Skeletal Muscle Oxygen Extraction Research Articles

Simultaneous exercise stress cardiac magnetic resonance and cardiopulmonary exercise testing to elucidate the Fick components of aerobic exercise capacity: a feasibility and reproducibility study and pilot study in hematologic cancer survivors

BackgroundPatients treated for hematologic malignancy often experience reduced exercise capacity and increased fatigue; however whether this reduction is related to cardiac dysfunction or impairment of skeletal muscle oxygen extraction during activity is unknown. Cardiopulmonary exercise testing (CPET) coupled with stress cardiac magnetic resonance (ExeCMR), may provide a noninvasive method to identify the abnormalities of cardiac function or skeletal muscle oxygen extraction. This study was performed to determine the feasibility and reproducibility of a ExeCMR + CPET technique to measure the Fick components of peak oxygen consumption (VO2) and pilot its discriminatory potential in hematologic cancer patients experiencing fatigue.MethodsWe studied 16 individuals undergoing ExeCMR to determine exercise cardiac reserve with simultaneous measures of VO2. The arteriovenous oxygen content difference (a-vO2diff) was calculated as the quotient of VO2/cardiac index (CI). Repeatability in measurements of peak VO2, CI, and a-vO2diff was assessed in seven healthy controls. Finally, we measured the Fick determinants of peak VO2 in hematologic cancer survivors with fatigue (n = 6) and compared them to age/gender-matched healthy controls (n = 6).ResultsStudy procedures were successfully completed without any adverse events in all subjects (N = 16, 100%). The protocol demonstrated good-excellent test-retest reproducibility for peak VO2 (intraclass correlation coefficient [ICC] = 0.992 [95%CI:0.955–0.999]; P < 0.001), peak CI (ICC = 0.970 [95%CI:0.838–0.995]; P < 0.001), and a-vO2diff (ICC = 0.953 [95%CI:0.744–0.992]; P < 0.001). Hematologic cancer survivors with fatigue demonstrated a significantly lower peak VO2 (17.1 [13.5–23.5] vs. 26.0 [19.7–29.5] mL·kg-1·min-1, P = 0.026) and lower peak CI (5.0 [4.7–6.3] vs. 7.4 [7.0-8.8] L·min-1/m2, P = 0.004) without a significant difference in a-vO2diff (14.4 [11.8–16.9] vs. 13.6 [10.9–15.4] mLO2/dL, P = 0.589).ConclusionsNoninvasive measurement of peak VO2 Fick determinants is feasible and reliable with an ExeCMR + CPET protocol in those treated for a hematologic malignancy and may offer insight into the mechanisms of exercise intolerance in those experiencing fatigue.

Adding heat stress to repeated-sprint training in hypoxia does not enhance performance improvements in canoe/kayak athletes.

The present study investigated the effects of adding heat stress to repeated-sprint training in hypoxia on performance and physiological adaptations in well-trained athletes. Sixteen canoe/kayak sprinters conducted 2weeks of repeated-sprint training consisting of three sets of 5 × 10s sprints with 20s active recovery periods under conditions of either normobaric hypoxia (RSH, FiO2: 14.5%, ambient temperature: 18 ℃, n = 8) or combined heat and normobaric hypoxia (RSHH, FiO2: 14.5%, ambient temperature: 38 ℃, n = 8). Before and after training, the 10 × 10s repeated-sprint ability (RSA) test and 500m time trial were performed on a canoe/kayak ergometer. Peak and average power outputs during the RSA test were significantly improved after training in both RSH (peak power: + 21.5 ± 4.6%, P < 0.001; average power: + 12.5 ± 1.9%, P < 0.001) and RSHH groups (peak power: + 18.8 ± 6.6%, P = 0.005; average power: + 10.9 ± 6.8%, P = 0.030). Indirect variables of skeletal muscle oxygen extraction (deoxygenated hemoglobin) and blood perfusion (total hemoglobin) during the RSA test were significantly increased after training in the RSH group (P = 0.041 and P = 0.034, respectively) but not in the RSHH group. In addition, finish time during the 500m time trial was significantly shortened after the training only in the RSH group (RSH: -3.9 ± 0.8%, P = 0.005; RSHH: -3.1 ± 1.4%, P = 0.078). Adding heat stress to RSH does not enhance performance improvement and may partially mask muscle tissue adaptation.

Effects of 12-Week Home-based Resistance Training on Peripheral Muscle Oxygenation in Children With Congenital Heart Disease: A CHAMPS Study.

A hallmark feature of children with congenital heart disease (CHD) is exercise intolerance. Whether a home-based resistance training intervention improves muscle oxygenation (as measured by tissue oxygenation index, TOI) and exercise tolerance (O2 reserve) during aerobic exercise in children with CHD compared with healthy children is unknown. We report findings for 10 children with CHD (female/male: 4/6; mean ± standard deviation age: 13 ± 1 years) and 9 healthy controls (female/male: 5/4; age: 12 ± 3 years). Children with CHD completed a 12-week home-based exercise programme in addition to 6 in-person sessions. Exercise tolerance was assessed with a peak exercise test. Vastus lateralis TOI was continuously sampled during the peak O2 test via near-infrared spectroscopy. There was a medium effect (Cohen's d= 0.67) of exercise training on lowering TOI at peak exercise (pre: 30 ± 16 %total labile signal vs post: 20 ± 13 % total labile signal; P= 0.099). Exercise training had a small effect (Cohen's d= 0.23) on increasing O2 reserve by 1.6 mL/kg/min (pre: 27.2 ± 5.7 mL/kg/min vs post: 29.4 ± 8.8 mL/kg/min; P= 0.382). There was also a small effect (Cohen's d= 0.27) of exercise on peak heart rate (pre: 175 ± 23 beats/min vs post: 169 ± 21 beats/min; P= 0.18). TOI, O2 reserve, and heart rate were generally lower than healthy control participants. Our findings indicate that home-based resistance training may enhance skeletal muscle oxygen extraction (lower TOI) and subsequently O2 reserve in children with CHD.

Physiological basis of brief, intense interval training to enhance maximal oxygen uptake: a mini-review.

Brief, intense interval training describes a style of exercise characterized by short bouts of strenuous effort interspersed with recovery periods. The method increases whole body maximal oxygen uptake (V̇o2max), but the underlying physiological basis is unclear. V̇o2max represents the functional limit of the integrative oxygen cascade, which refers to the physiological steps involved in oxygen transport and utilization from atmospheric air to mitochondrial metabolism. There is insufficient evidence to definitively state which steps in the oxygen cascade are responsible for the improvement in V̇o2max after brief, intense interval training. Studies typically focus on specific physiological variables that are often characterized as "central" or "peripheral" based in part on their location in the body. Recent work suggests that training for ≥6 wk improves V̇o2max in part by increasing maximal cardiac output and expanding blood volume, responses that are expected to augment central oxygen delivery. Other responses to brief, intense interval training, including increased capillary and mitochondrial density, may contribute to increases in V̇o2max via enhanced skeletal muscle oxygen extraction and/or increased muscle diffusing capacity. This is especially evident after relatively short-term training and despite no change in central oxygen delivery factors. Mechanistic investigations, particularly employing contemporary technologies, are needed to advance our understanding of the early time course of the V̇o2max response to brief, intense interval training and the extent to which changes in specific oxygen cascade processes compare with traditional endurance training.

Mechanisms Determining VO2peak During Single Leg Knee‐Extension Exercise in Heart Failure with Preserved Ejection Fraction Patients: Peripheral vs. Central Phenotypes

BackgroundHeart failure with preserved ejection fraction (HFpEF) is characterized by exercise intolerance, including a reduced maximal aerobic capacity that affects all aspects of daily living. The mechanisms responsible for the decreased exercise tolerance in HFpEF are incompletely understood. Our research group has characterized two unique HFpEF phenotypes based on cardiac output reserve relative to exercise metabolic work: those with either a “central” (Type A) or “peripheral” (Type B) limitation to exercise. We sought to investigate the peripheral limitations to exercise in these 2 phenotypes using single‐leg knee extension (SLKE) exercise, a modality that reduces the central limitations to exercise. Specifically, we tested the hypothesis that patients with the Type B phenotype would have lower leg VO2peak secondary to insufficient oxygen extraction (i.e., lower ∆a‐vO2diff) when compared to patients with the Type A phenotype.MethodsWe studied 20 HFpEF patients with either the Type A (n = 8; 68 ± 2yr; 5F) or Type B (n = 12; 70 ± 2yr; 7F) phenotype. Participants performed an incremental SLKE peak exercise test on a custom ergometer. Leg blood flow (LBF) was measured at the common femoral artery using duplex Doppler ultrasound. Average LBF (ml/min) at each workload was determined from measured blood velocity and vessel diameter. a‐vO2diff was calculated from hemoglobin and venous oxygen saturation directly from a femoral venous catheter, and arterial oxygen saturation via pulse oximetry. Leg VO2 (ml/min) was determined as the product of LBF and a‐vO2diff. All data are presented as mean ± SEM.ResultsParticipants with the Type A “central” phenotype reached a peak exercise workload of 20 ± 4 W and those with the Type B “peripheral” phenotype reached 15 ± 2 W (p = 0.18). Leg VO2peak was not different between the two phenotypes (Type A: 215 ± 23; Type B: 253 ± 34 ml/min; p = 0.42). The peak increase in LBF was ~ 50% greater in Type B (+1940 ± 243 ml/min) than Type A (+1309 ± 161 ml/min) patients, though this response was more variable (p = 0.07). Additionally, the ∆a‐vO2diff from rest to peak exercise was significantly lower in those with the Type B phenotype (Type A: +7.17 ± 0.87; Type B: +4.63 ± 0.46 ml O2/dl blood; p = 0.01). Finally, the ∆LBF/∆VO2 slope was lower in patients with the Type A phenotype (Type A: 6.78 ± 0.55; Type B: 8.72 ± 0.43; p = 0.01).ConclusionContrary to our hypothesis, there was no difference in leg VO2peak between phenotypes. Patients with Type B HFpEF had greater limitations in skeletal muscle oxygen extraction during exercise as evidenced by their diminished ability to increase a‐vO2diff during incremental SLKE, similar to the observed a‐vO2diff extraction impairments during whole body exercise. Importantly, by phenotyping HFpEF patients based on their limitations to exercise, we may be able to better individualize treatment strategies to improve exercise tolerance.

Abstract 9677: Therapeutic Improvements in Pulmonary Arterial Hypertension Are Related to Cardiopulmonary Function but Not Skeletal Muscle Oxygen Extraction

Introduction: World Symposium Group 1 pulmonary arterial hypertension (PAH) patients have impaired function from both central oxygen delivery and skeletal muscle oxygen extraction. The effect of PH-directed therapy on skeletal muscle oxygen extraction is unknown. The aim of this study is to determine if therapy associated changes in muscle extraction parallel changes in cardiopulmonary function. Methods: Retrospective analysis was performed on twenty-nine PAH patients (24 female, mean age 54±11.4 years) receiving prostacyclin therapy (18 on monotherapy). Subjects underwent invasive cardiopulmonary exercise testing (iCPET) for treatment response evaluation followed by repeat surveillance iCPET with mean follow-up of 10.4±5.2 months. Skeletal muscle oxygen extraction was quantified by arterio-venous difference indexed to hemoglobin (Ca-vO 2 /Hgb) and systemic oxygen extraction ratio (SER) (Ca-vO 2 /CaO 2 ). Central oxygen delivery (DO 2 ) was calculated as peak cardiac output X CaO2 at peak exercise. Functional capacity was semi-quantified by six-minute walk test (6MWT) distances between assessments (n=20). Subjects were stratified into two groups: those with improvement (n=10) vs unimproved (n=19) in currently accepted ERS/COMPERA score ( Figure ). Results: Improvements in ERS/COMPERA score were related to DO 2 (318.3±273.1 vs -38.3±684.9 mL/min, P=.016 ) and PVR (-4.8±3.0 vs -0.6±3.2 WU, P=.002 ) (Figure A &amp; B). However, there was not a detectible difference between assessments in Ca-vO 2 /hgb (-0.01±0.14 vs 0.00±0.27 mL/g, P=.573 ), SER (-0.01±0.10 vs 0.00±0.20, P=.573 ), or 6MWT (7 improved, 13 unimproved) (77±115 vs 25±104 meters, P=.877 ) ( Figure C &amp; D ). Conclusions: Although PH-directed therapy improves both PVR and oxygen delivery, its effects on skeletal muscle extraction are questionable. Clinicians should consider that oxygen extraction may influence functional capacity when evaluating therapeutic improvement.

Blood volume versus deoxygenated NIRS signal: computational analysis of the effects muscle O2 delivery and blood volume on the NIRS signals.

Near-infrared spectroscopy (NIRS) signals quantify the oxygenated (ΔHbMbO2) and deoxygenated (ΔHHbMb) heme group concentrations. ΔHHbMb has been preferred to ΔHbMbO2 in evaluating skeletal muscle oxygen extraction because it is assumed to be less sensitive to blood volume (BV) changes, but uncertainties exist on this assumption. To analyze this assumption, a computational model of oxygen transport and metabolism is used to quantify the effect of O2 delivery and BV changes on the NIRS signals from a canine model of muscle oxidative metabolism (Sun Y, Ferguson BS, Rogatzki MJ, McDonald JR, Gladden LB. Med Sci Sports Exerc 48: 2013-2020, 2016). The computational analysis accounts for microvascular (ΔHbO2, ΔHHb) and extravascular (ΔMbO2, ΔHMb) oxygenated and deoxygenated forms. Simulations predicted muscle oxygen uptake and NIRS signal changes well for blood flows ranging from resting to contracting muscle. Additional NIRS signal simulations were obtained in the absence or presence of BV changes corresponding to a heme groups concentration changes (ΔHbMb = 0-48 µM). Under normal delivery (Q = 1.0 L·kg-1·min-1) in contracting muscle, capillary oxygen saturation (So2) was 62% with capillary ΔHbO2 and ΔHHb of ± 41 µΜ for ΔHbMb = 0. An increase of BV (ΔHbMb = 24 µΜ) caused a ΔHbO2 decrease (16µΜ) almost twice as much as the increase observed for ΔHHb (9 µΜ). When So2 increased to more than 80%, only ΔHbO2 was significantly affected by BV changes. The analysis indicates that microvascular So2 is a key factor in determining the sensitivity of ΔHbMbO2 and deoxygenated ΔHHbMb to BV changes. Contrary to a common assumption, the ΔHHbMb is affected by BV changes in normal contracting muscle and even more in the presence of impaired O2 delivery.NEW & NOTEWORTHY Deoxygenated is preferred to the oxygenated near-infrared spectroscopy signal in evaluating skeletal muscle oxygen extraction because it is assumed to be insensitive to blood volume changes. The quantitative analysis proposed in this study indicates that even in absence of skin blood flow effects, both NIRS signals in presence of either normal or reduced oxygen delivery are affected by blood volume changes. These changes should be considered to properly quantify muscle oxygen extraction by NIRS methods.

Impairment of skeletal muscle oxygen extraction and cardiac output are matched in precapillary pulmonary hypertension.

In precapillary pulmonary hypertension, exercising muscles extract oxygen to a similar level seen in healthy individuals. Exercise limitation is a result of impaired oxygen delivery, which is matched to any impairment in skeletal muscle oxygen extraction. https://bit.ly/3hQUY8m

Mechanisms of reduced peak oxygen consumption in subjects with uncomplicated type 2 diabetes

BackgroundType 2 diabetes mellitus (T2D) increases the risk of incident heart failure (HF), whose earliest fingerprint is effort intolerance (i.e. impaired peak oxygen consumption, or VO2peak). In the uncomplicated T2D population, however, the prevalence of effort intolerance and the underpinning mechanistic bases are uncertain. Leveraging the multiparametric characterization allowed by imaging-cardiopulmonary exercise testing (iCPET), the aim of this study is to quantify effort intolerance in T2D and to dissect the associated cardiopulmonary alterations.MethodsEighty-eight adults with well-controlled and uncomplicated T2D and no criteria for HF underwent a maximal iCPET with speckle tracking echocardiography, vascular and endothelial function assessment, as well as a comprehensive biohumoral characterization. Effort intolerance was defined by a VO2peak below 80% of maximal predicted oxygen uptake.ResultsForty-eight patients (55%) had effort intolerance reaching a lower VO2peak than T2D controls (16.5 ± 3.2 mL/min/kg, vs 21.7 ± 5.4 mL/min/kg, p < 0.0001). Despite a comparable cardiac output, patients with effort intolerance showed reduced peak peripheral oxygen extraction (11.3 ± 3.1 vs 12.7 ± 3.3 mL/dL, p = 0.002), lower VO2/work slope (9.9 ± 1.2 vs 11.2 ± 1.4, p < 0.0001), impaired left ventricle systolic reserve (peak S’ 13.5 ± 2.8 vs 15.2 ± 3.0, p = 0.009) and global longitudinal strain (peak-rest ΔGLS 1.7 ± 1.5 vs 2.5 ± 1.8, p = 0.03) than subjects with VO2peak above 80%. Diastolic function, vascular resistance, endothelial function, biohumoral exams, right heart and pulmonary function indices did not differ between the two groups.ConclusionsEffort intolerance and reduced VO2peak is a severe and highly prevalent condition in uncomplicated, otherwise asymptomatic T2D. It results from a major defect in skeletal muscle oxygen extraction coupled with a subtle myocardial systolic dysfunction.

Reduced exercise capacity in patients with systemic sclerosis is associated with lower peak tissue oxygen extraction: a cardiovascular magnetic resonance-augmented cardiopulmonary exercise study

BackgroundExercise intolerance in systemic sclerosis (SSc) is typically attributed to cardiopulmonary limitations. However, problems with skeletal muscle oxygen extraction have not been fully investigated. This study used cardiovascular magnetic resonance (CMR)-augmented cardiopulmonary exercise testing (CMR-CPET) to simultaneously measure oxygen consumption and cardiac output. This allowed calculation of arteriovenous oxygen content gradient, a recognized marker of oxygen extraction. We performed CMR-CPET in 4 groups: systemic sclerosis (SSc); systemic sclerosis-associated pulmonary arterial hypertension (SSc-PAH); non-connective tissue disease pulmonary hypertension (NC-PAH); and healthy controls.MethodsWe performed CMR-CPET in 60 subjects (15 in each group) using a supine ergometer following a ramped exercise protocol until exhaustion. Values for oxygen consumption, cardiac output and oxygen content gradient, as well as ventricular volumes, were obtained at rest and peak-exercise for all subjects. In addition, T1 and T2 maps were acquired at rest, and the most recent clinical measures (hemoglobin, lung function, 6-min walk, cardiac and catheterization) were collected.ResultsAll patient groups had reduced peak oxygen consumption compared to healthy controls (p < 0.022). The SSc and SSc-PAH groups had reduced peak oxygen content gradient compared to healthy controls (p < 0.03). Conversely, the SSc-PAH and NC-PH patients had reduced peak cardiac output compared to healthy controls and SSc patients (p < 0.006). Higher hemoglobin was associated with higher peak oxygen content gradient (p = 0.025) and higher myocardial T1 was associated with lower peak stroke volume (p = 0.011).ConclusionsReduced peak oxygen consumption in SSc patients is predominantly driven by reduced oxygen content gradient and in SSc-PAH patients this was amplified by reduced peak cardiac output.Trial registration The study is registered with ClinicalTrials.gov Protocol Registration and Results System (ClinicalTrials.gov ID: 100358).

Oxygen transport and utilisation during exercise in cystic fibrosis: contributors to exercise intolerance.

What is the topic of this review? This review highlights the central and peripheral mechanisms that alter oxygen transport and utilisation and thereby contribute to exercise limitation in people with cystic fibrosis, considering also viable therapeutic targets for intervention. What advances does it highlight? Although traditionally considered a respiratory condition, pathological intramuscular and cardiovascular changes in people with cystic fibrosis appear to be key determinants of exercise intolerance up until the later stages of respiratory disease. Even young, habitually active patients with normal lung function experience multisystemic abnormalities, which play a role in exercise intolerance. Cystic fibrosis (CF) is a complex condition, commonly associated with exercise limitation. The mechanisms responsible for this in CF are of interest, given that lower aerobic fitness is associated with an increased risk of being hospitalised with pulmonary exacerbation, a poorer quality of life and a poorer prognosis. Pathophysiological changes in lung function are considered central to CF, and may contribute to exercise limitation. However, it is now clear that the pathogenesis of exercise limitation in this population is multifactorial, with alterations in cardiovascular, muscle and pulmonary function contributing. Whilst some of these changes are attributable to respiratory disease per se, the CF transmembrane conductance regulator protein is also found in skeletal muscle and the vascular endothelium and can directly alter central and localised oxygen delivery, as well as the ability to effectively extract and utilise oxygen at the myocyte level. Since intense exercise poses considerable challenges to arterial oxygen content and/or blood flow and its supply to the working skeletal muscle, evaluating the exercise physiology of people with CF has helped us understand the mechanisms underlying exercise intolerance. Through several investigations over recent years, we have collectively demonstrated that people with CF exhibit reduced skeletal muscle oxygen extraction and utilisation during exercise, with a lesser contribution from haemodynamic or chronotropic mechanisms. Taken together, our findings highlight the importance of targeting mechanisms of skeletal muscle oxygen utilisation in CF to improve exercise tolerance and we offer potential therapeutic interventional strategies.

Evaluating the correlation of the impairment between skeletal muscle and heart using MRI in a spontaneous type 2 diabetes mellitus rhesus monkey model.

To investigate the correlation of impairment in skeletal muscle and heart in spontaneous type 2 diabetes mellitus (T2DM) rhesus monkeys using magnetic resonance image (MRI). Fifteen T2DM monkeys and fourteen healthy control (HC) monkeys were included. The microcirculation of skeletal muscle [skeletal muscle blood flow (SMBF), skeletal muscle oxygen extraction fraction (SMOEF)] and the function and strain of heart were evaluated by MRI. Three regions of interests were chosen on the soleus muscle (SOL), gastrocnemius muscle (GAS) and tibialis anterior muscle (TA) for image analysis. Eight T2DM monkeys and eight HC monkeys were obtained the full data. The SMBF reserves and SMOEF reserves were found significantly decreased in T2DM during inflation in SOL, GAS and TA muscles (all p < 0.05), and the SMBF reserves decreased during hyperemia in GAS and TA muscles (all p < 0.05). In these monkeys, the global peak longitudinal strain (longitudinal PS), peak systolic longitudinal strain rate (longitudinal PSSR) and peak diastolic longitudinal strain rate (longitudinal PDSR) were seen significantly different in T2DM compared to HC monkeys (all p < 0.05). The longitudinal PSSR was found negatively correlated with SMBF reserves in SOL, GAS and TA during inflation in all monkeys. The impaired microcirculation of skeletal muscle and the myocardial deformation were found in T2DM monkeys with normal ejection fraction. And a negative correlation was existed in the longitudinal PSSR and the SMBF reserves.

INFLUENCE OF AGE DIFFERENCE IN RESPONSE TO MOTOR SKILL TRAINING ON THE PERFORMANCE OF ACTIVITIES OF DAILY LIVING BY PUPILS WITH CEREBRAL PALSY IN KISUMU KENYA

INTRODUCTION:Cerebral Palsy (CP) is a condition that restricts an individual's ability from independent living. Individuals with cerebral palsy are unable to perform precise movements of both fine and gross motor muscles required for self care activities such as dressing, toileting, feeding, cleaning amoung others. For individuals with cerebral palsy, self care abilities can be improved through training. This study evaluated the influence of age on response to motor skills training on the performance of activities of daily living by learners with cerebral palsy.According to (Olaf, et al., 2009), younger children with cerebral palsy respond faster to exercise on the performance of activities of daily living than adults.(Sekuler, Bennet, & Mamelak, 2005) observed that practice improved performance for both younger and older subjects. However, (Livingston, Stewart, Rosenbaum, & Russel, 2011) revealed that in South Africa, youths with severe physical disabilities have more difficulty performing cognitive skills than self-care skills when compared with younger ones. The study further revealed that most youths with severe physical challenges mastered the skills of activities of daily living even though with a lot of difficulties as compared to younger children with physical challenges. Younger children, more so those with disabilities enjoy self care activities being done for them. The difference between children with physical disabilities and those with Cerebral Palsy is that those with CP have unhealthy brain which may also detorroriate with age, it might therefore not be the age but the state of health of the brain when it comes to the abilities of learning the skills of daily living. In some cases older pupil can learn faster than younger learners and at times it can be vice -versa.LITERATURE REVIEW:(Fisher, 2010) studied cardio respiratory responses to exercise in children and adults in America. The study findings noted that maximum heart rate is a function of age, and children have very high maximal heart rates. Blood flow to working muscles is higher during exercise in children, this may partially compensate for the lower cardiac output. In contrast, during exercise, skeletal muscle oxygen extraction and muscle oxidative capacity are similar in the children and adults. Children require higher minute ventilation at any given oxygen consumption. The reason is the higher respiratory rate and shallower breathing in children. The study further found that respiratory muscles of children must work harder during exercise than those of adults. These differences in the cardio-vascular and respiratory system responses to exercise limit oxygen delivery to working muscles, resulting in a lower endurance exercise capacity in children. This does not mean that children cannot perform endurance exercises or improve endurance exercise capacity; rather it means that children cannot be expected to perform endurance exercises, or train for endurance events at the same level as adults. The study recommends exercise prescription for children which should approximately follow the general recommendations for enhancing motor skill functioning in children with physical disabilities. The reviewed study was done with children and adults with respiratory problems and not with children with cerebral palsy as it is in the present study.(Olaf, et al., 2009) conducted a study on the Gross Motor Function Classification System (GMFCS) among children with cerebral palsy in Europe. The study revealed that younger children with cerebral palsy responded faster to exercise on the performance of activities of daily living than adults.(Sekuler, Bennet, & Mamelak, 2005) carried out a study on age-related learning differences in USA. The study assessed how divided attention costs varied when initial performance levels were equated across the age groups at the start of practice. The result was that practice improved performance for both young and older subjects. …

Oximetric angiosome imaging in diabetic feet

PurposeTo develop a noncontrast oximetric angiosome imaging approach to assess skeletal muscle oxygenation in diabetic feet.Materials and MethodsIn four healthy and five subjects with diabetes, the feasibility of foot oximetry was examined using a 3T clinical magnetic resonance imaging (MRI) scanner. The subjects' feet were scanned at rest and during a toe‐flexion isometric exercise. The oxygen extraction fraction of skeletal muscle was measured using a susceptibility‐based MRI method. Our newly developed MR foot oximetric angiosome model was compared with the traditional angiosome model in the assessment of the distribution of oxygen extraction fraction.ResultsUsing the traditional angiosome during the toe‐flexion exercise, the oxygen extraction fraction in the medial foot of healthy subjects increased (4.9 ± 3%) and decreased (–2.7 ± 4.4%) in subjects with diabetes (difference = 7.6%; 95% confidence interval = –13.7 ± 1.4; P = 0.02). Using the oximetric angiosome, the percent difference in the areas of oxygen extraction fraction within the 0.7–1.0 range (expected oxygen extraction fraction during exercise) between rest and exercise was higher in healthy subjects (8 ± 4%) than in subjects with diabetes (4 ± 4%; P = 0.02).ConclusionThis study demonstrates the feasibility of measuring skeletal muscle oxygen extraction fraction in the foot muscle during a toe‐flexion isometric exercise. Instead of assessing oxygen extraction fraction in a foot muscle region linked to a supplying artery (traditional angiosome), the foot oximetric angiosome model assesses oxygen extraction fraction by its different levels in all foot muscle regions and thus may be more appropriate for assessing local ischemia in ulcerated diabetic feet. J. Magn. Reson. Imaging 2016. J. MAGN. RESON. IMAGING 2016;44:1–1.

Oximetric angiosome imaging in diabetic feet.

To develop a noncontrast oximetric angiosome imaging approach to assess skeletal muscle oxygenation in diabetic feet. In four healthy and five subjects with diabetes, the feasibility of foot oximetry was examined using a 3T clinical magnetic resonance imaging (MRI) scanner. The subjects' feet were scanned at rest and during a toe-flexion isometric exercise. The oxygen extraction fraction of skeletal muscle was measured using a susceptibility-based MRI method. Our newly developed MR foot oximetric angiosome model was compared with the traditional angiosome model in the assessment of the distribution of oxygen extraction fraction. Using the traditional angiosome during the toe-flexion exercise, the oxygen extraction fraction in the medial foot of healthy subjects increased (4.9 ± 3%) and decreased (-2.7 ± 4.4%) in subjects with diabetes (difference = 7.6%; 95% confidence interval = -13.7 ± 1.4; P = 0.02). Using the oximetric angiosome, the percent difference in the areas of oxygen extraction fraction within the 0.7-1.0 range (expected oxygen extraction fraction during exercise) between rest and exercise was higher in healthy subjects (8 ± 4%) than in subjects with diabetes (4 ± 4%; P = 0.02). This study demonstrates the feasibility of measuring skeletal muscle oxygen extraction fraction in the foot muscle during a toe-flexion isometric exercise. Instead of assessing oxygen extraction fraction in a foot muscle region linked to a supplying artery (traditional angiosome), the foot oximetric angiosome model assesses oxygen extraction fraction by its different levels in all foot muscle regions and thus may be more appropriate for assessing local ischemia in ulcerated diabetic feet. J. Magn. Reson. Imaging 2016. J. MAGN. RESON. IMAGING 2016;44:940-946.

Endurance Exercise Training in Young Adults with Barth Syndrome: A Pilot Study.

Barth syndrome (BTHS) is a rare X-linked disorder that is characterized by mitochondrial abnormalities, cardio-skeletal myopathy, exercise intolerance, and premature mortality. The effect on endurance exercise training on exercise tolerance, cardio-skeletal function, and quality of life in BTHS is unknown. Four young adults (23 ± 5 years, n = 4) with BTHS participated in a 12-week, supervised, individualized endurance exercise training program. Exercise training was performed on a cycle ergometer for 30-45' three times per week at a moderate intensity level. Exercise tolerance was measured by graded exercise testing and peak oxygen consumption, heart function via two-dimensional and M-mode echocardiography, skeletal muscle function by near-infrared spectroscopy, and quality of life through the Minnesota Living with Heart Failure questionnaire. There were no adverse events during exercise testing or training for any participant. Peak oxygen consumption modestly (~5%) improved in three or four participants. Mean quality of life questions regarding dyspnea and side effects from medications significantly improved following exercise training. Mean resting heart function or skeletal muscle oxygen extraction during exercise did not improve after exercise training. Endurance exercise training is safe and appears to modestly improve peak exercise tolerance and certain measures of quality of life in young adults with BTHS. However, compared to improvements resulting from endurance exercise training seen in other non-BTHS mitochondrial myopathies and heart failure, these improvements appear blunted. Further research into the most beneficial mode, intensity and frequency of exercise training in BTHS is warranted.

Greater physical fitness is associated with better air ventilation efficiency in firefighters

Firefighting is a hazardous task associated with a heavy workload where task duration may be limited by air cylinder capacity. Increased fitness may lead to better air ventilation efficiency and task duration at a given heavy work intensity. This study compared performance, air ventilation and skeletal muscle oxygen extraction during a maximal graded walking test (GWT), a 10 METS (metabolic equivalent) treadmill test (T10) and a simulated work circuit (SWC). Participants (n = 13) who performed the SWC in a shorter time had significantly lower air cylinder ventilation values on the T10 (r = −0.495), better peak oxygen consumption (r = −0.924) during the GWT and significantly greater skeletal muscle oxygen extraction during the SWC (HbDiff, r = 0.768). These results demonstrate that the fastest participants on the SWC had better air ventilation efficiency that could prolong interventions in difficult situations requiring air cylinder use.

Non‐invasive assessment of exercise performance in children with cystic fibrosis (CF) and non‐cystic fibrosis bronchiectasis: Is there a CF specific muscle defect?

Peripheral muscle dysfunction is increasingly recognized as complicating respiratory disease, but this is difficult to measure non-invasively. Can skeletal muscle function and efficiency be measured during exercise non-invasively using respiratory mass spectrometry (RMS); and is the known exercise dysfunction in cystic fibrosis (CF) children related in part to a disease specific defect of skeletal muscle, or a non-specific manifestation of chronic airway infection and inflammation. Calculations of effective pulmonary blood flow and stroke volume, blood oxygen content and oxygen dispatch from the lungs, skeletal muscle oxygen extraction and consumption, anerobic threshold and capacity, and gross, net and work efficiency in 106 controls and 36 children (18 CF) with bronchiectasis, all aged from 8 to 17 years. Normal values for control subjects are tabulated. CF and non-CF bronchiectatic subjects had similar physiology, and skeletal muscle abnormalities could not be detected. Reduced oxygen dispatch from the lungs, due to an inability to raise stroke volume, without an increase in functional residual capacity was the major factor in reduced exercise ability. Non-invasive RMS can be used to determine skeletal muscle function in children. The changes observed in CF subjects were very similar to non-CF bronchiectatic subjects and thus a CF specific defect was not demonstrated.

Measurement of skeletal muscle tissue oxygenation in the critically ill

Shock is a state of acutely reduced tissue oxygenation. In cardiogenic shock oxygen delivery (DO2) is reduced, but oxygen extraction is preserved. In septic shock DO2 is preserved, but oxygen extraction is decreased because of microvascular changes and disturbed metabolism. Global assessment of DO2 and oxygen consumption does not tell us enough about adequacy of regional perfusion. The aim of this study was to assess the value of near infrared spectroscopy (NIRS) in detecting skeletal muscle tissue oxygenation (StO2) in critically ill patients. Patients in cardiogenic shock (n=17), septic shock (n=14), without shock but with localized infection (n=14) and healthy volunteers (n=15) were included. Thenar StO2 was measured with NIRS before (baseline StO2, %), between (downward StO2 slope, %/min) and after 90 seconds of upper arm stagnant ischemia (hyperemic StO2, %). Muscle oxygen extraction (mOER) was calculated as follows: mOER (%) = (1-baselineStO2/hyperemic StO2)*100. Repeatability was assessed using the Bland Altman method (95 % of values within limits of agreement), comparing 55 pairs of measurements performed in 5-minute intervals. Repeatability of measurements was clinically acceptable. Compared to septic shock patients, cardiogenic shock patients had lower baseline StO2 (68.9 ± 10.0 % vs. 84.3 ± 10.4 %; p < 0.05) and hyperemic StO2 (80.8 ± 7.8 % vs. 91.8 ± 8.3 %; p < 0.05), and a higher downward StO2 slope (-17.4 ± 31.7 %/min vs. -9.1 ± 2.6 %/min; p < 0.05). mOER was higher in healthy volunteers (11.9 ± 3.8 %) and volunteers with cardiogenic shock (14.8 ± 7.3 %) compared to septic shock patients (8.1 ± 7.8 %) and those with localized infection (7.6 ± 5.4 %) (p < 0.05). Repeatability of baseline StO2 and hyperemic StO2 is clinically acceptable. Results support the hypothesis that skeletal muscle oxygen extraction capability is preserved and extraction is increased in cardiogenic shock compared to septic shock.

Endurance training and detraining in mitochondrial myopathies due to single large-scale mtDNA deletions

At present there are limited therapeutic interventions for patients with mitochondrial myopathies. Exercise training has been suggested as an approach to improve physical capacity and quality of life but it is uncertain whether it offers a safe and effective treatment for patients with heteroplasmic mitochondrial DNA (mtDNA) mutations. The objectives of this study were to assess the effects of exercise training and detraining in eight patients with single, large-scale mtDNA deletions to determine: (i) the efficacy and safety of endurance training (14 weeks) in this patient population; (ii) to determine the effect of more prolonged (total of 28 weeks) exercise training upon muscle and cardiovascular function and (iii) to evaluate the effect of discontinued training (14 weeks) upon muscle and cardiovascular function. Our results show that: (i) 14 weeks of exercise training significantly improved tolerance of submaximal exercise and peak capacity for work, oxygen utilization and skeletal muscle oxygen extraction with no change in the level of deleted mtDNA; (ii) continued training for an additional 14 weeks maintained these beneficial adaptations; (iii) the cessation of training (detraining) resulted in loss of physiological adaptation to baseline capacity with no overall change in mutation load. Patients' self assessment of quality of life as measured by the SF-36 questionnaire improved with training and declined with detraining. Whilst our findings of beneficial effects of training on physiological outcome and quality of life without increases in the percentage of deleted mtDNA are encouraging, we did not observe changes in mtDNA copy number. Therefore there remains a need for longer term studies to confirm that endurance exercise is a safe and effective treatment for patients with mitochondrial myopathies. The effects of detraining clearly implicate physical inactivity as an important mechanism in reducing exercise capacity and quality of life in patients with mitochondrial myopathy.