Publications

BACKGROUND: Older adults display wide individual variability (heterogeneity) in the effects of resistance exercise training on muscle strength. The mechanisms driving this heterogeneity are poorly understood. Understanding of these mechanisms could permit development of more targeted interventions and/or improved identification of individuals likely to respond to resistance training interventions. Thus, this study assessed potential physiological factors that may contribute to strength response heterogeneity in older adults: neural activation, muscle hypertrophy, and muscle contractility. METHODS: In 24 older adults (72.3 +/- 6.8 years), we measured the following parameters before and after 12 weeks of progressive resistance exercise training: i) isometric leg extensor strength; ii) isokinetic (60 degrees /sec) leg extensor strength; iii) voluntary (neural) activation by comparing voluntary and electrically-stimulated muscle forces (i.e., superimposed doublet technique); iv) muscle hypertrophy via dual-energy x-ray absorptiometry (DXA) estimates of regional lean tissue mass; and v) intrinsic contractility by electrically-elicited twitch and doublet torques. We examined associations between physiological factors (baseline values and relative change) and the relative change in isometric and isokinetic muscle strength. RESULTS: Notably, changes in quadriceps contractility were positively associated with the relative improvement in isokinetic (r = 0.37-0.46, p 0.05). Additionally, change in thigh lean mass was not significantly associated with relative improvement in isometric or isokinetic strength (r = 0.09 and -0.02, respectively; p > 0.05). Somewhat surprising was the lack of association between exercise-induced changes in isometric and isokinetic strength (r = 0.07). CONCLUSIONS: The strength response to resistance exercise in older adults appears to be contraction-type dependent. Therefore, future investigations should consider obtaining multiple measures of muscle strength to ensure that strength adaptations are comprehensively assessed. Changes in lean mass did not explain the heterogeneity in strength response for either contraction type, and the data regarding the influence of voluntary activation was inconclusive. For isokinetic contraction, the strength response was moderately explained by between-subject variance in the resistance-exercise induced changes in muscle contractility.

BACKGROUND: Weakness is a risk factor for physical limitations and death in older adults (OAs). We sought to determine whether OAs with clinically meaningful leg extensor weakness exhibit differences in voluntary inactivation (VIA) and measures of corticospinal excitability when compared to young adults (YAs) and OAs without clinically meaningful weakness. We also sought to estimate the relative contribution of indices of neural excitability and thigh lean mass in explaining the between-subject variability in OAs leg extensor strength. METHODS: In 66 OAs (75.1 +/- 7.0 years) and 20 YAs (22.0 +/- 1.9 years), we quantified leg extensor strength, thigh lean mass, VIA, and motor evoked potential (MEP) amplitude and silent period (SP) duration. OAs were classified into weakness groups based on previously established strength/body weight (BW) cut points (Weak, Modestly Weak, or Not Weak). RESULTS: The OAs had 63% less strength/BW when compared to YAs. Weak OAs exhibited higher levels of leg extensor VIA than Not Weak OAs (14.2 +/- 7.5% vs 6.1 +/- 7.5%). Weak OAs exhibited 24% longer SPs compared to Not Weak OAs, although this difference was insignificant (p = .06). The Weak OAs MEPs were half the amplitude of the Not Weak OAs. Regression analysis indicated that MEP amplitude, SP duration, and thigh lean mass explained  62% of the variance in strength, with the neural excitability variables explaining  33% of the variance and thigh lean mass explaining  29%. CONCLUSION: These findings suggest that neurotherapeutic interventions targeting excitability could be a viable approach to increase muscle strength in order to reduce the risk of physical impairments in late life.

Skeletal muscle function deficits associated with advancing age are due to several physiological and morphological changes including loss of muscle size and quality (conceptualized as a reduction in the intrinsic force-generating capacity of a muscle when adjusted for muscle size). Several factors can contribute to loss of muscle quality, including denervation, excitation-contraction uncoupling, increased fibrosis, and myosteatosis (excessive levels of inter- and intramuscular adipose tissue and intramyocellular lipids). These factors also adversely affect metabolic function. There is a major unmet need for tools to rapidly and easily assess muscle mass and quality in clinical settings with minimal patient and provider burden. Herein, we discuss the potential for electrical impedance myography (EIM) as a tool to evaluate muscle mass and quality in older adults. EIM applies weak, non-detectible (e.g., 400 muA), mutifrequency (e.g., 1 kHz-1 MHz) electrical currents to a muscle (or muscle group) through two excitation electrodes, and resulting voltages are measured via two sense electrodes. Measurements are fast ( 5 s/muscle), simple to perform, and unaffected by factors such as hydration that may affect other simple measures of muscle status. After nearly 2 decades of study, EIM has been shown to reflect muscle health status, including the presence of atrophy, fibrosis, and fatty infiltration, in a variety of conditions (e.g., developmental growth and maturation, conditioning/deconditioning, and obesity) and neuromuscular diseases states [e.g., amyotrophic lateral sclerosis (ALS) and muscular dystrophies]. In this article, we describe prior work and current evidence of EIM's potential utility as a measure of muscle health in aging and geriatric medicine.

In the 1990s and early 2000s, the common definition for sarcopenia was age-related loss of skeletal muscle, and low levels of muscle mass were central to sarcopenia diagnosis. In more recent consensus definitions, however, low muscle strength displaces low muscle mass as a defining feature of sarcopenia. The change stems from growing evidence that muscle weakness is a better predictor of adverse health outcomes (eg, mobility limitations) than muscle mass. This evidence accompanies an emerging recognition that central neural mechanisms are critical determinants of age-related changes in strength and mobility that can occur independently of variations in muscle mass. However, strikingly little practical attention is typically given to the potential role of the central nervous system in the etiology or remediation of sarcopenia (ie, low muscle function). In this article, we provide an overview of some mechanisms that mediate neural regulation of muscle contraction and control, and highlight the specific contributions of neural hypoexcitability, dopaminergic dysfunction, and degradation of functional and structural brain connectivity in relation to sarcopenia. We aim to enhance the lines of communication between the domains of sarcopenia and neuroscience. We believe that appreciation of the neural regulation of muscle contraction and control is fundamental to understanding sarcopenia and to developing targeted therapeutic strategies for its treatment.

Every second of every day, an older adult suffers a fall in the United States (>30 million older adults fall each year). More than 20% of these falls cause serious injury (e.g., broken bones, head injury) and result in 800,000 hospitalizations and 30,000 deaths annually. Bhasin and colleagues recently reported results from a pragmatic, cluster-randomized trial designed to evaluate the effectiveness of a multifactorial intervention to prevent fall injuries. The intervention did not result in a significantly lower rate of a first adjudicated serious fall injury among older adults at increased risk for fall injuries as compared with enhanced usual care. In this commentary we briefly review and highlight these recent findings. Additionally, we argue that the findings should not be discounted just because of the lack of statistical significance. The approximately 10% reduction compared to enhanced usual care is, arguably, meaningful at both the individual and public health level, especially when one considers that the control group had better outcomes than expected based on prior work. Moreover, we encourage future research as well as practitioners to give strong consideration to the nuances of the exercise interventions for reducing falls and fall-related injuries particularly as it relates to exercise programming specifics, namely intensity and volume, to enhance neuromuscular function and also to neurorehabilitation approaches to enhance motor function (e.g., balance, motor planning, and coordination).

Mal de Debarquement syndrome (MdDS), also known as disembarkment syndrome, is a benign neurological condition characterized by a feeling of rocking, bobbing, or swaying, usually presenting after an individual has been exposed to passive motion as from being on a cruise, long drive, turbulent air travel, or train. Clinical awareness about this condition is limited, as is research; thus, many patients go undiagnosed. In this case report, the authors describe a case of a severe headache as a major presenting symptom of MdDS in a 46-year-old woman who eventually attained full resolution of symptoms. This report aims to highlight this unique presentation and make practitioners more aware of the cardinal clinical features, to assist in prompt diagnosis of this disorder.

Mal de Debarquement syndrome (MdDS) is composed of constant phantom sensations of motion, which are frequently accompanied by increased sensitivity to light, inability to walk on a patterned floor, the sensation of ear fullness, head pressure, anxiety, and depression. This disabling condition generally occurs in premenopausal women within 2 days after prolonged passive motion (e.g., travel on a cruise ship, plane, or in a car). It has been previously hypothesized that MdDS is the result of maladaptive changes in the polysynaptic vestibulo-ocular reflex (VOR) pathway called velocity storage. Past research indicates that full-field optokinetic stimulation is an optimal way to activate velocity storage. Unfortunately, such devices are typically bulky and not commonly available. We questioned whether virtual reality (VR) goggles with a restricted visual field could effectively simulate a laboratory environment for MdDS treatment. A stripes program for optokinetic stimulation was implemented using Google Daydream Viewer. Five female patients (42 +/- 10 years; range 26-50), whose average MdDS symptom duration was 2 months, participated in this study. Four patients had symptoms triggered by prolonged passive motion, and in one, symptoms spontaneously occurred. Symptom severity was self-scored by patients on a scale of 0-10, where 0 is no symptoms at all and 10 is the strongest symptoms that the patient could imagine. Static posturography was obtained to determine objective changes in body motion. The treatment was considered effective if the patient's subjective score improved by at least 50%. All five patients reported immediate improvement. On 2-month follow-ups, symptoms returned only in one patient. These data provide proof of concept for the limited-visual-field goggles potentially having clinical utility as a substitute for full-field optokinetic stimulation in treating patients with MdDS in clinics or via telemedicine.