Jared T. Brizendine

Noninvasive evaluation of skeletal muscle mitochondrial capacity with near-infrared spectroscopy: correcting for blood volume changes

Near-infrared spectroscopy (NIRS) is a well-known method used to measure muscle oxygenation and hemodynamics in vivo. The application of arterial occlusions allows for the assessment of muscle oxygen consumption (mVo(2)) using NIRS. The aim of this study was to measure skeletal muscle mitochondrial capacity using blood volume-corrected NIRS signals that represent oxygenated hemoglobin/myoglobin (O(2)Hb) and deoxygenated hemoglobin/myoglobin (HHb). We also assessed the reliability and reproducibility of NIRS measurements of resting oxygen consumption and mitochondrial capacity. Twenty-four subjects, including four with chronic spinal cord injury, were tested using either the vastus lateralis or gastrocnemius muscles. Ten healthy, able-bodied subjects were tested on two occasions within a period of 7 days to assess the reliability and reproducibility. NIRS signals were corrected for blood volume changes using three different methods. Resting oxygen consumption had a mean coefficient of variation (CV) of 2.4% (range 1-32%). The recovery of oxygen consumption (mVo(2)) after electrical stimulation at 4 Hz was fit to an exponential curve, which represents mitochondrial capacity. The time constant for the recovery of mVo(2) was reproducible with a mean CV of 10% (range 1-22%) only when correcting for blood volume changes. We also examined the effects of adipose tissue thickness on measurements of mVo(2). We found the mVo(2) measurements using absolute units to be influenced by adipose tissue thickness (ATT), and this relationship was removed when an ischemic calibration was performed, supporting its use to compare mVo(2) between individuals of varying ATT. In conclusion, in vivo oxidative capacity can be assessed using blood volume-corrected NIRS signals with a high degree of reliability and reproducibility.

Skeletal muscle metabolism in endurance athletes with near-infrared spectroscopy.

PURPOSE To determine whether near-infrared spectroscopy (NIRS) measurements of muscle mitochondrial function could detect the expected differences between endurance-trained athletes (n = 8) and inactive subjects (n = 8). METHODS Muscle oxygen consumption (mV˙O2) of the vastus lateralis was measured with continuous-wave NIRS using transient arterial occlusions. The recovery rate of mV˙O2 after electrical stimulation was fit to an exponential curve, with the time constant (Tc) used as an index of mitochondrial capacity. Whole-body peak oxygen uptake was determined by indirect calorimetry during a continuous ramp protocol on a cycle ergometer. RESULTS Whole-body peak oxygen uptake values for endurance-trained and inactive controls were 73.5 ± 9.1 and 33.7 ± 5.9 mL·kg·min, respectively (P < 0.001). The recovery rates of mV˙O2 after exercise for endurance training were 18.4 ± 3.2 and 18.8 ± 2.5 s, whereas those for inactive controls were 32.4 ± 5.2 and 34.9 ± 5.9 s for the shallow and deep channels, respectively (P < 0.001 for comparison between groups). Resting mV˙O2 was 0.52%·s ± 0.22%·s for endurance athletes and 0.77%·s ± 0.82%·s for inactive controls (P = 0.42). CONCLUSIONS The recovery rates of mV˙O2 after exercise in endurance athletes were almost twofold faster than inactive subjects measured with NIRS, consistent with previous studies using muscle biopsies and magnetic resonance spectroscopy. Our results support the use of NIRS measurements of the recovery of oxygen consumption to assess muscle oxidative capacity.

Activity-induced changes in skeletal muscle metabolism measured with optical spectroscopy.

PURPOSE Previous studies have used near-infrared spectroscopy (NIRS) to measure skeletal muscle mitochondrial capacity. This study tested the hypothesis that NIRS-measured mitochondrial capacity would improve with endurance exercise training and decline with detraining. METHODS Nine young participants performed 4 wk of progressively increasing endurance exercise training of the wrist flexor muscles followed by approximately 5 wk of inactivity. The rate of recovery of muscle oxygen consumption (mV(˙)O₂) was measured with NIRS every 3-7 d, indicating mitochondrial oxidative capacity. RESULTS A linear increase in mitochondrial capacity (NIRS rate constant) was found with a group average of 64% ± 37% improvement after 4 wk of exercise training (P < 0.05). Mitochondrial capacity declined exponentially upon cessation of exercise training, with a mean half-time of approximately 7.7 d. CONCLUSIONS Both the magnitude and the time course of mitochondrial adaptations to exercise training and detraining measured with NIRS was consistent with previous studies using both in vitro and in vivo techniques. These findings show that NIRS-based measurements can detect meaningful changes in mitochondrial capacity.

A comparison of exercise type and intensity on the noninvasive assessment of skeletal muscle mitochondrial function using near-infrared spectroscopy

Near-infrared spectroscopy (NIRS) can be used to measure muscle oxygen consumption (mVO(2)) using arterial occlusions. The recovery rate of mVO(2) after exercise can provide an index of skeletal muscle mitochondrial function. The purpose of this study was to test the influence of exercise modality and intensity on NIRS measurements of mitochondrial function. Three experiments were performed. Thirty subjects (age: 18-27 yr) were tested. NIRS signals were corrected for blood volume changes. The recovery of mVO(2) after exercise was fit to a monoexponential curve, and a rate constant was calculated (directly related to mitochondrial function). No differences were found in NIRS rate constants for VOL and ES exercises (2.04 ± 0.57 vs. 2.01 ± 0.59 min(-1) for VOL and ES, respectively; P = 0.317). NIRS rate constants were independent of the contraction frequency for both VOL and ES (VOL: P = 0.166 and ES: P = 0.780). ES current intensity resulted in significant changes to the normalized time-tension integral (54 ± 11, 82 ± 7, and 100 ± 0% for low, medium, and high currents, respectively; P < 0.001) but did not influence NIRS rate constants (2.02 ± 0.54, 1.95 ± 0.44, 2.02 ± 0.46 min(-1) for low, medium, and high currents, respectively; P = 0.771). In summary, NIRS measurements of skeletal muscle mitochondrial function can be compared between VOL and ES exercises and were independent of the intensity of exercise. NIRS represents an important new technique that is practical for testing in research and clinical settings.

Electrically Induced Resistance Training in Individuals With Motor Complete Spinal Cord Injury

OBJECTIVE To examine the effects of 16 weeks of electrically induced resistance training on insulin resistance and glucose tolerance, and changes in muscle size, composition, and metabolism in paralyzed muscle. DESIGN Pre-post intervention. SETTING University-based trial. PARTICIPANTS Participants (N=14; 11 men and 3 women) with chronic (>2y post spinal cord injury), motor complete spinal cord injury. INTERVENTION Home-based electrically induced resistance exercise training twice weekly for 16 weeks. MAIN OUTCOME MEASURES Plasma glucose and insulin throughout a standard clinical oral glucose tolerance test, thigh muscle and fat mass via dual-energy x-ray absorptiometry, quadriceps and hamstrings muscle size and composition via magnetic resonance imaging, and muscle oxidative metabolism using phosphorus magnetic resonance spectroscopy. RESULTS Muscle mass increased in all participants (mean ± SD, 39%±27%; range, 5%-84%). The mean change ± SD in intramuscular fat was 3%±22%. Phosphocreatine mean recovery time constants ± SD were 102±24 and 77±18 seconds before and after electrical stimulation-induced resistance training, respectively (P<.05). There was no improvement in fasting blood glucose levels, homeostatic model assessment calculated insulin resistance, 2-hour insulin, or 2-hour glucose. CONCLUSIONS Sixteen weeks of electrical stimulation-induced resistance training increased muscle mass, but did not reduce intramuscular fat. Similarly, factors associated with insulin resistance or glucose tolerance did not improve with training. We did find a 25% improvement in mitochondrial function, as measured by phosphocreatine recovery rates. Larger improvements in mitochondrial function may translate into improved glucose tolerance and insulin resistance.

SKELETAL MUSCLE MITOCHONDRIAL FUNCTION AND INTERMITTENT CLAUDICATION IN PATIENTS WITH PERIPHERAL ARTERIAL DISEASE FOLLOWING SUPERVISED TREADMILL TRAINING

background: Abnormalities in skeletal muscle oxygen delivery and mitochondrial oxygen utilization are thought to contribute to the pathophysiology of claudication in subjects with lower extremity peripheral arterial disease (PAD). Non-invasive measurement of tissue oxygen delivery as well as oxygen utilization (reflecting muscle mitochondrial function independent of oxygen delivery) can be performed with near-infrared spectroscopy (NIRS).

Postcontractile blood flow as a window to cardiovascular disease

a historically important topic in physiology is the control of arterial blood flow ([1][1]). Numerous studies have shown that multiple vasodilatory mechanisms exist and that there is enough redundancy and compensatory interaction to make studying the control of blood flow a difficult topic ([5][2