Skeletal muscle chemoreflex and pHi in exercise ventilatory control

1998 ◽  
Vol 84 (2) ◽  
pp. 676-682 ◽  
Author(s):  
David A. Oelberg ◽  
Allison B. Evans ◽  
Mirko I. Hrovat ◽  
Paul P. Pappagianopoulos ◽  
Samuel Patz ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Minute Ventilation ◽  
Venous Blood ◽  
Hydrogen Ion ◽  
Positive Pressure ◽  
Resonance Spectroscopy ◽  
Ventilatory Control ◽  
Ventilatory Drive ◽  
Repetition Time ◽  
Muscle Chemoreflex

Oelberg, David A., Allison B. Evans, Mirko I. Hrovat, Paul P. Pappagianopoulos, Samuel Patz, and David M. Systrom. Skeletal muscle chemoreflex and pHi in exercise ventilatory control. J. Appl. Physiol. 84(2): 676–682, 1998.—To determine whether skeletal muscle hydrogen ion mediates ventilatory drive in humans during exercise, 12 healthy subjects performed three bouts of isotonic submaximal quadriceps exercise on each of 2 days in a 1.5-T magnet for 31P-magnetic resonance spectroscopy (31P-MRS). Bilateral lower extremity positive pressure cuffs were inflated to 45 Torr during exercise (BLPPex) or recovery (BLPPrec) in a randomized order to accentuate a muscle chemoreflex. Simultaneous measurements were made of breath-by-breath expired gases and minute ventilation, arterialized venous blood, and by 31P-MRS of the vastus medialis, acquired from the average of 12 radio-frequency pulses at a repetition time of 2.5 s. With BLPPex, end-exercise minute ventilation was higher (53.3 ± 3.8 vs. 37.3 ± 2.2 l/min; P < 0.0001), arterialized[Formula: see text] lower (33 ± 1 vs. 36 ± 1 Torr; P = 0.0009), and quadriceps intracellular pH (pHi) more acid (6.44 ± 0.07 vs. 6.62 ± 0.07; P = 0.004), compared with BLPPrec. Blood lactate was modestly increased with BLPPex but without a change in arterialized pH. For each subject, pHi was linearly related to minute ventilation during exercise but not to arterialized pH. These data suggest that skeletal muscle hydrogen ion contributes to the exercise ventilatory response.

Influence of inspiratory assistance on ventilatory control during moderate exercise

1987 ◽  
Vol 62 (2) ◽  
pp. 551-560 ◽  
Author(s):  
C. S. Poon ◽  
S. A. Ward ◽  
B. J. Whipp
Keyword(s):  
Mechanical Load ◽  
Minute Ventilation ◽  
Constant Load ◽  
Positive Pressure ◽  
Moderate Exercise ◽  
Ventilatory Control ◽  
Mechanical Unloading ◽  
Ventilatory Drive ◽  
End Tidal ◽  
Control Exercise

In five healthy subjects, we studied the effects of controlled mechanical unloading of the respiratory system on ventilatory control during moderate exercise, utilizing a modified positive-pressure ventilator (IEEE Trans. Biomed. Eng. BME-33: 361–365, 1986). We were especially interested in whether isocapnia was maintained when a portion of the normal ventilatory response to constant-load cycling was subserved by the ventilator. The mechanical unloading was achieved by “assisting” airflow throughout inspiration in a constant proportion to instantaneous flow. Two modest degrees of assistance (A1 = 1.5 and A2 = 3.0 cmH2O X l-1 X s) were imposed. The assistance caused minute ventilation (VE) to increase immediately (inspiratory time shortening and tidal volume rising) and end-tidal PCO2 (PETCO2) to fall. Some 10–15 s later, inspiratory occlusion pressure (P100) decreased, and in the new steady-state VE and PETCO2 were virtually restored to their control exercise levels. The modest residual hyperventilation [delta PETCO2 = -0.9 Torr (A1) and -1.6 Torr (A2)], which was not significant statistically, contrasted markedly with the much larger increase predicted for VE had there been no compensatory reduction in ventilatory drive (as evidenced by the fall in P100). Consistent with earlier studies utilizing resistive loading (J. Appl. Physiol. 35: 361–366, 1973 and Acta Physiol. Scand. 120: 557–565, 1984), these observations suggest that ventilatory drive during moderate exercise is controlled to compensate for modest changes in respiratory-mechanical load, so that VE is preserved at a level appropriate to metabolic rate or nearly so.

Skeletal muscle ECF pH error signal for exercise ventilatory control

1998 ◽  
Vol 84 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Allison B. Evans ◽  
Larry W. Tsai ◽  
David A. Oelberg ◽  
Homayoun Kazemi ◽  
David M. Systrom
Keyword(s):  
Skeletal Muscle ◽  
Magnetic Resonance ◽  
Extracellular Fluid ◽  
Muscle Metabolism ◽  
Respiratory Alkalosis ◽  
Resonance Spectroscopy ◽  
Error Signal ◽  
Ventilatory Control ◽  
Arterial Ph ◽  
Sciatic Nerve Stimulation

Evans, Allison B., Larry W. Tsai, David A. Oelberg, Homayoun Kazemi, and David M. Systrom. Skeletal muscle ECF pH error signal for exercise ventilatory control. J. Appl. Physiol. 84(1): 90–96, 1998.—An autonomic reflex linking exercising skeletal muscle metabolism to central ventilatory control is thought to be mediated by neural afferents having free endings that terminate in the interstitial fluid of muscle. To determine whether changes in muscle extracellular fluid pH (pHe) can provide an error signal for exercise ventilatory control, pHe was measured during electrically induced contraction by31P-magnetic resonance spectroscopy and the chemical shift of a phosphorylated, pH-sensitive marker that distributes to the extracellular fluid (phenylphosphonic acid). Seven lightly anesthetized rats underwent unilateral continuous 5-Hz sciatic nerve stimulation in an 8.45-T nuclear magnetic resonance magnet, which resulted in a mixed lactic acidosis and respiratory alkalosis, with no net change in arterial pH. Skeletal muscle intracellular pH fell from 7.30 ± 0.03 units at rest to 6.72 ± 0.05 units at 2.4 min of stimulation and then rose to 7.05 ± 0.01 units ( P < 0.05), despite ongoing stimulation and muscle contraction. Despite arterial hypocapnia, pHeshowed an immediate drop from its resting baseline of 7.40 ± 0.01 to 7.16 ± 0.04 units ( P < 0.05) and remained acidic throughout the stimulation protocol. During the on- and off-transients for 5-Hz stimulation, changes in the pH gradient between intracellular and extracellular compartments suggested time-dependent recruitment of sarcolemmal ion-transport mechanisms. pHe of exercising skeletal muscle meets temporal and qualitative criteria necessary for a ventilatory metaboreflex mediator in a setting where arterial pH does not.

Cellular P O 2 as a determinant of maximal mitochondrial O2consumption in trained human skeletal muscle

1999 ◽  
Vol 87 (1) ◽  
pp. 325-331 ◽  
Author(s):  
R. S. Richardson ◽  
J. S. Leigh ◽  
P. D. Wagner ◽  
E. A. Noyszewski
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Venous Blood ◽  
Saturation Pressure ◽  
Knee Extensor ◽  
Resonance Spectroscopy ◽  
Flow Measurements ◽  
Trained Subjects ◽  
Blood Flow Measurements ◽  
Mitochondrial Capacity

Previously, by measuring myoglobin-associated [Formula: see text](PMb o 2) during maximal exercise, we have demonstrated that 1) intracellular[Formula: see text] is 10-fold less than calculated mean capillary [Formula: see text] and 2) intracellular[Formula: see text] and maximum O2 uptake (V˙o 2 max) fall proportionately in hypoxia. To further elucidate this relationship, five trained subjects performed maximum knee-extensor exercise under conditions of normoxia (21% O2), hypoxia (12% O2), and hyperoxia (100% O2) in balanced order. Quadriceps O2 uptake (V˙o 2) was calculated from arterial and venous blood O2concentrations and thermodilution blood flow measurements. Magnetic resonance spectroscopy was used to determine myoglobin desaturation, and an O2 half-saturation pressure of 3.2 Torr was used to calculate PMb o 2from saturation. Skeletal muscleV˙o 2 max at 12, 21, and 100% O2 was 0.86 ± 0.1, 1.08 ± 0.2, and 1.28 ± 0.2 ml ⋅ min−1 ⋅ ml−1, respectively. The 100% O2 values approached twice that previously reported in human skeletal muscle. PMb o 2values were 2.3 ± 0.5, 3.0 ± 0.7, and 4.1 ± 0.7 Torr while the subjects breathed 12, 21, and 100% O2, respectively. From 12 to 21% O2,V˙o 2 and PMb o 2were again proportionately related. However, 100% O2 increasedV˙o 2 max relatively less than PMb o 2, suggesting an approach to maximal mitochondrial capacity with 100% O2. These data 1) again demonstrate very low cytoplasmic [Formula: see text] atV˙o 2 max, 2) are consistent with supply limitation of V˙o 2 maxof trained skeletal muscle, even in hyperoxia, and 3) reveal a disproportionate increase in intracellular [Formula: see text] in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscleV˙o 2 are being approached.

Dietary effects on exercising muscle metabolism and performance by 31P-MRS

1994 ◽  
Vol 77 (3) ◽  
pp. 1108-1115 ◽  
Author(s):  
D. E. Larson ◽  
R. L. Hesslink ◽  
M. I. Hrovat ◽  
R. S. Fishman ◽  
D. M. Systrom
Keyword(s):  
Minute Ventilation ◽  
Muscle Metabolism ◽  
Exercise Duration ◽  
Quadriceps Muscle ◽  
Peak Exercise ◽  
Crossover Fashion ◽  
Resonance Spectroscopy ◽  
Phosphorylation Potential ◽  
Beneficial Effects ◽  
Muscle Ph

To determine how diet modulates short-term exercise capacity, skeletal muscle pH and bioenergetic state were examined by 31P-magnetic resonance spectroscopy in nine healthy volunteers. Subjects performed incremental quadriceps exercise to exhaustion after 5 days of high-carbohydrate (HCHO) or high-fat (HFAT) diet randomly assigned in crossover fashion and separated by a 2.5-day period of ad libitum mixed diet. Simultaneous measurements were made of pulmonary gas exchange, minute ventilation, and quadriceps muscle pH and phosphorylation potential. At rest and peak exercise, respiratory exchange ratio and minute ventilation were higher after HCHO than after HFAT (P < 0.05), reflecting greater CHO utilization. Peak O2 consumption (VO2) was not increased after HCHO (P > 0.05), but exercise duration was (339 +/- 34 s for HCHO vs. 308 +/- 25 s for HFAT; P < 0.05). HCHO was associated with a blunted early fall of phosphocreatine (PCr)/Pi vs. VO2 (-4.1 +/- 0.7 x 10(-2) min/ml for HCHO vs. -5.6 +/- 1.2 x 10(-2) min/ml for HFAT; P < 0.05). On both study days, the slope of PCr/Pi vs. VO2, before and after the PCr threshold, was correlated with exercise time. The results suggest that a diet rich in CHO improves exercise efficiency through beneficial effects on intracellular phosphorylation potential.

scholarly journals Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in heart failure patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Kagami Hirabayashi ◽  
Mayumi Yamato ◽  
Shingo Takada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Aerobic Capacity ◽  
Plantar Flexion ◽  
Exercise Intolerance ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Systemic Oxidative Stress

AbstractOxidative stress plays a role in the progression of chronic heart failure (CHF). We investigated whether systemic oxidative stress is linked to exercise intolerance and skeletal muscle abnormalities in patients with CHF. We recruited 30 males: 17 CHF patients, 13 healthy controls. All participants underwent blood testing, cardiopulmonary exercise testing, and magnetic resonance spectroscopy (MRS). The serum thiobarbituric acid reactive substances (TBARS; lipid peroxides) were significantly higher (5.1 ± 1.1 vs. 3.4 ± 0.7 μmol/L, p < 0.01) and the serum activities of superoxide dismutase (SOD), an antioxidant, were significantly lower (9.2 ± 7.1 vs. 29.4 ± 9.7 units/L, p < 0.01) in the CHF cohort versus the controls. The oxygen uptake (VO2) at both peak exercise and anaerobic threshold was significantly depressed in the CHF patients; the parameters of aerobic capacity were inversely correlated with serum TBARS and positively correlated with serum SOD activity. The phosphocreatine loss during plantar-flexion exercise and intramyocellular lipid content in the participants' leg muscle measured by 31phosphorus- and 1proton-MRS, respectively, were significantly elevated in the CHF patients, indicating abnormal intramuscular energy metabolism. Notably, the skeletal muscle abnormalities were related to the enhanced systemic oxidative stress. Our analyses revealed that systemic oxidative stress is related to lowered whole-body aerobic capacity and skeletal muscle dysfunction in CHF patients.

scholarly journals AB0185 PROSPECTIVE PROFILE OF URINE METABOLOME IN RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1392.2-1392
Author(s):  
M. De Oliveira ◽  
P. V. Alabarse ◽  
M. Farinon ◽  
R. Cavalheiro Do Espírito Santo ◽  
R. Xavier
Keyword(s):  
Rheumatoid Arthritis ◽  
Skeletal Muscle ◽  
Disease Activity ◽  
Pearson Correlation ◽  
Statistical Significance ◽  
Resonance Spectroscopy ◽  
Metabolome Analysis ◽  
Orthogonal Projections ◽  
Urine Metabolome

Background:Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by increased mortality and associated with metabolic disorders. Since the metabolomic profile is known to vary in response to different inflammatory conditions, metabolome analysis could substantially improve diagnosis and prognosis of RA.Objectives:To analyze the urine metabolome profile in RA patients and correlate it with disease activity changes over 12 monthsMethods:Seventy-nine RA patients, according to ACR/EULAR 2010 classification criteria, between 40 and 70 years old, were recruited and followed for 12 months. Metabolome analysis was performed by Nuclear Magnetic Resonance spectroscopy (NMR), resulting in the identification of 93 metabolites in urine collected at the baseline and after 12 months. Frequency analysis, Pearson Correlation and Multivariate data analysis with orthogonal projections to latent structures (OPLS) method were performed and a statistical significance was considered as p<0.05.Results:The study population was characterized by the majority of women (86.7%), mean age of 56 years old, around 80% with positive anti-CCP or Rheumatoid Factor. During the one year of follow-up, there was no substantial variation in the DAS28 measurement (baseline: 3.8, after 12 months: 4.0). There was no significant correlation between the metabolome pattern and DAS28 score (p>0.05) over time. However, multivariate analysis (OPLS-DA) demonstrated an adequate differentiation of the population with 0.92 of accuracy (Q2: 0.72 and R2: 0.89).There was a significant increase of L-cysteine, choline, L-Phenylalanin, creatine, L-histidine, oxalacetic acid and xanthine, and a decrease of L-threonine, taurine, butyric and gluconic acid (p<0.05) during the follow-up, metabolites that are involved in the skeletal muscle metabolism.Conclusion:The observed biomarkers indicate,as expected, that the RA metabolic profile is associated with inflammation injury and skeletal muscle amino acid metabolism. Correlations with disease activity changes was compromised by the stable disease status during the 12 months. More studies evaluating correlations with skeletal muscle function and mass are underway.Acknowledgments:Disclosure of interest: Marianne Oliveira: None declared, Rafaela Santo: None declared, Mirian Farinon: None declared, Ricardo Xavier Consultant of: Abbvie, Pfizer, Novartis, Janssen, Lilly, RocheDisclosure of Interests:Marianne de Oliveira: None declared, Paulo Vinicius Alabarse: None declared, Mirian Farinon: None declared, Rafaela Cavalheiro do Espírito Santo: None declared, Ricardo Xavier Consultant of: AbbVie, Pfizer, Novartis, Janssen, Eli Lilly, Roche

scholarly journals Early metabolic changes measured by 1H MRS in healthy and dystrophic muscle after injury

2012 ◽  
Vol 113 (5) ◽  
pp. 808-816 ◽  
Author(s):  
Su Xu ◽  
Stephen J. P. Pratt ◽  
Espen E. Spangenburg ◽  
Richard M. Lovering
Keyword(s):  
Skeletal Muscle ◽  
Muscle Injury ◽  
Tibialis Anterior Muscle ◽  
Metabolic Changes ◽  
Mdx Mice ◽  
Resonance Spectroscopy ◽  
Dystrophic Muscle ◽  
1H Mrs ◽  
Skeletal Muscle Injury

Skeletal muscle injury is often assessed by clinical findings (history, pain, tenderness, strength loss), by imaging, or by invasive techniques. The purpose of this work was to determine if in vivo proton magnetic resonance spectroscopy (1H MRS) could reveal metabolic changes in murine skeletal muscle after contraction-induced injury. We compared findings in the tibialis anterior muscle from both healthy wild-type (WT) muscles (C57BL/10 mice) and dystrophic ( mdx mice) muscles (an animal model for human Duchenne muscular dystrophy) before and after contraction-induced injury. A mild in vivo eccentric injury protocol was used due to the high susceptibility of mdx muscles to injury. As expected, mdx mice sustained a greater loss of force (81%) after injury compared with WT (42%). In the uninjured muscles, choline (Cho) levels were 47% lower in the mdx muscles compared with WT muscles. In mdx mice, taurine levels decreased 17%, and Cho levels increased 25% in injured muscles compared with uninjured mdx muscles. Intramyocellular lipids and total muscle lipid levels increased significantly after injury but only in WT. The increase in lipid was confirmed using a permeable lipophilic fluorescence dye. In summary, loss of torque after injury was associated with alterations in muscle metabolite levels that may contribute to the overall injury response in mdx mice. These results show that it is possible to obtain meaningful in vivo 1H MRS regarding skeletal muscle injury.

scholarly journals Evidence that a higher ATP cost of muscular contraction contributes to the lower mechanical efficiency associated with COPD: preliminary findings

2011 ◽  
Vol 300 (5) ◽  
pp. R1142-R1147 ◽  
Author(s):  
Gwenael Layec ◽  
Luke J. Haseler ◽  
Jan Hoff ◽  
Russell S. Richardson
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Energy Cost ◽  
Plantar Flexion ◽  
Mechanical Efficiency ◽  
Exercise Intolerance ◽  
Chronic Obstructive ◽  
Small Subset ◽  
Resonance Spectroscopy ◽  
Muscle Energetics

Impaired metabolism in peripheral skeletal muscles potentially contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). We used 31P-magnetic resonance spectroscopy (31P-MRS) to examine the energy cost and skeletal muscle energetics in six patients with COPD during dynamic plantar flexion exercise compared with six well-matched healthy control subjects. Patients with COPD displayed a higher energy cost of muscle contraction compared with the controls (control: 6.1 ± 3.1% of rest·min−1·W−1, COPD: 13.6 ± 8.3% of rest·min−1·W−1, P = 0.01). Although, the initial phosphocreatine resynthesis rate was also significantly attenuated in patients with COPD compared with controls (control: 74 ± 17% of rest/min, COPD: 52 ± 13% of rest/min, P = 0.04), when scaled to power output, oxidative ATP synthesis was similar between groups (6.5 ± 2.3% of rest·min−1·W−1 in control and 7.8 ± 3.9% of rest·min−1·W−1 in COPD, P = 0.52). Therefore, our results reveal, for the first time that in a small subset of patients with COPD a higher ATP cost of muscle contraction may substantially contribute to the lower mechanical efficiency previously reported in this population. In addition, it appears that some patients with COPD have preserved mitochondrial function and normal energy supply in lower limb skeletal muscle.

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