scholarly journals NIRS-derived skeletal muscle oxidative capacity is correlated with aerobic fitness and independent of sex

2020 ◽  
Vol 129 (3) ◽  
pp. 558-568
Author(s):  
Austin T. Beever ◽  
Thomas R. Tripp ◽  
Jenny Zhang ◽  
Martin J. MacInnis

Near-infrared spectroscopy (NIRS) can be used to measure skeletal muscle oxidative capacity. Here, we demonstrated that NIRS-derived skeletal muscle oxidative capacity of the vastus lateralis was independent of sex, reliable across and within days, and correlated with maximal and submaximal indices of aerobic fitness, including maximal oxygen uptake, lactate threshold, and respiratory compensation point. These findings highlight the utility of NIRS for investigating skeletal muscle oxidative capacity in females and males.

2006 ◽  
Vol 31 (1) ◽  
pp. 48-55 ◽  
Author(s):  
Kotaro Kawaguchi ◽  
Yukiko Hayashi ◽  
Kiyokazu Sekikawa ◽  
Mitsuru Tabusadani ◽  
Tsutomu Inamizu ◽  
...  

This study examined the relationship between acute cardiorespiratory and muscle oxygenation and blood volume changes during prolonged exercise. Eight healthy male volunteers (mean maximum oxygen uptake ([Formula: see text]O2max) = 41.6 ± 2.4 mL/kg/min) performed 60 min submaximal cycling at 50% [Formula: see text]O2max. Oxygen uptake ([Formula: see text]O2) was measured by indirect spirometry, cardiac output (CO) was estimated using a PortapresTM, and right vastus lateralis oxyhemoglobin/ myoglobin (oxyHb/Mb), deoxyhemoglobin/myoglobin (deoxyHb/Mb), and total hemoglobin/myoglobin (total Hb/Mb) were recorded using near-infrared spectroscopy (NIRS). After 40 min of exercise, there was a significant increase in [Formula: see text]O2 due to a significantly higher arteriovenous oxygen difference ((a - v)O2diff). After 30 min of exercise CO remained unchanged, but there was a significant decrease in stroke volume and a proportionate increase in heart rate, thus indicating the occurrence of cardiovascular drift. During the first few minutes of exercise, there was a decline in oxyHb/Mb and total Hb/Mb, whereas deoxyHb/Mb remained unchanged. Thereafter, oxyHb/Mb and total Hb/Mb increased systematically until the termination of exercise while deoxyHb/Mb declined. After 40 min of exercise, these changes were significantly different from the baseline values. There were no significant correlations between the changes in the NIRS variables and systemic [Formula: see text]O2 or mixed (a - v)O2diff during exercise. These results suggest that factors other than localized changes in muscle oxygenation and blood volume account for the increased [Formula: see text]O2 during prolonged submaximal exercise. Key words: near infrared spectroscopy, cardiovascular drift, systemic oxygen consumption.


2020 ◽  
Vol 15 (2) ◽  
pp. 278-284
Author(s):  
Nicola Giovanelli ◽  
Lea Biasutti ◽  
Desy Salvadego ◽  
Hailu K. Alemayehu ◽  
Bruno Grassi ◽  
...  

Purpose: To evaluate the effects of a trail-running race on muscle oxidative function by measuring pulmonary gas exchange variables and muscle fractional O2 extraction. Methods: Eighteen athletes were evaluated before (PRE) and after (POST) a trail-running competition of 32 or 50 km with 2000 or 3500 m of elevation gain, respectively. During the week before the race, runners performed an incremental uphill running test and an incremental exercise by utilizing a 1-leg knee extension ergometer. The knee extension exercise was repeated after the end of the race. During the knee extension test, the authors measured oxygen uptake () and micromolar changes in deoxygenated hemoglobin (Hb)+myoglobin (Mb) concentrations (Δ[deoxy(Hb+Mb)]) on vastus lateralis with a portable near-infrared spectroscopy. Results: was lower at POST versus PRE (−23.9% [9.0%]; P < .001). at POST was lower than at the same workload at PRE (−8.4% [15.6%]; P < .050). Peak power output and time to exhaustion decreased at POST by −23.7% (14.3%) and −18.3% (11.3%), respectively (P < .005). At POST, the increase of Δ[deoxy(Hb+Mb)] as a function of work rate, from unloaded to peak, was less pronounced (from 20.2% [10.1%] to 64.5% [21.1%] of limb ischemia at PRE to 16.9% [12.7%] to 44.0% [18.9%] at POST). Peak Δ[deoxy(Hb+Mb)] values were lower at POST (by −31.2% [20.5%]; P < .001). Conclusions: Trail running leads to impairment in skeletal muscle oxidative metabolism, possibly related to muscle damage from repeated eccentric contractions. In association with other mechanisms, the impairment of skeletal muscle oxidative metabolism is likely responsible for the reduced exercise capacity and tolerance during and following these races.


2018 ◽  
Vol 50 (5S) ◽  
pp. 149-150
Author(s):  
Brian A. Irving ◽  
Timothy D. Allerton ◽  
Guillaume Spielmann ◽  
Stefany Primeaux ◽  
Arnold Nelson ◽  
...  

2013 ◽  
Vol 115 (12) ◽  
pp. 1757-1766 ◽  
Author(s):  
Terence E. Ryan ◽  
W. Michael Southern ◽  
Mary Ann Reynolds ◽  
Kevin K. McCully

The purpose of this study was to cross-validate measurements of skeletal muscle oxidative capacity made with near-infrared spectroscopy (NIRS) measurements to those made with phosphorus magnetic resonance spectroscopy (31P-MRS). Sixteen young (age = 22.5 ± 3.0 yr), healthy individuals were tested with both 31P-MRS and NIRS during a single testing session. The recovery rate of phosphocreatine was measured inside the bore of a 3-Tesla MRI scanner, after short-duration (∼10 s) plantar flexion exercise as an index of skeletal muscle oxidative capacity. Using NIRS, the recovery rate of muscle oxygen consumption was also measured using repeated, transient arterial occlusions outside the MRI scanner, after short-duration (∼10 s) plantar flexion exercise as another index of skeletal muscle oxidative capacity. The average recovery time constant was 31.5 ± 8.5 s for phosphocreatine and 31.5 ± 8.9 s for muscle oxygen consumption for all participants ( P = 0.709). 31P-MRS time constants correlated well with NIRS time constants for both channel 1 (Pearson's r = 0.88, P < 0.0001) and channel 2 (Pearson's r = 0.95, P < 0.0001). Furthermore, both 31P-MRS and NIRS exhibit good repeatability between trials (coefficient of variation = 8.1, 6.9, and 7.9% for NIRS channel 1, NIRS channel 2, and 31P-MRS, respectively). The good agreement between NIRS and 31P-MRS indexes of skeletal muscle oxidative capacity suggest that NIRS is a valid method for assessing mitochondrial function, and that direct comparisons between NIRS and 31P-MRS measurements may be possible.


2013 ◽  
Vol 113 (9) ◽  
pp. 2275-2283 ◽  
Author(s):  
Melissa Lynn Erickson ◽  
Terence E. Ryan ◽  
Hui-Ju Young ◽  
Kevin K. McCully

2018 ◽  
Vol 50 (9) ◽  
pp. 688-690 ◽  
Author(s):  
Alessandra Adami ◽  
Brian D. Hobbs ◽  
Merry-Lynn N. McDonald ◽  
Richard Casaburi ◽  
Harry B. Rossiter ◽  
...  

Muscle oxidative capacity is a major determinant of maximum oxygen uptake (V̇O2max). V̇O2max predicts survival in humans. Muscle oxidative capacity is low in chronic obstructive pulmonary disease (COPD) and can be assessed from the muscle oxygen consumption recovery rate constant ( k) by near-infrared spectroscopy. We hypothesized that 11 SNPs, previously associated with the increase in V̇O2max following exercise training, would correlate with k in 152 non-Hispanic White and African American smokers with and without COPD. Associations were adjusted for age, weight, FEV1% predicted, steps/day, and principal components of genetic ancestry. No SNPs were significantly associated with k. rs2792022 within BTAF1 (β = 0.130, P = 0.053) and rs24575771 within SLC22A3 (β = 0.106, P = 0.058) approached nominal significance. Case-control stratification identified three SNPs nominally associated with k in moderate-to-severe COPD ( rs6481619 within SVIL β = 0.152, P = 0.013; BTAF1 β = 0.196, P = 0.046; rs7386139 within DEPTOR β = 0.159, P = 0.047). These data support further study of the genomic contributions to skeletal muscle dysfunction in COPD.


2016 ◽  
Vol 121 (3) ◽  
pp. 636-645 ◽  
Author(s):  
Stephan van der Zwaard ◽  
C. Jo de Ruiter ◽  
Dionne A. Noordhof ◽  
Renske Sterrenburg ◽  
Frank W. Bloemers ◽  
...  

V̇o2 max during whole body exercise is presumably constrained by oxygen delivery to mitochondria rather than by mitochondria's ability to consume oxygen. Humans and animals have been reported to exploit only 60-80% of their mitochondrial oxidative capacity at maximal oxygen uptake (V̇o2 max). However, ex vivo quantification of mitochondrial overcapacity is complicated by isolation or permeabilization procedures. An alternative method for estimating mitochondrial oxidative capacity is via enzyme histochemical quantification of succinate dehydrogenase (SDH) activity. We determined to what extent V̇o2 max attained during cycling exercise differs from mitochondrial oxidative capacity predicted from SDH activity of vastus lateralis muscle in chronic heart failure patients, healthy controls, and cyclists. V̇o2 max was assessed in 20 healthy subjects and 28 cyclists, and SDH activity was determined from biopsy cryosections of vastus lateralis using quantitative histochemistry. Similar data from our laboratory of 14 chronic heart failure patients and 6 controls were included. Mitochondrial oxidative capacity was predicted from SDH activity using estimated skeletal muscle mass and the relationship between ex vivo fiber V̇o2 max and SDH activity of isolated single muscle fibers and myocardial trabecula under hyperoxic conditions. Mitochondrial oxidative capacity predicted from SDH activity was related ( r2 = 0.89, P < 0.001) to V̇o2 max measured during cycling in subjects with V̇o2 max ranging from 9.8 to 79.0 ml·kg−1·min−1. V̇o2 max measured during cycling was on average 90 ± 14% of mitochondrial oxidative capacity. We conclude that human V̇o2 max is related to mitochondrial oxidative capacity predicted from skeletal muscle SDH activity. Mitochondrial oxidative capacity is likely marginally limited by oxygen supply to mitochondria.


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