Publications

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.

Our understanding the neurophysiologic characteristics of the human paraspinal muscles has historically been hindered by the lack of experimental techniques to examine these muscles function in vivo. In this article we describe a paired-pulse transcranial magnetic stimulation (TMS) protocol to quantify intracortical facilitation (ICF) and short-interval intracortical inhibition (SICI) of the lumbar paraspinal muscles, and an electromechanical tapping protocol to measure the amplitude of the short-latency stretch reflex. Test-retest reliability of these protocols was examined across two sessions separated by 30-min in healthy adults. We assessed relative reliability by calculating the intraclass correlation coefficient (ICC), and absolute reliability was assessed via coefficient of variation (CV). ICF and SICI in the lumbar paraspinal muscles exhibited the classical facilitatory and inhibitory responses observed in appendicular skeletal muscles ( approximately 30% facilitation and inhibition, respectively). The motor evoked potential amplitude (MEP), ICF, SICI, and stretch reflex amplitude measurements did not significantly differ between the two testing sessions (p>0.05). The MEP amplitude, ICF and stretch reflex amplitude exhibited the highest relative and absolute reliability (ICC=0.89-0.91, CV=10.6-11.1%); whereas the SICI measure exhibited somewhat lower reliability (ICC=0.75, CV=20.1%). The stretch reflex protocol performed in the first testing session did not influence the TMS outcome measures in the second testing session (p>0.05). These innovative methods may be useful in studying basic physiology, the pathology of low back pain, as well as the mechanisms of action of treatment interventions.

Aging is associated with dramatic reductions in muscle strength and motor control, and many of these agerelated changes in muscle function result from adaptations in the central nervous system. Aging is associated with widespread qualitative and quantitative changes of the motor cortex. For example, advancing age has been suggested to result in cortical atrophy, reduced cortical excitability, reduced cortical plasticity, as well as neurochemical abnormalities.The associated functional effects of these changes likely influence numerous aspects of muscle performance such as muscle strength and motor control. For example, there is evidence to suggest that the muscle weakness associated with aging is partially due to impairments in the nervous system's ability to fully activate motor neurons- particularly in the larger proximal muscle groups. In this review article we discuss age-related changes in the motor cortex, as well as the abilityor lack thereof- of older adults to voluntarily activate skeletal muscle. We also provide perspectives on scientific and clinical questions that need to be addressed in the near future.

This study evaluated the effect of 4 weeks of low-load resistance exercise with blood flow restriction (BFRE) on increasing strength in comparison with high-load resistance exercise (HLE), and assessed changes in blood, vascular and neural function. Healthy adults performed leg extension BFRE or HLE 3 days/week at 30% and 80% of strength, respectively. During BFRE, a cuff on the upper leg was inflated to 30% above systolic blood pressure. Strength, pulse-wave velocity (PWV), ankle-brachial index (ABI), prothrombin time (PT) and nerve conduction (NC) were measured before and after training. Markers of coagulation (fibrinogen and D-dimer), fibrinolysis [tissue plasminogen activator (tPA)] and inflammation [high sensitivity C-reactive protein (hsCRP)] were measured in response to the first and last exercise bouts. Strength increased 8% with BFRE and 13% with HLE (P0.01). No changes in PWV, ABI, PT or NC were observed following training for either group (P>0.05). tPA antigen increased 30-40% immediately following acute bouts of BFRE and HLE (P=0.01). No changes were observed in fibrinogen, D-dimer or hsCRP (P>0.05). These findings indicate that both protocols increase the strength without altering nerve or vascular function, and that a single bout of both protocols increases fibrinolytic activity without altering selected markers of coagulation or inflammation in healthy individuals.

BACKGROUND: While there is growing evidence for the efficacy of SM to treat LBP, little is known on the mechanisms and physiologic effects of these treatments. Accordingly, the purpose of this study was to determine whether SM alters the amplitude of the motor evoked potential (MEP) or the short-latency stretch reflex of the erector spinae muscles, and whether these physiologic responses depend on whether SM causes an audible joint sound. METHODS: We used transcranial magnetic stimulation to elicit MEPs and electromechanical tapping to elicit short-latency stretch reflexes in 10 patients with chronic LBP and 10 asymptomatic controls. Neurophysiologic outcomes were measured before and after SM. Changes in MEP and stretch reflex amplitude were examined based on patient grouping (LBP vs. controls), and whether SM caused an audible joint sound. RESULTS: SM did not alter the erector spinae MEP amplitude in patients with LBP (0.80+/-0.33 vs. 0.80+/-0.30 muV) or in asymptomatic controls (0.56+/-0.09 vs. 0.57+/-0.06 muV). Similarly, SM did not alter the erector spinae stretch reflex amplitude in patients with LBP (0.66+/-0.12 vs. 0.66+/-0.15 muV) or in asymptomatic controls (0.60+/-0.09 vs. 0.55+/-0.08 muV). Interestingly, study participants exhibiting an audible response exhibited a 20% decrease in the stretch reflex (p0.05). CONCLUSIONS: These findings suggest that a single SM treatment does not systematically alter corticospinal or stretch reflex excitability of the erector spinae muscles (when assessed 10-minutes following SM); however, they do indicate that the stretch reflex is attenuated when SM causes an audible response. This finding provides insight into the mechanisms of SM, and suggests that SM that produces an audible response may mechanistically act to decrease the sensitivity of the muscle spindles and/or the various segmental sites of the Ia reflex pathway.