Publications

OBJECTIVE: Resistance exercise (RE) stimulates growth hormone (GH) secretion in a load-dependent manner, with heavier loads producing larger GH responses. However, new research demonstrates that low-load RE performed with blood flow restriction (BFR) produces potent GH responses that are similar to or exceed those produced following high-load RE. We hypothesized that low-load RE with vascular restriction would attenuate the known age-related reduction in GH response to RE. DESIGN: In a randomized crossover design, ten young (28 +/- 7.8 years) and ten older (67.4 +/- 4.6 years) men performed bilateral knee extension RE with low-load [20% of one-repetition maximum (1RM)] with BFR and high-load (80% 1RM) without BFR. GH and lactate were measured every 10 minutes throughout a 150-minute testing session (30 minutes prior to and 120 minutes following completion of the exercise); IGF-I was measured at baseline and 60 minutes post-exercise. RESULTS: Area under the GH curve indicated that both age groups responded similarly to each exercise condition. However, young men had a significantly greater maximal GH response to low-load RE with BFR than the high-load condition without BFR. Additionally, younger men had greater maximal GH concentrations to low-load RE with BFR than older men (p=0.02). The GH responses were marginally correlated to lactate concentration (r=0.13, p=0.002) and IGF-I levels were unchanged with RE. CONCLUSIONS: GH responses to low-load RE with vascular restriction are slightly higher than high-load RE without vascular restriction in young men. However, low-load RE with vascular restriction did not attenuate the known age-related reduction in GH response with exercise. These data suggest that while low-load RE with vascular restriction is as effective for inducing a GH response than traditionally-based high-load RE, there is a more potent response in young men.

In 2008, we published an article arguing that the age-related loss of muscle strength is only partially explained by the reduction in muscle mass and that other physiologic factors explain muscle weakness in older adults (Clark BC, Manini TM. Sarcopenia =/= dynapenia. J Gerontol A Biol Sci Med Sci. 2008;63:829-834). Accordingly, we proposed that these events (strength and mass loss) be defined independently, leaving the term "sarcopenia" to be used in its original context to describe the age-related loss of muscle mass. We subsequently coined the term "dynapenia" to describe the age-related loss of muscle strength and power. This article will give an update on both the biological and clinical literature on dynapenia-serving to best synthesize this translational topic. Additionally, we propose a working decision algorithm for defining dynapenia. This algorithm is specific to screening for and defining dynapenia using age, presence or absence of risk factors, a grip strength screening, and if warranted a test for knee extension strength. A definition for a single risk factor such as dynapenia will provide information in building a risk profile for the complex etiology of physical disability. As such, this approach mimics the development of risk profiles for cardiovascular disease that include such factors as hypercholesterolemia, hypertension, hyperglycemia, etc. Because of a lack of data, the working decision algorithm remains to be fully developed and evaluated. However, these efforts are expected to provide a specific understanding of the role that dynapenia plays in the loss of physical function and increased risk for disability among older adults.

PURPOSE: Sprint training is associated with several beneficial adaptations in skeletal muscle, including an enhancement of sarcoplasmic reticulum (SR) Ca(2+) release. Unfortunately, several patient populations (e.g., the elderly, those with cardiac dysfunction) that might derive great benefit from sprint exercise are unlikely to tolerate it. The purpose of this report was to describe the development of a tolerable neuromuscular electrical stimulation (NMES) protocol that induces skeletal muscle adaptations similar to those observed with sprint training. METHODS: Our NMES protocol was modeled after a published sprint exercise protocol and used a novel electrode configuration and stimulation sequence to provide adequate training stimulus while maintaining subject tolerance. Nine young, healthy subjects (four men) began and completed the training protocol of the knee extensor muscles. RESULTS: All subjects completed the protocol, with ratings of discomfort far less than those reported in studies of traditional NMES. Training induced significant increases in SR Ca(2+) release and citrate synthase activity ( 16% and 32%, respectively), but SR Ca(2+) uptake did not change. The percentage of myosin heavy chain IIx isoform was decreased significantly after training. At the whole muscle level, neither central activation nor maximum voluntary isometric contraction force were significantly altered, although isometric force did exhibit a trend toward an increase ( 3%, P = 0.055). Surprisingly, the NMES training produced a significant increase in muscle cross-sectional area ( 3%, P = 0.04). CONCLUSIONS: It seems that an appropriately designed NMES protocol can mimic many of the benefits of sprint exercise training, with a low overall time commitment and training volume. These findings suggest that NMES has the potential to bring the benefits of sprint exercise to individuals who are unable to tolerate traditional sprint training.

The deterioration of skeletal muscle with advancing age has long been anecdotally recognized and has been of scientific interest for more than 150 years. Over the past several decades, the scientific and medical communities have recognized that skeletal muscle dysfunction (e.g., muscle weakness, poor muscle coordination, etc.) is a debilitating and life-threatening condition in the elderly. For example, the age-associated loss of muscle strength is highly associated with both mortality and physical disability. It is well-accepted that voluntary muscle force production is not solely dependent upon muscle size, but rather results from a combination of neurologic and skeletal muscle factors, and that biologic properties of both of these systems are altered with aging. Accordingly, numerous scientists and clinicians have used the term "muscle quality" to describe the relationship between voluntary muscle strength and muscle size. In this review article, we discuss the age-associated changes in the neuromuscular system-starting at the level of the brain and proceeding down to the subcellular level of individual muscle fibers-that are potentially influential in the etiology of dynapenia (age-related loss of muscle strength and power).

Mal de debarquement syndrome (MdDS) is a disorder of phantom perception of self-motion of unknown cause. The purpose of this work was to describe the quality of life (QOL) of patients with MdDS and to estimate the economic costs associated with this disorder. A modified version of a QOL survey used for another neurological disease (multiple sclerosis; MSQOL-54) was used to assess the impact of MdDS on QOL in 101 patients. The estimated economic costs were based on self-reported direct and indirect costs of individuals living in the United States using Medicare reimbursement payment rates for 2011 in 79 patients. Patients with MdDS reported a poor overall QOL as indicated by a mean composite QOL score of 59.26 +/- 1.89 (out of 100). The subcategories having the lowest QOL rating were role limitations due to physical problems (18.32 +/- 3.20), energy (34.24 +/- 1.47), and emotional problems (36.30 +/- 4.00). The overall physical health composite score including balance was 49.40 +/- 1.69, and the overall mental health composite score was 52.40 +/- 1.83. The cost to obtain a diagnosis was $2,997 +/- 337, which included requiring an average of 19 physician visits per patient. The direct cost of MdDS medical care was $826 +/- 140 per patient per year, which mainly included diagnostic imaging and physician visits. The indirect costs (i.e., lost wages) were $9,781 +/- 2,347 per patient per year. Among 65 patients who were gainfully employed when they acquired MdDS, the indirect costs were $11,888 +/- 2,786 per patient per year. Thus, the total annual cost of the disorder ranged from $11,493 +/- 2,341 to $13,561 +/- 2,778 per patient per year depending on employment status prior to developing MdDS. MdDS negatively and dramatically impacts QOL, and also imposes a substantial economic burden on MdDS patients. These findings underscore the need for further basic and clinical research on MdDS.

The purpose of this study was to determine if non-thrust manual therapy (MT) attenuated side-to-side differences (asymmetry) of the erector spinae (ES) stretch reflex amplitude in nine patients with chronic LBP. We used electromechanical tapping to elicit short-latency stretch reflexes (SR) from the ES muscles before and after non-thrust MT. A large asymmetry in the SR was observed at baseline, with the higher of the paraspinal sides exhibiting a 100.2+/-28.2% greater value than the lower side. Following the intervention, this SR asymmetry was reduced (100.2+/-28.2% to 36.6+/-23.1%; p=0.03). This change was largely due to reduced amplitude on the side that was higher at baseline (35% reduction following treatment; p=0.05), whereas no change over time was observed in the low side (p=0.23). Additionally, there was no difference between the respective sides following the intervention (p=0.38), indicating that the asymmetry was normalized following treatment. These findings provide insight into the mechanism(s) of action of non-thrust MT, and suggest that it acts to down regulate the gain of the muscle spindles and/or the various sites of the Ia reflex pathway. Ultimately, developing a better understanding of the physiologic effects of manual therapies will assist in optimizing treatment strategies for patients with LBP.

Transcranial magnetic stimulation (TMS) has been in use for more than 20 years, and has grown exponentially in popularity over the past decade. While the use of TMS has expanded to the study of many systems and processes during this time, the original application and perhaps one of the most common uses of TMS involves studying the physiology, plasticity and function of the human neuromuscular system. Single pulse TMS applied to the motor cortex excites pyramidal neurons transsynaptically (Figure 1) and results in a measurable electromyographic response that can be used to study and evaluate the integrity and excitability of the corticospinal tract in humans. Additionally, recent advances in magnetic stimulation now allows for partitioning of cortical versus spinal excitability. For example, paired-pulse TMS can be used to assess intracortical facilitatory and inhibitory properties by combining a conditioning stimulus and a test stimulus at different interstimulus intervals. In this video article we will demonstrate the methodological and technical aspects of these techniques. Specifically, we will demonstrate single-pulse and paired-pulse TMS techniques as applied to the flexor carpi radialis (FCR) muscle as well as the erector spinae (ES) musculature. Our laboratory studies the FCR muscle as it is of interest to our research on the effects of wrist-hand cast immobilization on reduced muscle performance, and we study the ES muscles due to these muscles clinical relevance as it relates to low back pain. With this stated, we should note that TMS has been used to study many muscles of the hand, arm and legs, and should iterate that our demonstrations in the FCR and ES muscle groups are only selected examples of TMS being used to study the human neuromuscular system.

Each year, more than 18 million adults in the United States receive manual therapies, at a total annual out-of-pocket cost of $3.9 billion. Although there is growing evidence supporting the efficacy of manual therapies, little is known about the mechanisms underlying these treatments. This lack of basic knowledge significantly limits the development of rational strategies for the use of these treatments and potentially hinders their acceptance by the wider scientific and health care communities. Many authors have hypothesized that manual therapies act by disrupting the pain-spasm-pain cycle, but relatively little experimental evidence has supported this hypothesis. The authors have tested this hypothesis and summarize their work on the biology of manual therapies.

Dynapenia (pronounced dahy-nuh-pe-ne-a, Greek translation for poverty of strength, power, or force) is the age-associated loss of muscle strength that is not caused by neurologic or muscular diseases. Dynapenia predisposes older adults to an increased risk for functional limitations and mortality. For the past several decades, the literature has largely focused on muscle size as the primary cause of dynapenia; however, recent findings have clearly demonstrated that muscle size plays a relatively minor role. Conversely, subclinical deficits in the structure and function of the nervous system and/or impairments in the intrinsic force-generating properties of skeletal muscle are potential antecedents to dynapenia. This review highlights in the contributors to dynapenia and the etiology and risk factors that predispose individuals to dynapenia. In addition, we address the role of nutrition in the muscular and neurologic systems for the preservation of muscle strength throughout the life span.