Publications

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.

This study evaluated the effect of passive-heat stress on the neuromuscular properties of the wrist flexor muscles, which are commonly used in manual labour hand tasks. A combination of techniques were utilised, involving nerve stimulation and paired-pulse transcranial magnetic stimulation to assess changes in muscle strength, contractile properties, fatigue-resistance and central activation as well as indices of intracortical excitability in 10healthy humans who were exposed to a passive heat stress protocol as well as a normothermia control protocol. Passive-heat stress increased core body temperature ∼1°C (37.2 ± 0.4 to 38.2 ± 0.4°C ; p < 0.01), mean skin temperature (34.5 ± 0.7°C to 37.3 ± 1.1°C; p < 0.01), and heart rate (79.5 ± 20.0 to 110.0 ± 23.0 beats/min; p = 0.04). No effect was observed on muscle strength, contractile properties, muscle fatigability, central activation orindices of intracortical excitability (p > 0.05). These data indicate that allowing internal temperatures of workers to increase ≤1.0°C does not affect neuromuscular properties of the wrist flexors.

AIM: Resistance exercise performed at low loads (20-30% of maximal strength) with blood flow restriction (BFR) acutely increases protein synthesis and induces hypertrophy when performed chronically. We investigated myogenic and proteolytic mRNA expression 8 h following an acute bout of knee extension exercise. METHODS: Fifteen subjects (22.8 +/- 3.7 years, eight men and seven women) were randomized to two exercise conditions: BFR or control exercise. All participants performed four sets of exercise (30, 15, 15 and 15 repetitions) at 20% of maximal strength. Persons in the BFR group had a cuff placed on the upper thigh inflated to 1.5 times brachial systolic blood pressure (cuff pressure range: 135-186 mmHg). Muscle biopsies from the vastus lateralis were excised 24 h before and 8 h following the exercise. RESULTS: RT-PCR analysis demonstrated no change in myogenic gene expression (insulin-like growth factor-1, MyoD, myogenin, myostatin - a negative regulator) with either exercise condition (P > 0.123). However, BFR exercise downregulated mRNA expression in transcripts associated with proteolytic pathways (FOXO3A, Atrogin-1 and MuRF-1) with no change in the control exercise condition. Specifically, median mRNA expression of FOXO3A decreased by 1.92-fold (P = 0.01), Atrogin-1 by 2.10-fold (P = 0.01) and MuRF-1 by 2.44-fold (P = 0.01). CONCLUSION: These data are consistent with the downregulation of proteolytic transcripts observed following high-load resistance exercise. In summary, myogenic genes are unchanged and proteolytic genes associated with muscle remodelling are reduced 8 h following low-load BFR exercise.

Time to task failure of trunk extensor muscles during seated submaximal isometric exertions was assessed in 18 healthy participants using 2 different load types. One required supporting an inertial load (position-matching task) whereas the 2nd required maintaining an equivalent torque against a rigid restraint (force-matching task). Time to task failure was significantly longer for position-matching tasks compared to the force-matching tasks. This finding is opposite to that reported for the appendicular muscles. A subset of 4 individuals completed a 2nd experiment to test the time to task failure of the elbow flexors in the position- and force-matching tasks. Time to task failure of the elbow flexors was significantly longer for the force-matching tasks compared to position matching. Thus, the same population shows that the effects of load type on time to task failure are opposite for the appendicular and axial muscles. This could be an important issue in understanding the mechanisms of task failure, and the endurance capacity of the trunk extensor muscles.