Publications

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.

BACKGROUND: Aging results in decreased neuromuscular function, which is likely associated with neurologic alterations. At present little is known regarding age-related changes in intracortical properties. METHODS: In this study we used transcranial magnetic stimulation (TMS) to measure intracortical facilitation (ICF), short- and long-interval intracortical inhibition (SICI and LICI), motor evoked potential amplitude, and silent period duration in young and older adults (21.4+/-0.8years and 70.9+/-1.8years). These variables were assessed from the flexor carpi radialis muscle of the non-dominant arm under resting conditions, and during a submaximal contraction (intensity 15% maximum strength). RESULTS: Older adults exhibited increased SICI and LICI in comparison to young adults (SICI: 29.0+/-9.2% vs. 46.2+/-4.8% of unconditioned pulse; LICI: 6.5+/-1.7% vs. 15.8+/-3.3% of unconditioned pulse; P=0.04), and less ICF under resting conditions (74.6+/-8.7% vs. 104.9+/-6.9% of unconditioned pulse; P=0.02). These age-related differences disappeared during contraction, although the older adults did exhibit a longer silent period during contraction (112.5+/-6.5 vs. 84.0+/-3.9ms; P0.01). CONCLUSIONS: Collectively, these findings suggest increased GABA mediated intracortical inhibition with age.

Sex differences in muscle fatigue-resistance have been observed in a variety of muscles and under several conditions. This study compared the time to task failure (TTF) of a sustained isometric elbow extensor (intensity 15% of maximal strength) contraction in young men (n = 12) and women (n = 11), and examined if their neurophysiologic adjustments to fatigue differed. Motor-evoked potential amplitude (MEP), silent period duration, interference electromyogram (EMG) amplitude, maximal muscle action potential (M (max)), heart rate, and mean arterial pressure were measured at baseline, during the task, and during a 2-min ischemia period. Men and women did not differ in TTF (478.2 +/- 31.9 vs. 500.4 +/- 41.3 s; P = 0.67). We also performed an exploratory post hoc cluster analysis, and classified subjects as low (n = 15) or high endurance (n = 8) based on TTF (415.3 +/- 16.0 vs. 626.7 +/- 25.8 s, respectively). The high-endurance group exhibited a lower MEP and EMG at baseline (MEP 16.3 +/- 4.1 vs. 37.2 +/- 3.0% M (max), P 0.01; EMG 0.98 +/- 0.18 vs. 1.85 +/- 0.26% M (max), P = 0.03). These findings suggest no sex differences in elbow extensor fatigability, in contrast to observations from other muscle groups. The cluster analyses results indicated that high- and low-endurance groups displayed neurophysiologic differences at baseline (before performing the fatigue task), but that they did not differ in fatigue-induced changes in their neurophysiologic adjustments to the task.

Immobilization reduces muscle performance, and despite these performance losses being associated with neural impairments little is known regarding adaptations in cortical properties. We utilized transcranial magnetic stimulation to assess changes in flexor carpi radialis (FCR) intracortical facilitation (ICF), and short- and long-interval intracortical inhibition (SICI and LICI) in healthy humans undergoing 3 weeks of immobilization. Measurements were obtained at rest and during contraction (15% intensity). Central activation and the Hoffman reflex (H-reflex) were also assessed. Strength decreased 43.2% +/- 6.1% following immobilization, and central activation also decreased (97.5% +/- 2.4% to 73.2% +/- 8.3%). No changes in ICF, SICI, or LICI were observed at rest; however, LICI was increased during contraction (67.5% +/- 6.9% to 53.1% +/- 6.7% of unconditioned response). The increase in LICI correlated with the loss of strength (r = -0.63). The H-reflex increased following immobilization. These findings suggest that immobilization increases intracortical inhibition during contraction, and this increase is primarily mediated by GABA(B) receptors.

PURPOSE OF REVIEW: The economic burden due to the sequela of sarcopenia (muscle wasting in the elderly) are staggering and rank similarly to the costs associated with osteoporotic fractures. In this article, we discuss the societal burden and determinants of the loss of physical function with advancing age, the physiologic mechanisms underlying dynapenia (muscle weakness in the elderly), and provide perspectives on related critical issues to be addressed. RECENT FINDINGS: Recent epidemiological findings from longitudinal aging studies suggest that dynapenia is highly associated with both mortality and physical disability even when adjusting for sarcopenia indicating that sarcopenia may be secondary to the effects of dynapenia. These findings are consistent with the physiologic underpinnings of muscle strength, as recent evidence demonstrates that alterations in muscle quantity, contractile quality and neural activation all collectively contribute to dynapenia. SUMMARY: Although muscle mass is essential for regulation of whole body metabolic balance, overall neuromuscular function seems to be a critical factor for maintaining muscle strength and physical independence in the elderly. The relative contribution of physiologic factors contributing to muscle weakness are not fully understood and further research is needed to better elucidate these mechanisms between muscle groups and across populations.

For nearly half a century, high mechanical loading and mechanotransduction pathways have guided exercise recommendations for inducing muscle hypertrophy. However, emerging research on low-intensity exercise with blood flow restriction challenges this paradigm. This article will describe the BFR exercise model and discuss its efficacy, potential mechanisms, and clinical viability.