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PURPOSE: Different strategies for near-infrared spectroscopy (NIRS)-derived muscle oxidative capacity assessment have been reported. This study compared and evaluated (I) approaches for averaging trials; (II) NIRS signals and blood volume correction equations; (III) the assessment of vastus lateralis (VL) and tibialis anterior (TA) muscles in two fitness levels groups. METHODS: Thirty-six participants [18 chronically trained (CT: 14 males, 4 females) and 18 untrained (UT: 10 males, 8 females)] participated in this study. Two trials of twenty transient arterial occlusions were performed for NIRS-derived muscle oxidative capacity assessment. Muscle oxygen consumption ( V ˙ O2m) was estimated from deoxygenated hemoglobin (HHb), corrected for blood volume changes following Ryan (HHbR) and Beever (HHbB) equations, and from oxygen saturation (StO2) in VL and TA. RESULTS: Superimposing or averaging V ˙ O2m or averaging the rate constants (k) from the two trials resulted in equivalent k values [two one-sided tests (TOST) procedure with 5% equivalence margin-P < 0.001]. Whereas HHbR (2.35 ± 0.61 min-1) and HHbB (2.34 ± 0.58 min-1) derived k were equivalent (P < 0.001), StO2 derived k (2.81 ± 0.92 min-1) was greater (P < 0.001) than both. k values were greater in CT vs UT in both muscles (VL: + 0.68 min-1, P = 0.002; TA: + 0.43 min-1, P = 0.01). CONCLUSION: Different approaches for averaging trials lead to similar k. HHb and StO2 signals provided different k, although different blood volume corrections did not impact k. Group differences in k were detected in both muscles.

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Purpose: Near-infrared spectroscopy (NIRS) indices during arterial occlusion-reperfusion maneuver have been used to examine the muscle's oxidative metabolism and microvascular function-important determinants of whole-body aerobic-fitness. The association of NIRS-derived parameters with whole-body VO2max was previously examined using a method requiring exercise (or electrical stimulation) followed by multiple arterial occlusions. We examined whether NIRS-derived indices of muscle deoxygenation and microvascular reactivity assessed during a single occlusion-reperfusion at rest are (a) associated with maximal/submaximal indices of whole-body aerobic-fitness and (b) could discriminate individuals with different VO2max. We, also, investigated which NIRS-parameter during occlusion-reperfusion correlates best with whole-body aerobic-fitness. Methods: Twenty-five young individuals performed an arterial occlusion-reperfusion at rest. Changes in oxygenated- and deoxygenated-hemoglobin (O2Hb and HHb, respectively) in vastus-lateralis were monitored; adipose tissue thickness (ATT) at NIRS-application was assessed. Participants also underwent a maximal incremental exercise test for VO2max, maximal aerobic velocity (MAV), and ventilatory-thresholds (VTs) assessments. Results: The HHbslope and HHbmagnitude of increase (occlusion-phase) and O2Hbmagnitude of increase (reperfusion-phase) were strongly correlated with VO2max (r = .695-.763, p < .001) and moderately with MAV (r = .468-.530; p < .05). O2Hbmagnitude was moderately correlated with VTs (r = .399-.414; p < .05). After controlling for ATT, the correlations remained significant for VO2max (r = .672-.704; p < .001) and MAV (r = .407; p < .05). Individuals in the high percentiles after median and tritile splits for HHbslope and O2Hbmagnitude had significantly greater VO2max vs. those in low percentiles (p < .01-.05). The HHbslope during occlusion was the best predictor of VO2max. Conclusion: NIRS-derived muscle deoxygenation/reoxygenation indices during a single arterial occlusion-reperfusion maneuver are strongly associated with whole-body maximal indices of aerobic-fitness (VO2max, MAV) and may discriminate individuals with different VO2max.

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Skeletal muscle wasting related to aging or pathological conditions is critically associated with the increased incidence and prevalence of secondary diseases including cardiovascular diseases, metabolic syndromes, and chronic inflammations. Much effort is made to develop agents to enhance muscle metabolism and function. Inonotus obliquus (I. obliquus; IO) is a mushroom popularly called chaga and has been widely employed as a folk medicine for inflammation, cardiovascular diseases, diabetes, and cancer in Eastern Europe and Asia. However, its effect on muscle health has not been explored. Here, we aimed to investigate the beneficial effect of IO extract in muscle regeneration and metabolism. The treatment of IO in C2C12 myoblasts led to increased myogenic differentiation and alleviation of dexamethasone-induced myotube atrophy. Network pharmacological analysis using the identified specific chemical constituents of IO extracts predicted protein kinase B (AKT)-dependent mechanisms to promote myogenesis and muscle regeneration. Consistently, IO treatment resulted in the activation of AKT, which suppressed muscle-specific ubiquitin E3 ligases induced by dexamethasone. IO treatment in mice improved the regeneration of cardiotoxin-injured muscles accompanied by elevated proliferation and differentiation of muscle stem cells. Furthermore, it elevated the mitochondrial content and muscle oxidative metabolism accompanied by the induction of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). Our current data suggest that IO is a promising natural agent in enhancing muscle regenerative capacity and oxidative metabolism thereby preventing muscle wasting.

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Following acute coronavirus disease 2019 (COVID-19), a substantial proportion of patients showed symptoms and sequelae for several months, namely the postacute sequelae of COVID-19 (PASC) syndrome. Major phenomena are exercise intolerance, muscle weakness, and fatigue. We aimed to investigate the physiopathology of exercise intolerance in patients with PASC syndrome by structural and functional analyses of skeletal muscle. At least 3 mo after infection, nonhospitalized patients with PASC (n = 11, age: 54 ± 11 yr; PASC) and patients without long-term symptoms (n = 12, age: 49 ± 9 yr; CTRL) visited the laboratory on four nonconsecutive days. Spirometry, lung diffusion capacity, and quality of life were assessed at rest. A cardiopulmonary incremental exercise test was performed. Oxygen consumption (V̇o2) kinetics were determined by moderate-intensity exercises. Muscle oxidative capacity (k) was assessed by near-infrared spectroscopy. Histochemical analysis, O2 flux (JO2) by high-resolution respirometry, and quantification of key molecular markers of mitochondrial biogenesis and dynamics were performed in vastus lateralis biopsies. Pulmonary and cardiac functions were within normal range in all patients. V̇o2peak was lower in PASC than CTRL (24.7 ± 5.0 vs. 32.9 ± 7.4 mL·min-1·kg-1, respectively, P < 0.05). V̇o2 kinetics was slower in PASC than CTRL (41 ± 12 vs. 30 ± 9 s-1, P < 0.05). k was lower in PASC than CTRL (1.54 ± 0.49 vs. 2.07 ± 0.51 min-1, P < 0.05). Citrate synthase, peroxisome proliferator-activated receptor-γ coactivator (PGC)1α, and JO2 for mitochondrial complex II were significantly lower in PASC vs. CTRL (all P values <0.05). In our cohort of patients with PASC, we showed limited exercise tolerance mainly due to "peripheral" determinants. Substantial reductions were observed for biomarkers of mitochondrial function, content, and biogenesis. PASC syndrome, therefore, appears to negatively impact skeletal muscle function, although the disease is a heterogeneous condition.NEW & NOTEWORTHY Several months after mild acute SARS-CoV-2 infection, a substantial proportion of patients present persisting, and often debilitating, symptoms and sequelae. These patients show reduced quality of life due to exercise intolerance, muscle weakness, and fatigue. The present study supports the hypothesis that "peripheral" impairments at skeletal muscle level, namely, reduced mitochondrial function and markers of mitochondrial biogenesis, are major determinants of exercise intolerance and fatigue, "central" phenomena at respiratory, and cardiac level being less relevant.

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The objectification of acute fatigue (during isometric muscle contraction) and cumulative fatigue (due to multiple intermittent isometric muscle contractions) plays an important role in sport climbing. The data of 42 participants were used in the study. Climbing performance was operationalized using maximal climbing-specific holding time (CSHT) by performing dead hangs. The test started with an initial measurement of handgrip strength (HGS) followed by three intermittent measurements of CSHT and HGS. During the test, finger flexor muscle oxygen saturation (SmO2) was measured using a near-infrared spectroscopy wearable biosensor. Significant reductions in CSHT and HGS could be found (p < 0.001), which indicates that the consecutive maximal isometric holding introduces cumulative fatigue. The reduction in CSHT did not correlate with a reduction in HGS over multiple consecutive maximal dead hangs (p > 0.35). Furthermore, there were no significant differences in initial SmO2 level, SmO2 level at termination, SmO2 recovery, and mean negative slope of the SmO2 saturation reduction between the different measurements (p > 0.24). Significant differences were found between pre-, termination-, and recovery- (10 s after termination) SmO2 levels (p < 0.001). Therefore, monitoring acute fatigue using athletes' termination SmO2 saturation seems promising. By contrast, the measurement of HGS and muscle oxygen metabolism seems inappropriate for monitoring cumulative fatigue during intermittent isometric climbing-specific muscle contractions.

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Progress in understanding physiological mechanisms often consists of discrete discoveries made across different models and species. Accordingly, understanding the mechanistic bases for how altering nitric oxide (NO) bioavailability impacts exercise tolerance (or not) depends on integrating information from cellular energetics and contractile regulation through microvascular/vascular control of O2 transport and pulmonary gas exchange. This review adopts state-of-the-art concepts including the intramyocyte power grid, the Wagner conflation of perfusive and diffusive O2 conductances, and the Critical Power/Critical Speed model of exercise tolerance to address how altered NO bioavailability may, or may not, affect physical performance. This question is germane from the elite athlete to the recreational exerciser and particularly the burgeoning heart failure (and other clinical) populations for whom elevating O2 transport and/or exercise capacity translates directly to improved life quality and reduced morbidity and mortality. The dearth of studies in females is also highlighted, and areas of uncertainty and questions for future research are identified.

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Near-infrared spectroscopy (NIRS) has been utilized as a noninvasive method to evaluate skeletal muscle mitochondrial function in humans, by calculating muscle V̇o2 (V̇o2m) recovery (off-) kinetics following short light-intensity plantar flexion exercise. The aim of the present study was to determine V̇o2m off- kinetics following standard cycle ergometer exercise of different intensities. Fifteen young physically active healthy men performed an incremental exercise (INCR) up to exhaustion and two repetitions of constant work-rate (CWR) exercises at 80% of gas exchange threshold (GET; MODERATE) and at 40% of the difference between GET and peak pulmonary V̇o2 (V̇o2p; HEAVY). V̇o2p and vastus lateralis muscle fractional O2 extraction by NIRS (Δ[deoxy(Hb+Mb)]) were recorded continuously. Transient arterial occlusions were carried out at rest and during the recovery for V̇o2m calculation. All subjects tolerated the repeated occlusions protocol without problems. The quality of the monoexponential fitting for V̇o2m off-kinetics analysis was excellent (0.93≤r2≤0.99). According to interclass correlation coefficient, the test-retest reliability was moderate to good. V̇o2m values at the onset of recovery were ~27, ~38, and ~35 times higher (in MODERATE, HEAVY, and INCR, respectively) than at rest. The time constants (τ) of V̇o2m off-kinetics were lower (P < 0.001) following MODERATE (29.1 ± 6.8 s) vs. HEAVY (40.8 ± 10.9) or INCR (42.9 ± 10.9), suggesting an exercise intensity dependency of V̇o2m off-kinetics. Only following MODERATE the V̇o2m off-kinetics were faster than the V̇o2p off-kinetics. V̇o2m off-kinetics, determined noninvasively by the NIRS repeated occlusions technique, can be utilized as a functional evaluation tool of skeletal muscle oxidative metabolism also following conventional cycle ergometer exercise.NEW & NOTEWORTHY This is the first study in which muscle V̇o2 recovery kinetics, determined noninvasively by near-infrared spectroscopy (NIRS) by utilizing the repeated occlusions method, was applied following standard cycle ergometer exercise of different intensities. The results demonstrate that muscle V̇o2 recovery kinetics, determined noninvasively by the NIRS repeated occlusions technique, can be utilized as a functional evaluation tool of skeletal muscle oxidative metabolism also following conventional cycle ergometer exercise, overcoming significant limitations associated with the traditionally proposed protocol.

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In the last 20 yr, near-infrared diffuse correlation spectroscopy (DCS) has been developed for providing a noninvasive estimate of microvascular blood flow (BF) as a BF index (BFi) in the human skin, muscle, breast, brain, and other tissue types. In this study, we proposed a new motion correction algorithm for DCS-derived BFi able to remove motion artifacts during cycling exercise. We tested this algorithm on DCS data collected during cycling exercise and demonstrated that DCS can be used to quantify muscle BFi during dynamic high-intensity exercise. In addition, we measured tissue regional oxygen metabolic rate (MRO2i) by combining frequency-domain multidistance near-infrared spectroscopy (FDNIRS) oximetry with DCS flow measures. Recreationally active subjects (n = 12; 31 ± 8 yr, 183 ± 4 cm, 79 ± 10 kg) pedaled at 80-100 revolutions/min until volitional fatigue with a work rate increase of 30 W every 4 min. Exercise intensity was normalized in each subject to the cycling power peak (Wpeak). Both rectus femoris BFi and MRO2i increased from 15% up to 75% Wpeak and then plateaued to the end of the exercise. During the recovery at 30 W cycling power, BFi remained almost constant, whereas MRO2i started to decrease. The BFi/MRO2i plateau was associated with the rising of the lactate concentration, indicating the progressive involvement of the anaerobic metabolism. These findings further highlight the utility of DCS and FDNIRS oximetry as effective, reproducible, and noninvasive techniques to assess muscle BFi and MRO2i in real time during a dynamic exercise such as cycling.NEW & NOTEWORTHY To the best of our knowledge, this study is the first to demonstrate that diffuse correlation spectroscopy in combination with frequency-domain near-infrared spectroscopy can monitor human quadriceps microvascular blood flow and oxygen metabolism with high temporal resolution during a cycling exercise. The optically measured parameters confirm the expected relationship between blood flow, muscle oxidative metabolism, and lactate production during exercise.

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KEY POINTS: Superposition of hypoxia on 21 day bed rest did not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone. A significant impairment of maximal oxidative performance was identified downstream of cardiovascular O2 delivery, involving both the intramuscular matching between O2 supply and utilization and mitochondrial respiration. These chronic adaptations appear to be relevant in terms of exposure to spaceflights and reduced gravity habitats (Moon or Mars), as characterized by low gravity and hypoxia, in patients with chronic diseases characterized by hypomobility/immobility and hypoxia, as well as in ageing. ABSTRACT: Skeletal muscle oxidative function was evaluated in 11 healthy males (mean ± SD age 27 ± 5 years) prior to (baseline data collection, BDC) and following a 21 day horizontal bed rest (BR), carried out in normoxia ( PIO2  = 133 mmHg; N-BR) and hypoxia ( PIO2  = 90 mmHg; H-BR). H-BR was aimed at simulating reduced gravity habitats. The effects of a 21 day hypoxic ambulatory confinement ( PIO2  = 90 mmHg; H-AMB) were also assessed. Pulmonary O2 uptake ( V̇O2 ), vastus lateralis fractional O2 extraction (changes in deoxygenated haemoglobin + myoglobin concentration, Δ[deoxy(Hb + Mb)]; near-infrared spectroscopy) and femoral artery blood flow (ultrasound Doppler) were evaluated during incremental one-leg knee-extension exercise (reduced constraints to cardiovascular O2 delivery) carried out to voluntary exhaustion in a normoxic environment. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibres. V̇O2peak decreased (P < 0.05) after N-BR (0.98 ± 0.13 L min-1 ) and H-BR (0.96 ± 0.17 L min-1 ) vs. BDC (1.05 ± 0.14 L min-1 ). In the presence of a decreased (by ∼6-8%) thigh muscle volume, V̇O2peak normalized per unit of muscle mass was not affected by both interventions. Δ[deoxy(Hb + Mb)]peak decreased (P < 0.05) after N-BR (65 ± 13% of limb ischaemia) and H-BR (62 ± 12%) vs. BDC (73 ± 13%). H-AMB did not alter V̇O2peak or Δ[deoxy(Hb + Mb)]peak . An overshoot of Δ[deoxy(Hb + Mb)] was evident during the first minute of unloaded exercise after N-BR and H-BR. Arterial blood flow to the lower limb during both unloaded and peak knee extension was not affected by any intervention. Maximal ADP-stimulated mitochondrial respiration decreased (P < 0.05) after all interventions vs. control. In 21 day N-BR, a significant impairment of oxidative metabolism occurred downstream of cardiovascular O2 delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O2 supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.

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BACKGROUND: Parkinson's Disease (PD) is characterized by progressive and disabling symptoms. An impaired oxidative metabolism efficiency was supposed to be involved in the systemic impairment. Rehabilitative treatment represents a valid tool in promoting skeletal muscle's adaptations, even if no solid studies on muscle metabolic features are still available. OBJECTIVE: To evaluate the efficiency of skeletal muscle oxidative metabolism in PD patients in comparison with age-matched controls and test the role of an intensive aerobic treatment on muscle oxidative metabolism and its clinical effects. METHODS: 60 PD patients and 32 age-matched healthy controls participated. Haematic lactate values were detected during and after a submaximal incremental exercise on treadmill. The number of steps completed during the exercise was recorded. From these patients 10 underwent to an intensive aerobic treatment on treadmill (4 sessions/week for 4 weeks). Haematic lactate values and functional scales were recorded before (T0) and after (T1) treatment. RESULTS: At rest no significant difference in hematic lactate values between PD and control subjects was found. Lactate blood levels were significantly higher (p < 0,001) after the aerobic exercise test in PD patients compared to controls. These values remained higher at any time during recovery period (p < 0,001). No significant relationship between lactate values and the number of completed steps was found. After the rehabilitation treatment haematic value of lactate showed a significant reduction (p < 0,05) at 0, 5 and 10 minutes of recovery period with a normalization of value at 30'. All functional scales showed an improvement trend at T1, in particular Berg Balance Scale and 6 Meter Walking Test showed a significant reduction (p < 0,001 and p < 0,05 respectively). CONCLUSION: Our data clearly show an impaired muscle oxidative efficiency in PD subjects. The intensive rehabilitation program on treadmill showed a beneficial effect on muscle oxidative metabolism, endurance and balance, confirming the focal role of rehabilitation in PD patients.

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Measurement of muscle oxidative metabolism is of interest for monitoring the training status in athletes and the rehabilitation process in patients. Time domain near infrared spectroscopy (TD NIRS) is an optical technique that allows the non-invasive measurement of the hemodynamic parameters in muscular tissue: concentrations of oxy- and deoxy-hemoglobin, total hemoglobin content, and tissue oxygen saturation. In this paper, we present a novel TD NIRS medical device for muscle oxidative metabolism. A custom-printed 3D probe, able to host optical elements for signal acquisition from muscle, was develop for TD NIRS in vivo measurements. The system was widely characterized on solid phantoms and during in vivo protocols on healthy subjects. In particular, we tested the in vivo repeatability of the measurements to quantify the error that we can have by repositioning the probe. Furthermore, we considered a series of acquisitions on different muscles that were not yet previously performed with this custom probe: a venous-arterial cuff occlusion of the arm muscle, a cycling exercise, and an isometric contraction of the vastus lateralis.

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Cardiac function, skeletal (soleus) muscle oxidative metabolism, and the effects of exercise training were evaluated in a transgenic murine model (Tgαq*44) of chronic heart failure during the critical period between the occurrence of an impairment of cardiac function and the stage at which overt cardiac failure ensues (i.e., from 10 to 12 mo of age). Forty-eight Tgαq*44 mice and 43 wild-type FVB controls were randomly assigned to control groups and to groups undergoing 2 mo of intense exercise training (spontaneous running on an instrumented wheel). In mice evaluated at the beginning and at the end of training we determined: exercise performance (mean distance covered daily on the wheel); cardiac function in vivo (by magnetic resonance imaging); soleus mitochondrial respiration ex vivo (by high-resolution respirometry); muscle phenotype [myosin heavy chain (MHC) isoform content; citrate synthase (CS) activity]; and variables related to the energy status of muscle fibers [ratio of phosphorylated 5'-AMP-activated protein kinase (AMPK) to unphosphorylated AMPK] and mitochondrial biogenesis and function [peroxisome proliferative-activated receptor-γ coactivator-α (PGC-1α)]. In the untrained Tgαq*44 mice functional impairments of exercise performance, cardiac function, and soleus muscle mitochondrial respiration were observed. The impairment of mitochondrial respiration was related to the function of complex I of the respiratory chain, and it was not associated with differences in CS activity, MHC isoforms, p-AMPK/AMPK, and PGC-1α levels. Exercise training improved exercise performance and cardiac function, but it did not affect mitochondrial respiration, even in the presence of an increased percentage of type 1 MHC isoforms. Factors "upstream" of mitochondria were likely mainly responsible for the improved exercise performance.NEW & NOTEWORTHY Functional impairments in exercise performance, cardiac function, and soleus muscle mitochondrial respiration were observed in transgenic chronic heart failure mice, evaluated in the critical period between the occurrence of an impairment of cardiac function and the terminal stage of the disease. Exercise training improved exercise performance and cardiac function, but it did not affect the impaired mitochondrial respiration. Factors "upstream" of mitochondria, including an enhanced cardiovascular O2 delivery, were mainly responsible for the functional improvement.

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