Age-related skeletal muscle atrophy appears to be a muscle group-specific process, yet only a few specific muscles have been investigated and our understanding in this area is limited. This review provides a comprehensive summary of the available information on age-related skeletal muscle atrophy in a muscle-specific manner, nearly half of which comes from the quadriceps. Decline in muscle-specific size over ~50yr of aging was determined from 47 cross-sectional studies of 982 young (~25yr) and 1,003 old (~75yr) individuals and nine muscle groups: elbow extensors (-20%, -0.39%/yr), elbow flexors (-19%, -0.38%/yr), paraspinals (-24%, -0.47%/yr), psoas (-29%, -0.58%/yr), hip adductors (-13%, -0.27%/yr), hamstrings (-19%, -0.39%/yr), quadriceps (-27%, -0.53%/yr), dorsiflexors (-9%, -0.19%/yr), and triceps surae (-14%, -0.28%/yr). Muscle-specific atrophy rate was also determined for each of the subcomponent muscles in the hamstrings, quadriceps, and triceps surae. Of all the muscles included in this review, there was more than a 5-fold difference between the least (-6%, -0.13%/yr, soleus) to the most (-33%, -0.66%/yr, rectus femoris) atrophying muscles. Muscle activity level, muscle fiber type, sex, and timeline of the aging process all appeared to have some influence on muscle-specific atrophy. Given the large range of muscle-specific atrophy and the large number of muscles that have not been investigated, more muscle-specific information could expand our understanding of functional deficits that develop with aging and help guide muscle-specific interventions to improve the quality of life of aging women and men.

Skeletal muscle health has been shown to benefit from regular consumption of cyclooxygenase (COX) inhibiting drugs. Aspirin, especially at low doses, is one of the most commonly consumed COX inhibitors, yet investigations of low dose aspirin effects on skeletal muscle are nonexistent. The goal of this study was to examine the efficacy of low dose aspirin on skeletal muscle COX production of the inflammatory regulator prostaglandin (PG) E2 at rest and following exercise. Skeletal muscle biopsies (vastus lateralis) were taken from eight individuals (4M, 4W; 25±1y; 81.4±3.4kg; VO2max: 3.33±0.21L/min) before and 3.5 hours after 40 minutes of cycling at 70% of VO2max for the measurement of ex vivo PGE2 production. Muscle strips were incubated in Krebs-Henseleit buffer (control) or supplemented with one of two aspirin concentrations that reflected blood levels following a low (10µM; typical oral dose: 75-325mg) or standard (100µM; typical oral dose: 975-1000mg) dose. Low (-22±5%) and standard (-28±5%) dose aspirin concentrations both reduced skeletal muscle PGE2 production, independent of exercise (P<0.05). There was no difference in PGE2suppression between the two doses (P>0.05). In summary, low dose aspirin levels are sufficient to inhibit the COX enzyme in skeletal muscle and significantly reduce production of PGE2, a known regulator of skeletal muscle health. Aerobic exercise does not appear to alter the inhibitory efficacy of aspirin. These findings may have implications for the tens of millions of individuals that chronically consume low dose aspirin.

Skeletal muscle size is an important factor in assessing adaptation to exercise training and detraining, athletic performance, age-associated atrophy and mobility decline, clinical conditions associated with cachexia, and overall skeletal muscle health. Magnetic resonance (MR) imaging and computed tomography (CT) are widely accepted as the gold standard methods for skeletal muscle size quantification. However, it is not always feasible to use these methods (e.g., field studies, bedside studies, large cohort studies). Ultrasound has been available for skeletal muscle examination for more than 50 years and the development, utility, and validity of ultrasound imaging are underappreciated. It is now possible to use ultrasound in situations where MR and CT imaging are not suitable. This review provides a comprehensive summary of ultrasound imaging and human skeletal muscle size assessment. Since the first study in 1968, more than 600 articles have used ultrasound to examine the cross-sectional area and/or volume of 107 different skeletal muscles in more than 27,500 subjects of various ages, health status, and fitness conditions. Data from these studies, supported by decades of technological developments, collectively show that ultrasonography is a valid tool for skeletal muscle size quantification. Considering the wide-ranging connections between human health and function and skeletal muscle mass, the utility of ultrasound imaging will allow it to be employed in research investigations and clinical practice in ways not previously appreciated or considered.

Prostaglandin (PG) E2 has been linked to increased inflammation and attenuated resistance exercise adaptations in skeletal muscle. Nonaspirin cyclooxygenase (COX) inhibitors have been shown to reduce these effects. This study examined the effect of low‐dose aspirin on skeletal muscle COX production of PGE2 at rest and following resistance exercise. Skeletal muscle (vastus lateralis) biopsies were taken from six individuals (4 M/2 W) before and 3.5 hr after a single bout of resistance exercise for ex vivo PGE2 production under control and low (10 μM)‐ or standard (100 μM)‐dose aspirin conditions. Sex‐specific effects of aspirin were also examined by combining the current findings with our previous similar ex vivo skeletal muscle investigations (n = 20, 10 M/10 W). Low‐dose aspirin inhibited skeletal muscle PGE2 production (p < 0.05). This inhibition was similar to standard‐dose aspirin (p > 0.05) and was not influenced by resistance exercise (p > 0.05) (overall effect: −18 ± 5%). Men and women had similar uninhibited skeletal muscle PGE2 production at rest (men: 1.97 ± 0.33, women: 1.96 ± 0.29 pg/mg wet weight/min; p > 0.05). However, skeletal muscle of men was 60% more sensitive to aspirin inhibition than women (p < 0.05). In summary, the current findings 1) confirm low‐dose aspirin inhibits the PGE2/COX pathway in human skeletal muscle, 2) show that resistance exercise does not alter aspirin inhibitory efficacy, and 3) suggest the skeletal muscle of men and women could respond differently to long‐term consumption of low‐dose aspirin, one of the most common chronically consumed drugs in the world.

There is some evidence that the age-associated change in skeletal muscle mass is muscle specific, yet the number of specific muscles that have been studied to form our understanding in this area is limited. In addition, few aging investigations have examined multiple muscles in the same individuals. This longitudinal investigation compared changes in skeletal muscle size via computed tomography of the quadriceps (rectus femoris, vastus lateralis, vastus medialis, vastus intermedius), hamstrings (biceps femoris short and long heads, semitendinosus, semimembranosus), psoas, rectus abdominis, lateral abdominals (obliques and transversus abdominis), and paraspinal muscles (erector spinae and multifidi) of older individuals from the Health ABC study at baseline and 5.0±0.1 years later (n=469, 73±3yr & 78±3yr, 49% women, 33% black). Skeletal muscle size decreased (p<0.05) in quadriceps (-3.3%), hamstrings (-5.9%), psoas (-0.4%), and rectus abdominis (-7.0%). The hamstrings and rectus abdominis atrophied approximately twice as much as the quadriceps (p<0.05), while the quadriceps atrophied substantially more than the psoas (p<0.05). The lateral abdominals (+5.9%) and paraspinals (+4.3%) hypertrophied (p<0.05) to a similar degree (p>0.05) over the 5 years. These data suggest that older individuals experience skeletal muscle atrophy and hypertrophy in a muscle group-specific fashion in the eighth decade, a critical time period in the aging process. A broader understanding of muscle group-specific skeletal muscle aging is needed to better guide exercise programs and other interventions that mitigate decrements in physical function with aging.