Aging Muscle
Like many powerlifters, I have been strength training seriously for most of my life. While mostly training alone in my garage, I have participated over the years in powerlifting meets through the USAPL, USPA, and other organizations. I reached the Powerlifting USA Top 100 list in the deadlift on two occasions. Now that I am in my 50s, I find myself worrying about how much my strength will decline as I age. I also look towards the many aging lifting icons whose feats of strength I followed through the years and wonder how long they can keep moving impressive weights. We can find inspirational examples of older lifters. In 2010, Bob Gaynor pulled a 680 lb deadlift at a bodyweight of under 200 lbs when he was already well into his 60’s (16)! While Gaynor’s lifting feats are clearly incredible, he is just one of the many masters lifters who continue to post astounding lifts well past what we might assume to be their prime years. These accomplishments by aging strength athletes suggest that some of our strength losses may be more a state of mind than inevitable predicament. They should inspire us to keep setting goals and training with intensity.
It is well established that regular exercise plays a central role in good health. A recent study of more than 100,000 patients from the Cleveland Clinic reported a significant relationship between cardiorespiratory fitness and reduced risk for all-cause mortality (12). Here, I will make the case that lifelong strength training in particular has scientifically founded benefits. Changes to skeletal muscle structure and function with age have been studied intensively over the past several decades and aging muscle continues to represent a very active field of research. This body of research provides a scientific look into what we can reasonably expect as we age, as well as providing motivation to keep training with purpose.
First the bad news. Most of us begin losing muscle at about the age of 40 – even earlier for those who don’t exercise regularly. The general consensus is that we lose about 1 – 2 % of our muscle mass per year, which means that if we are fortunate enough to reach the age of 80, we might have lost 40 – 50% of our formal skeletal muscle mass! What’s worse, contractile strength declines at an even faster rate of about 2 – 4% per year beginning around age 40 (9, 13). Muscle power is lost at an even faster rate than strength, because our muscles also become slower as we age (13). Before you say to yourself, ‘but that won’t happen to me because I will continue to train!’, think again. Studies of muscle power in aging athletes have documented steady declines in muscle power and performance beginning at around age 50 (14). This rate of decline becomes more precipitous after age 70 and plummets into a frightening free fall after age 80. The significance of these studies of master record holders and other aging competitive athletes is that it can be difficult for researchers to tease out differences between losses in strength due to disuse versus strength declines specifically from aging. Inactivity at any age leads to loss of muscle mass and strength, but this loss is especially pernicious in older people. Since these competitive athletes are highly motivated and maintain dedicated training schedules, their declines in performance represent the best cases scenarios for staving off the effects of aging. Training can help slow age associated loss skeletal muscle mass and function, but it cannot be entirely halted or reversed (8).
Muscle biologists have a name for the loss of skeletal muscle with aging: sarcopenia. The name sarcopenia translates from Greek as ‘poverty of flesh’, alluding to the loss of lean skeletal muscle mass with age (6). Although precise definitions of sarcopenia are subject to debate, some include the decline in muscle strength as being another facet of sarcopenia. More recently, another related term of dynapenia, ‘poverty of strength’, was introduced into the literature after researchers recognized that muscle strength actually declines more rapidly than muscle mass in aging subjects (5, 13). Sarcopenia and dynapenia may well be viewed as normal biological processes, but from the standpoint of the health impacts of aging, they represent major challenges. Indeed, sarcopenia fits within a whole spectrum of serious muscle wasting conditions that include cancer cachexia, sepsis, and rapid skeletal muscle loss following glucocorticoid treatment (13). Losses in muscle mass and function result in a decline in quality of life and the loss of skeletal muscle mass is even an independent risk factor for mortality (7, 17). The factors leading to the loss of voluntary muscle strength aren’t fully understood, but may follow malnutrition, declining circulating hormones like testosterone, and a number of other factors (11). The resulting deficits in the neuromuscular system are related to the loss of motor units, inefficient excitation-contraction coupling, and especially to changes within the muscle tissues themselves (2).
Whole skeletal muscles are assembled from hundreds of smaller functional contractile entities called motor units. A motor unit is comprised of a single motor neuron within the anterior horn of the spinal cord and all of the muscle fibers it controls, or innervates. A typical motor unit includes hundreds of individual fibers controlled by a single motor neuron and these fibers generate force when they receive the command to contract from the motor neuron . An essential mechanism for controlling voluntary muscle force is through motor unit recruitment, which means ‘turning on’ as many motor units needed for a particular task. When we generate maximal force, whether squatting, pressing, or closing a gripper, our ability to generate that force is directly dependent on our ability to recruit as many motor units as possible. Unfortunately, one of the well documented effects of muscle aging is the loss of motor units as a function of age (8, 11, 13). An extreme version of a loss of motor neurons occurs in amyotrophic lateral sclerosis (ALS) – also known as Lou Gehrig’s Disease. In that degenerative condition, the progressive loss of motor neurons eventually and inevitably leads to death. In the case of aging, the number of motor units appear to remain constant up until about age 50, but then steadily declines over time so that by age 80 approximately 50% of the original number of motor units may have been lost (2, 8). The maximum number of muscle fibers within our muscles is fixed by the time of birth and new fibers or motor units are not generated. This means that once a motor unit is lost it may be gone forever.
In some cases, when a muscle fiber loses its motor neuron through degeneration or injury, it may become ‘reinnervated’, when an adjacent motor neuron forms a new synapse with the fiber (2, 11). One of the hallmarks of aging muscle when viewed at a microscopic scale is a clumping of muscle fiber types that is thought to result from this process of neuron loss and reinnervation (2, 3). In healthy young muscle, fiber types are distributed in a more evenly spaced ‘checkerboard’ pattern throughout the muscle. The characteristic observation of these grouped fiber types within the muscles of elderly individuals suggests that the denervation followed by reinnervation represents a common process of aging (3). Even though some denervated fibers may be rescued through reinnervation, the total number of muscle fibers within aging muscles declines with age at approximately the same rate as motor unit loss. Many studies over the years have also reported that during aging, type II motor units disproportionately disappear from muscles, resulting in relative increase in the proportion of type I motor units (1, 8, 11). In the broadest terms, type II motor units are ‘fast’ motor neurons controlling ‘fast’ muscle fibers. These are the motor units most important for explosive force generation (think sprinting, jumping, or heavy squats and power cleans). Slow jogging and other types of endurance training rely more on the slower, type I, motor units. So as we age, our skeletal muscles not only grow smaller, but we are also susceptible to losing our most powerful motor units.
Another likely culprit for the loss in strength with aging is a decline in the ability of a motor neuron to effectively elicit muscular contraction through a process known as excitation-contraction coupling (ECC) (11). The first step in ECC is through the release of the neurotransmitter acetylcholine at the synapse that connects the motor neuron to the muscle fiber. In skeletal muscles, the complex synapse referred to as the neuromuscular junction (NMJ), is where the end of a motor neuron is structurally and functionally connected to the muscle fiber. ECC is based upon a complex series of events that functions like a line of dominos set up to knock one another down. Each individual step in the process ECC depends on the effective completion of the previous step, with the final event being the generation of muscle force. Recent studies have documented changes within the NMJ that lead to a loss in the effectiveness of ECC (11). This means that even when our motor neurons send the signal to contract, our muscle fibers cannot respond as efficiently as they did when we were younger. Research into the functional changes of the NMJ and ECC with aging is ongoing.
It is also well known that changes to the muscle tissues themselves contribute directly to a loss of effective function. In addition to the cited loss of motor units and skeletal muscle fiber number, the remaining fibers typically atrophy. Muscle atrophy describes the reduction of individual muscle fiber diameter and occurs with disuse, aging, and other pathological conditions. Muscle force is functionally related to muscle fiber cross sectional area, so atrophy directly causes muscle weakening. Studies have also revealed that everything else being equal, the muscles from older individuals generate less force and are slower than comparable fibers from younger people. These changes reflect the decline of what is sometimes referred to as ‘muscle quality’, meaning that contractile force and speed is lower in older muscles, even if muscle size is maintained. One aspect of declining muscle quality is that as muscle fibers atrophy, fatty tissue and other connective tissues expand into the spaces left by the retreating muscle tissue. Moreover, studies have documented decline in muscle tissue itself at the cellular and molecular levels that aren’t yet fully understood.
As many readers will already understand, the mechanism of strength gains through resistance training stem from an increase in muscle size known as hypertrophy. Many studies have demonstrated that strength training counteracts the effects of atrophy and that these benefits are even observed when the elderly engage in resistance training. Significantly, the more powerful type II fibers in particular are especially impacted through heavy resistance training. Studies of the cellular and molecular composition of skeletal muscles in bodybuilders and lifters have consistently reported that although both fast and slow fiber types are increased in size, the faster type II fibers comprise a larger proportion of the total muscle. This knowledge should compel any of us interested in maintaining functional strength to fight to maintain our type II muscle fibers. The best way to do that is to train them regularly through heavy resistance training and other kinds of explosive movements like jumping, sprinting, or throwing (1). Don’t expect your general practitioner to have an understanding of the intensity of these exercises, or why they are important for developing and maintaining functional strength. Like most of the general public, many clinicians fail to appreciate the differences between bodybuilding, weightlifting, and other kinds of strength performance training.
In spite of the knowledge that muscle size and function decline with aging, there are numerous studies that provide incentives to keep training and striving for personal bests. Most biological processes following the ‘use it or lose it’ principle and our bodies are no different. Probably the best way to maintain our motor neurons and their muscle fibers is to work them regularly (2). Multiple research studies have reported that resistance training in the elderly results in increases in muscular strength and power, in similar patterns observed for younger individuals (4, 15). The general consensus is that adaptive responses are blunted when compared with younger muscles, but the responses are significant none the less. One study of master athletes (aged 70 – 74 years) found that life-long strength trained athletes exhibited greater strength, rate of force development, and a higher proportion of type II muscle fibers than untrained subjects (1). A new study from the Human Performance Lab at Ball State University reported that life-long endurance training maintained skeletal muscle capillary supply and metabolic enzymes to levels similar to the muscles of younger endurance trained individuals (10). Estimates of physiological age based on maximal exercise performance ranged from 19 – 37 years younger than the chronological age of the master athletes in that study! Many master powerlifters continue to compete into their 60’s and 70’s and post impressive lifts. In my own training, I look for a variety of ways to work my neuromuscular system and challenge myself. In addition to my core powerlifting training, I rotate in rope climbing, trail running, sprinting, box jumps, and kettlebells. I train my grip strength using Captains of Crush grippers, static pinch holds, and juggling shots. My hope is that these training challenges not only keep me engaged mentally, but also exercise my neuromuscular system in unique ways.
Knowing that we are all facing the natural processes of skeletal muscle decline should keep us motivated to stay committed to serious training for functional strength. Challenging ourselves to achieve goals and benchmarks in powerlifting, strongman, or odd lifts can help maintain functional strength across our lifespan. In addition to the obvious benefits to maintaining strength through training, skeletal muscle mass also fulfills other critical functions like serving as a reservoir for amino acids, burning excess energy and staving off obesity, combating insulin resistance and type II diabetes, secreting myokines that communicate with other organs, and in recovering from illness and injury (7, 17). Serious strength training may seem like an odd pursuit to the general public, but the harder we train the longer and healthier lives we may enjoy.
References
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