Abstract

The ability to sustain submaximal exercise is largely dependent on the oxidative capacity of mitochondria within skeletal muscle, and impairments in oxidative metabolism have been implicated in many neurologic and cardiovascular pathologies. Here we review studies which have demonstrated the utility of Near-infrared spectroscopy (NIRS) as a method of evaluating of skeletal muscle mitochondrial dysfunction in clinical human populations. NIRS has been previously used to noninvasively measure tissue oxygen saturation, but recent studies have demonstrated the utility of NIRS as a method of evaluating skeletal muscle oxidative capacity using post-exercise recovery kinetics of oxygen metabolism. In comparison to historical methods of measuring muscle metabolic dysfunction in vivo, NIRS provides a more versatile and economical method of evaluating mitochondrial oxidative capacity in humans. These advantages generate great potential for the clinical applicability of NIRS as a means of evaluating muscle dysfunction in clinical populations.

Highlights

  • Mitochondria serve critical roles in bioenergetics and cellular signaling

  • More recent studies have demonstrated that near-infrared spectroscopy (NIRS) can be used in a similar manner to measure the recovery of oxygen metabolism following a brief bout exercise as an assessment of mitochondrial oxidative capacity (Ryan et al, 2012, 2013c, 2014a)

  • Erickson et al found no significant relationship between FEV1 and Near-infrared spectroscopy (NIRS) measures of muscle mitochondrial capacity, which is in agreement with previous studies evaluating the relationship between whole body exercise capacity and mortality

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Summary

INTRODUCTION

Mitochondria serve critical roles in bioenergetics and cellular signaling. mitochondria have been widely recognized for their ability to produce cellular free energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation. More recent studies have demonstrated that near-infrared spectroscopy (NIRS) can be used in a similar manner to measure the recovery of oxygen metabolism following a brief bout exercise as an assessment of mitochondrial oxidative capacity (Ryan et al, 2012, 2013c, 2014a). Increases in the rate of oxygen metabolism as measured by NIRS during periods of ischemia following exercise reflect the increases in cellular respiration required to restore PCr in the muscle (Paganini et al, 1997; Ryan et al, 2013c). There has been increasing interests in the ability of NIRS to quickly and noninvasively measure muscle mitochondrial function in clinical populations that may be affected by declines in oxidative capacity (Erickson et al, 2013, 2015, 2016; Bossie et al, 2016). Several recent studies have employed this methodology to evaluate mitochondrial function in various clinical populations, and the findings are providing novel insight into pathophysiology and rehabilitation interventions (McCully et al, 2011; Erickson et al, 2013, 2015, 2016; Ryan et al, 2013d, 2014b; Bossie et al, 2016)

Neurological Injury and Disease
Cardiovascular an Respiratory Disease
Mitochondrial Disease
DISCUSSION
Findings
CONCLUSION
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