Muscle strength mediates the relationship between mitochondrial energetics and walking performance.

Ariel C Zane,David A Reiter,Eleanor M Simonsick,Stephanie A Studenski,Luigi Ferrucci,Michelle Shardell,Kenneth W Fishbein,Donnie Cameron,Richard G Spencer

doi:10.1111/acel.12568

Abstract

SummarySkeletal muscle mitochondrial oxidative capacity declines with age and negatively affects walking performance, but the mechanism for this association is not fully clear. We tested the hypothesis that impaired oxidative capacity affects muscle performance and, through this mechanism, has a negative effect on walking speed. Muscle mitochondrial oxidative capacity was measured by in vivo phosphorus magnetic resonance spectroscopy as the postexercise phosphocreatine resynthesis rate, kPC r, in 326 participants (154 men), aged 24–97 years (mean 71), in the Baltimore Longitudinal Study of Aging. Muscle strength and quality were determined by knee extension isokinetic strength, and the ratio of knee extension strength to thigh muscle cross‐sectional area derived from computed topography, respectively. Four walking tasks were evaluated: a usual pace over 6 m and for 150 s, and a rapid pace over 6 m and 400 m. In multivariate linear regression analyses, kPC r was associated with muscle strength (β = 0.140, P = 0.007) and muscle quality (β = 0.127, P = 0.022), independent of age, sex, height, and weight; muscle strength was also a significant independent correlate of walking speed (P < 0.02 for all tasks) and in a formal mediation analysis significantly attenuated the association between kPC r and three of four walking tasks (18–29% reduction in β for kPC r). This is the first demonstration in human adults that mitochondrial function affects muscle strength and that inefficiency in muscle bioenergetics partially accounts for differences in mobility through this mechanism.

Highlights

Walking independently is essential for performing daily living activities and maintaining independence throughout the human lifespan (Halter et al, 2009)
In a previous study conducted on participants drawn from the Baltimore Longitudinal Study of Aging (BLSA), we demonstrated that skeletal muscle mitochondrial oxidative capacity is a strong independent predictor of walking speed, and this association between oxidative capacity and walking speeds is especially strong for more challenging gait tasks (Choi et al, 2016)
These findings suggested that diminished bioenergetic reserve (Schrack et al, 2013) and/or impaired bioenergetic synthetic capacity is in part responsible for slower walking speeds in older persons

Summary

Introduction

Walking independently is essential for performing daily living activities and maintaining independence throughout the human lifespan (Halter et al, 2009). In a previous study conducted on participants drawn from the Baltimore Longitudinal Study of Aging (BLSA), we demonstrated that skeletal muscle mitochondrial oxidative capacity (as measured by in vivo phosphorus magnetic resonance spectroscopy, 31P MRS, in the quadriceps) is a strong independent predictor of walking speed, and this association between oxidative capacity and walking speeds is especially strong for more challenging gait tasks (Choi et al, 2016) These findings suggested that diminished bioenergetic reserve (Schrack et al, 2013) and/or impaired bioenergetic synthetic capacity is in part responsible for slower walking speeds in older persons. This hypothesis is consistent with the progressive decline in muscle mass and strength (with the decline in strength outpacing that of muscle mass) (Goodpaster et al, 2006; Newman et al, 2006) often observed in older persons and attributed in part to higher prevalence of chronic diseases (McDermott et al, 2004) and lower physical activity in older compared with younger persons (Cesari et al, 2009)

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Discussion

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