ABSTRACT
The mechanisms responsible for increased walking metabolic cost among older adults are poorly understood. We recently proposed a theoretical premise by which age-related reductions in Achilles tendon stiffness (k AT ) can disrupt the neuromechanics of calf muscle behavior and contribute to faster rates of oxygen consumption during walking. The purpose of this study was to objectively evaluate this premise. We quantified k AT at a range of matched activations prescribed using electromyographic biofeedback and walking metabolic cost in a group of 15 younger (age: 23±4 yrs) and 15 older adults (age: 72±5 yrs). Older adults averaged 44% less k AT than younger adults at matched triceps surae activations (p=0.046). This effect appeared to arise not only from altered tendon length-tension relations with age, but also from differences in the operating region of those length-tension relations between younger and older adults. Older adults also walked with a 17% higher net metabolic power than younger adults (p=0.017). In addition, we discovered empirical evidence that lesser k AT exacts a metabolic penalty and was positively correlated with higher net metabolic power during walking (r=-0.365, p=0.048). These results pave the way for interventions focused on restoring ankle muscle-tendon unit structural stiffness to improve walking energetics in aging.
ABSTRACT
Ultrasonic techniques are being developed to detect changes in cancellous bone caused by osteoporosis. The goal of this study was to test the relative in vivo performance of eight backscatter parameters developed over the last several years for ultrasonic bone assessment: apparent integrated backscatter (AIB), frequency slope of apparent backscatter (FSAB), frequency intercept of apparent backscatter (FIAB), normalized mean of the backscatter difference (nMBD), normalized slope of the backscatter difference (nSBD), normalized intercept of the backscatter difference (nIBD), normalized backscatter amplitude ratio (nBAR) and backscatter amplitude decay constant (BADC). Backscatter measurements were performed on the left and right femoral necks of 80 adult volunteers (age = 25 ± 11 y) using an imaging system equipped with a convex array transducer. For comparison, additional ultrasonic measurements were performed at the left and right heel using a commercially available heel-bone ultrasonometer that measured the stiffness index. Six of the eight backscatter parameters (all but nSBD and nIBD) exhibited similar and highly significant (p < 0.000001) left-right correlations (0.51 ≤ R ≤ 0.68), indicating sensitivity to naturally occurring variations in bone tissue. Left-right correlations for the stiffness index measured at the heel (R = 0.75) were not significantly better than those produced by AIB, FSAB and FIAB. The short-term precisions of AIB, nMBD, nBAR and BADC (7.8%-11.7%) were comparable to that of the stiffness index measured with the heel-bone ultrasonometer (7.5%).
Subject(s)
Femur Neck , Ultrasonics , Adolescent , Adult , Bone Density , Femur Neck/diagnostic imaging , Humans , Scattering, Radiation , Ultrasonics/methods , Ultrasonography/methods , Young AdultABSTRACT
Ultrasonic backscatter techniques are being developed to detect changes in bone caused by osteoporosis. The present study introduces a new technique that measures the exponential decay in the amplitude of the backscatter signal quantified by a parameter called the backscatter amplitude decay constant (BADC). Measurements were performed on 54 specimens of cancellous bone from 14 human femurs using a 3.5-MHz transducer. Six methods were tested to determine BADC. The recommended method measures the time slope of the natural log of the rectified signal. Measured values of BADC ranged from approximately 0.1 µs-1 to 0.6 µs-1. Moderate to strong correlations (Spearman's ρ >0.7) were found between BADC and the density and microstructural characteristics of the specimens determined using X-ray microcomputed tomography. The results of this study suggest that BADC may be able to detect changes in the density and microstructure of cancellous bone caused by osteoporosis and other diseases.