With increasing survival rates in people with spinal cord injuries (SCI), detection and prevention of metabolic and cardiovascular disease have become increasingly important. Few studies have evaluated in vivo mitochondrial function in paralyzed skeletal muscle. The purpose of this study was to compare oxidative muscle metabolism using the rate of phosphocreatine (PCr) resynthesis measured by magnetic resonance spectroscopy (MRS) in people with SCI and able-bodied (AB) controls. Eight subjects with complete SCI (American Spinal Injury Association Impairment Scale A, levels T3–T12, injury duration 2–13 years) were compared with 12 AB controls. T1-weighted¹H MR images of the thigh were taken to identify skeletal muscle. Phosphorous MRS was performed with a 13 × 13-cm²surface coil placed on the right vastus lateralis in a 3 Tesla clinical MRI scanner. PCr resynthesis was measured after electrical stimulation for 60 s at 4 Hz in SCI and AB and in AB subjects after 39 s of voluntary isometric contractions. Resting metabolites were not different between SCI and AB, except for an elevated phosphodiester peak. PCr recovery was slower in AB subjects using electrical stimulation compared with voluntary exercise (28.4 ± 6.1 vs. 41.5 ± 4.3 s; P < 0.05). PCr recovery rates and calculated muscle maximum oxidative capacity in SCI were both 52% of electrically stimulated AB ( P < 0.001). In vivo oxidative metabolism was reduced in paralyzed muscle to a similar extent as seen in people with mitochondrial myopathies and heart failure.

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. Near-infrared spectroscopy (NIRS) has been previously used to noninvasively measure tissue oxygen saturation in humans, 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.

Repeated bouts of eccentric exercise reduce the amount of exercise-induced muscle injury.Purpose:This study sought to evaluate the importance of neural adaptations by comparing the repeated bout effect on muscle injury caused by voluntary and electrically stimulated eccentric exercise.Method

Near-infrared spectroscopy (NIRS) uses the relative absorption of light at 850 and 760 nm to determine skeletal muscle oxygen saturation. Previous studies have used the ratio of both signals to report muscle oxygen saturation. Purpose: The purpose of this pilot study is to assess the different approaches used to represent muscle oxygen saturation and to evaluate the pulsations of oxygenated hemoglobin/myoglobin (O₂heme) and deoxygenated hemoglobin/myoglobin (Heme) signals. Method: Twelve participants, aged 20–29 years, were tested on the forearm flexor muscles using continuous-wave NIRS at rest. Measurements were taken during 2–3 min rest, physiological calibration (5 min ischemia), and reperfusion. Ten participants were included in the study analysis. Results: There was a significant difference in pulse size between O₂heme and Heme signals at the three locations (p < 0.05). Resting oxygen saturation was 58.8% + 9.2%, 69.6% + 3.9%, and 89.2% + 6.9% when calibrated using O₂heme, the tissue oxygenation/saturation index (TSI), and Heme, respectively. Conclusion: The difference in magnitude of O₂heme and Heme pulses with each heartbeat might suggest different anatomical locations of these signals, for which calibrating with just one of the signals instead of the ratio of both is proposed. Calculations of physiological calibration must account for increased blood volume in the tissue because of the changes in blood volume, which appear to be primarily from the O₂heme signal. Resting oxygen levels calibrated with Heme agree with theoretical oxygen saturation.