on the risks associated with usual aging and strategies to modify them should help elucidate how a transition from usual to successful aging can be facilitated.
Astrand further states that “physical training can readily produce a profound improvement of function essential for physical fitness in old age and thus effectively postpone physical deterioration for some 10 to 20 years”. These are bold statements; but Rogers and Evans have concluded that the muscle’s decline in force generating capacity should not be considered an inevitable consequence of aging. Research by Klitgaard et al. supports this theory. In a study comparing young 28 year old subjects to 68 year old sedentary controls, strength trainers, swimmers, and runners the findings were nothing short of amazing. The elderly exercisers had all been training for at least a decade prior to participation in the study, with the strength trainers having 12-17 years of strength training experience. The strength trained seniors demonstrated similar performance capabilities when compared to the 28 year olds. Klitgaard reports, “the elderly strength trained subjects had maximal isometric torques, speed of movement, cross-sectional area, specific tensions and content of myosin and tropomyosin isoforms in both muscles studied identical to those of the young controls.” As previously reported, the study found, “these results seem to suggest that strength training can counteract the age related changes in function and morphology of the aging human skeletal muscle”. The study compared the vastus lateralis and the biceps brachii in 28-year-old sedentary controls, elderly sedentary controls, elderly runners, elderly swimmers, and elderly strength trainers. Table 3A shows the fiber type distribution in the vastus lateralis.
A. Fiber Type by Percentage – Vastus Lateralis
|Type I||Type Ila||Type IIb||Type Ilc|
|Old, controls||57+5||26+3||16+3||1 ±O|
|Old, swimmers||57+5||32+4||10+4||1 ±O|
|Old, strength trained||44+6||42+2||13+4||1 ±O|
The percentage of Type II fibers, those fibers whose area and number had been specifically shown to decline with aging, demonstrate a 31% increase in
fiber type percentage compared to the untrained controls! The results of similar measurements using the biceps brachii demonstrate an even more significant change in fiber type composition with strength training in elderly males; as demonstrated in Table 3 B.
B. Fiber Type by Percentage – Biceps Brachii
|Type I||Type IIa||Type IIb||Type Ilc|
|Old, swimmers||57+5||16±4||26+5||1 ±0|
|Old, strength trained||0||53+5||38+4||19+4|
Aging, Cardiovascular Function, and Exercise
Maximal heart rate peaks at about 10 years of age and decreases from that point at a rate of about 1 beat per minute per year. Research has shown that the maximal heart rate does not adapt to chronic exercise and therefore is not a mutable factor in maximal cardiac output. The reasons for this decline are unknown at the present time though various hypotheses exist; from those pinpointing changes in catecholamine effects on the heart which diminish with age, to changes in the number of pacemaker cells, to changes in the volume of the sinoatrial node with aging. The hypothesized causes vary from the heart itself to the neural input for cardiac control.
The fact that aging results in a decline in maximal oxygen uptake, maximal heart rate, and metabolic rate is fairly well established. The rate of decline has been the subject of a number of studies as well. The purpose of this section is to provide the reader with an overview of the pertinent findings related to cardiovascular function and exercise.
The standard measure of overall fitness, Maximal Oxygen Consumption (Max VO2) declines with age. This age related decline is thought to be, at least partially, the result of the decline of maximal cardiac output. Cardiac output is the product of heart rate (number of beats per minute) and stroke volume (amount of blood pumped with each beat). The causes of the age-related decline in maximal heart rate are unknown and are not amenable to exercise training. The decrement in maximal stroke volume can be improved by exercise training and this capability is preserved with advancing age. Elderly subjects have demonstrated enhanced systolic and diastolic properties following training. The diastolic filling capability of the aged heart can be improved with endurance exercise, leading to an increased maximal stroke volume. The rate of systolic function, or ejection, (pumping the blood out of the heart) appears faster in older trained subjects. The general consensus is that, physical activity can stimulate gene expression in the heart, leading to improved cardiac function, though it is unknown whether this is possible throughout the entire lifespan.
Another explanation for the age-related decrease in Max V02 is the loss of skeletal muscle in the elderly . Since Max V02, is a measure of oxygen extraction capability, the loss of metabolically active tissue would definitely affect the use of oxygen. A significant loss of muscle tissue would, theoretically, reduce the body’s ability to use oxygen and could account for most of the decline observed in elderly subjects.
Long term endurance training leads to cardiovascular and neuromuscular adaptations that increase the functional capacity of the individual. Most, if not all of these adaptations are evident throughout the lifespan. All systems are affected in these changes and a complex interrelationship exists among the observed adaptations. The following is a list of some of the adaptations that could help improve the functional capabilities of the elderly.
- Resting bradycardia, (decreased resting heart rate).
- Decreased heart rate and systolic blood pressure response at any submaximal workrate, thereby reducing myocardial oxygen requirements, resting blood pressure, and possibly reducing or eliminating the need for anti-hypertensive medications.
- More rapid recovery after exercise.
- Increased blood flow to exercising skeletal muscles, possibly resulting in greater functional capabilities in ADLs and increases in vascularization of ischemic musculature, especially in patients with peripheral vascular disease.
- Increased maximal cardiac output, as a result of better systolic and diastolic function of the heart.
- Increased arterial-venous oxygen differences caused by greater extraction of oxygen by working muscle, enables increased oxidative metabolism of fuel substrates and the regeneration of more high energy phosphates for the performance of muscular work. The capability for increased oxidative metabolism may result in longer periods of activity and shorter periods of inactivity, resulting in greater caloric expenditure, therefore reducing the need for dieting to control changes in body fatness.
- Increased whole body insulin sensitivity, reducing the risk for Type II diabetes and possibly reducing the insulin dosage for older Type I diabetics.
Aging, Bone Loss, and Exercise
Bone loss with advancing age is generally accepted as a given. In older, postmenopausal women, leg and hand fractures are increased by 40 to 80% for each standard deviation reduction in appendicular bone mass (measured at the radius and calcaneus). Research has demonstrated that appendicular bone mass can be used to predict the risk of nonspinal fractures and bone mass in the hip and spine.
A number of factors are related to bone mass in older women. Multivariate regression analysis found that estrogen use, Type II diabetes, thiazide use,increased weight, greater muscular strength, later onset of menopause, and greater height were independently and positively associated with greater bone mass in 9704 ambulatory, nonblack women (average age at enrollment in the study – 71.1 years).
A strong inverse relationship existed between age and bone mass with an average decrease of 1% per year after age 65. Grip strength, elbow extensor torque, hip abductor torque, and knee extensor torque were all found to be positively related to bone mass, even after adjusting for individual differences in body weight. Bone mass measured at the distal radius demonstrated an almost perfect 1% increase per 1 kg increase in grip strength (4.9%/5 kg).
A 10 cm increase in height resulted in a 5.7% increase in calcaneal bone mass. An exercise program resulting in a 2000 kCal/week energy expenditure (approximately 20 minutes of jogging per day for 5 days) was associated with a 2% increase in distal radius bone mass and a 3.9% increase in calcaneal bone mass.
Interestingly, in Bauer et al.’s study, no association was found between the use of calcium or vitamin D supplements and increased bone mass. However, a weak association existed for current calcium intake from dietary sources (1.1% increase in distal radius bone mass). Calcium intake from milk as a
teenager, between 18 and 50, and after 50, adjusted for current intake, was related to increased bone mass. Women who drank milk at every meal from ages 18 to 50, had 3.1% greater bone mass than women who rarely or never drank milk.
Increased body weight and muscular strength were found to be two of the strongest predictors of increased bone mass, while age was one of the best predictors of decreased bone mass. The authors of this study state that their findings do not support the idea that increased physical activity leads to increased bone mass in older women, however two of their strongest predictors – body weight and muscular strength tend to dispute that finding.
Logic, Wolff’s Law, and the Law of Conservation of Energy require that the bone mass of a heavier person be greater than the bone mass of a lighter person. The strength and energetic demands of performing ADLs for a heavier person are greater than those same demands for a lighter person. A frequently overlooked fact in weight loss programs is the fact that overweight persons have increased their muscle mass simply by moving their bodies on a daily basis. Carrying 20 to 30 extra pounds of fat is equivalent to putting on a weighted vest and going through the day; it amounts to an overload. In fact the process of gaining weight is, in reality, a perverse form of progressive resistance exercise.
All of the previous information on bone mass and aging was derived from the study by Bauer et al.. Its significance lies in the sample size and the large number of variables investigated. A literature review by Gutin and Kasper provides a better view of what research has shown with regards to osteoporosis and exercise. One hundred and fourteen papers were reviewed in this article.
The authors conclude that cross sectional studies fail to present a consistent picture of the relationship between activity and bone mass. The fact that athletes involved in strength/power sports have greater bone mineral density and hypertrophy is confounded by the possibility that individuals with
better bone mass may choose to participate in those types of sports rather than the sport participation leading to greater bone mass and bone mineral density.
Prospective studies are reported to, at least partially, support the idea that vigorous and varied weight bearing regimens can increase bone mass and bone mineral density. Strenuous aerobic and strength training exercise have been shown, in number of studies, to enhance bone health in humans. At least a dozen studies cited, using postmenopausal women as subjects, have demonstrated either increases in bone mass or reduced rates of bone loss. Some of these studies are thought to demonstrate a reversing of postmenopausal bone loss. The need to continue the training in order to maintain the desired effect and the trainability of very old persons are emphasized in this paper.
The key findings of research related to bone loss with aging are the following:
- Older individuals, who have consistently been active over their
lifespan, generally, exhibit enhanced bone mineral density and bone mass.
- Increased muscular strength and body mass are related to increased bone mass.
- Exercise programs that include vigorous aerobic activity and strength training lead to increased bone mass and density, however mere weight bearing exercise (like walking) is relatively ineffective in reducing or preventing bone loss in postmenopausal women.
- The ability of the elderly to benefit from vigorous exercise intervention to reduce bone loss is good, their trainability does not to appear to be seriously compromised.
- The best exercise intervention for improved bone health should include not only vigorous aerobic exercise but a total body strengthening program using resistive exercises done two to five times per week.
While many scientists are adverse to supposing that association or even strong correlation implies causation, we believe many researchers are missing the forest for the trees when speaking about the relationship between activity and bone mass. Strength training and vigorous activity are not just related to skeletal strength, as we have previously stated, such activities may logically be assumed to cause adaptation that increases the strength of the skeletal system.
A 1996 review article by Bailey, Faulkner, and McKay affirms this point of view. One of the article’s conclusions is that activities which increase muscular strength and work all large muscle groups should be encouraged since these activities “can enhance bone acquisition.”
Our discussion of exercise’s effects on bone mass will close with an excerpt from Bailey et al., which restates our point about the reluctance of some scientists to take the “leap of faith” and advocate the theory that strength training and vigorous activity causes improvements in bone mass and increases in bone mineral density.
Heavy and prolonged physical activity has always been a major determinant of human structure and function. The genetic makeup of humans remains adapted for circumstances as they existed 10,000 years ago, before the domestication of plants and animals and the rise of agriculture. Humans evolved as active animals designed for an environment demanding high levels of activity. Thus,
our present relatively sedentary lives may be out of step with our genetic makeup, which remains adapted to another time.
Human energy expenditure requirements have declined over the past 10,000 years, and the decline has been most marked during the twentieth century. Taking this lifestyle difference into consideration, one would expect early humans to have a relatively greater skeletal mass and denser skeletons than present-day people, and anthropological studies have confirmed this. Although this genetic argument does not prove that physical activity is necessary for skeletal health, it does suggest that we may be playing a dangerous game with our heritage and that we should not forget the preeminent role played by mechanical loading through physical activity, as it applies to bone mineral acquisition during growth.