Melissa L. Erickson

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 Oxidative Capacity in Patients with Cystic Fibrosis

What is the central question of this study? Do patients with cystic fibrosis have reduced skeletal muscle oxidative capacity, measured with near‐infrared spectroscopy, compared with demographically matched control subjects? What is the main finding and is its importance? Patients with cystic fibrosis have impairments in skeletal muscle oxidative capacity. This reduced skeletal muscle oxidative capacity not only appears to be accelerated by age, but it may also contribute to exercise intolerance in patients with cystic fibrosis.

Skeletal muscle oxidative capacity in amyotrophic lateral sclerosis

Introduction: Mitochondrial dysfunction in the motor neuron has been suspected in amyotrophic lateral sclerosis (ALS). If mitochondrial abnormalities are also found in skeletal muscle, assessing skeletal muscle could serve as an important biomarker of disease progression. Methods: Using 31P magnetic resonance (31P‐MRS) and near infrared (NIRS) spectroscopy, we compared the absolute values and reproducibility of skeletal muscle oxidative capacity in people with ALS (n = 6) and healthy adults (young, n = 7 and age‐matched, n = 4). Results: ALS patients had slower time constants for phosphocreatine (PCr) and muscle oxygen consumption (mVO2) compared with young, but not age‐matched controls. The coefficient of variation for the time constant was 10% (SD = 2.8%) and 17% (SD = 6.2%) for PCr and mVO2, respectively. Conclusions: People with ALS had, on average, a small but not statistically significant, impairment in skeletal muscle mitochondrial function measured by both 31P‐MRS and NIRS. Both methods demonstrated good reproducibility. Muscle Nerve 50: 767–774, 2014

Endurance neuromuscular electrical stimulation training improves skeletal muscle oxidative capacity in individuals with motor-complete spinal cord injury.

Introduction: Spinal cord injury (SCI) results in skeletal muscle atrophy, increases in intramuscular fat, and reductions in skeletal muscle oxidative capacity. Endurance training elicited with neuromuscular electrical stimulation (NMES) may reverse these changes and lead to improvement in muscle metabolic health. Methods: Fourteen participants with complete SCI performed 16 weeks of home‐based endurance NMES training of knee extensor muscles. Skeletal muscle oxidative capacity, muscle composition, and blood metabolic and lipid profiles were assessed pre‐ and post‐training. Results: There was an increase in number of contractions performed throughout the duration of training. The average improvement in skeletal muscle oxidative capacity was 119%, ranging from –14% to 387% (P = 0.019). There were no changes in muscle composition or blood metabolic and lipid profiles. Conclusion: Endurance training improved skeletal muscle oxidative capacity, but endurance NMES of knee extensor muscles did not change blood metabolic and lipid profiles. Muscle Nerve 55: 669–675, 2017

Postmeal exercise blunts postprandial glucose excursions in people on metformin monotherapy

Metformin is used clinically to reduce fasting glucose with minimal effects on postprandial glucose. Postmeal exercise reduces postprandial glucose and may offer additional glucose-lowering benefit beyond that of metformin alone, yet controversy exists surrounding exercise and metformin interactions. It is currently unknown how postmeal exercise and metformin monotherapy in combination will affect postprandial glucose. Thus, we examined the independent and combined effects of postmeal exercise and metformin monotherapy on postprandial glucose. A randomized crossover design was used to assess the influence of postmeal exercise on postprandial glucose excursions in 10 people treated with metformin monotherapy (57 ± 10 yr, HbA1C = 6.3 ± 0.6%). Each participant completed the following four conditions: sedentary and postmeal exercise (5 × 10-min bouts of treadmill walking at 60% V̇o2max) with metformin and sedentary and postmeal exercise without metformin. Peak postprandial glucose within a 2-h time window and 2-h total area under the curve was assessed after a standardized breakfast meal, using continuous glucose monitoring. Postmeal exercise significantly blunted 2-h peak (P = 0.001) and 2-h area under the curve (P = 0.006), with the lowest peak postprandial glucose excursion observed with postmeal exercise and metformin combined (P < 0.05 vs. all other conditions: metformin/sedentary: 12 ± 3.4, metformin/exercise: 9.7 ± 2.3, washout/sedentary: 13.3 ± 3.2, washout/exercise: 11.1 ± 3.4 mmol/l). Postmeal exercise and metformin in combination resulted in the lowest peak postprandial glucose excursion compared with either treatment modality alone. Exercise timed to the postprandial phase may be important for optimizing glucose control during metformin monotherapy.NEW & NOTEWORTHY The interactive effects of metformin and exercise on key physiological outcomes remain an area of controversy. Findings from this study show that the combination of metformin monotherapy and moderate-intensity postmeal exercise led to beneficial reductions in postprandial glucose excursions. Postmeal exercise may be a useful strategy for the management of postprandial glucose in people on metformin.

A wellness program for individuals with disabilities: Using a student wellness coach approach.

BACKGROUND Individuals with disabilities are at higher risk of health conditions; thus, there is a need to provide hands-on opportunities for pre-healthcare professionals to interact with individual with disabilities as well as deliver wellness services to this population. OBJECTIVE Examine the feasibility and effectiveness of a student-led wellness program for individuals with disabilities. METHODS Thirty-two undergraduate student wellness coaches between the ages of 19-23 years, and fifteen participants with disabilities, ranging in ages from 28 to 74 years were included in this study. Every participant was assigned to at least 1 student wellness coach with the purpose of establishing an individualized wellness plan. RESULTS After 3 months (fall 2013 academic semester), all wellness coaches demonstrated improved clinical interaction and confidence toward working with the participants. The participants had an average weight loss of 2.0 ± 2.9 kg, ranging from 0.0 to 9.0 kg. All participants had improved functionality and fitness and reported high satisfaction toward the program. CONCLUSIONS This study demonstrated the impact of a unique program on the education of pre-healthcare professionals and the overall wellness of participants with disabilities. The program model has the potential to provide clinical health education among pre-healthcare professionals through interacting with individuals with disabilities.

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

Rebuttal from Paula Rodriguez-Miguelez, Melissa L. Erickson, Kevin K. McCully and Ryan A. Harris

We read with great interest the opposing view presented by Hulzebos et al. (2017), which provides evidence that skeletal muscle oxidative capacity is preserved in patients with cystic fibrosis (CF). It is clear that both of our positions acknowledge the strong importance of understanding how skeletal muscle function contributes to exercise intolerance in patients with CF. Nonetheless, Hulzebos and colleagues (2017) defend the viewpoint that a reduction in muscle mass, not muscle function, is the underlying mechanism of exercise intolerance in patients with CF. Patients with CF spend less time performing moderate and/or vigorous physical activities compared to healthy controls, even during periods of enhanced wellbeing (Troosters et al. 2009; Ward et al. 2013). It is therefore logical to consider that physical inactivity can contribute to quantitative impairments of skeletal muscle (i.e. muscle deconditioning and smaller muscle mass), which can result in exercise intolerance (de Meer et al. 1999). However, reductions in muscle strength and peak power during exercise have been observed in physically active, competitive athletes with CF compared to their healthy peers (Selvadurai et al. 2003). Importantly, these results were supported by the presence of similar muscle and bone cross-sectional area between patients and healthy controls, ruling out the possibility of skeletal muscle deconditioning in this athletic CF cohort. The data that indicate a preserved skeletal muscle function in patients with CF are scant. In contrast, there are a handful of studies that provide compelling data to support an impaired mitochondrial oxidative metabolism in patients with CF compared to controls (de Meer et al. 1995; Selvadurai et al. 2003; Wells et al. 2011; Erickson et al. 2015), even when controlling for skeletal muscle cross-sectional area (Selvadurai et al. 2003; Wells et al. 2011). It is likely that the disparity in findings can be explained by inclusion of a younger, healthier CF population (Werkman et al. 2016) and/or the evaluation of different muscle groups that are composed of different fibre-type proportions (Decorte et al. 2017). In conclusion, there are convincing data that document both qualitative and quantitative impairments of skeletal muscle in patients with CF. Results from different studies provide strong evidence to support the existence of mitochondrial dysfunction and altered skeletal muscle oxidative metabolism in CF, independent of muscle mass. Although it is reasonable to speculate that reductions in both muscle mass and muscle function contribute to exercise intolerance in CF, further investigation of the link between skeletal muscle function and exercise capacity in CF is certainly warranted.