Progressive decrease of intramyocellular accumulation of H+ and Pi in human skeletal muscle during repeated isotonic exercise

2003 ◽  
Vol 284 (6) ◽  
pp. C1490-C1496 ◽  
Author(s):  
J. Rico-Sanz
Keyword(s):  
Skeletal Muscle ◽  
Perceived Exertion ◽  
Plantar Flexion ◽  
High Energy ◽  
Rating Of Perceived Exertion ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Hydrogen Ions ◽  
Isotonic Exercise ◽  
Wet Weight

The purpose of this study was to evaluate the hypotheses that accumulation of hydrogen ions and/or inorganic phosphate (Pi) in skeletal muscle increases with repeated bouts of isotonic exercise. 31P-Magnetic resonance spectroscopy was used to examine the gastrocnemius muscle of seven highly aerobically trained females during four bouts of isotonic plantar flexion. The exercise bouts ( EX1- 4) of 3 min and 18 s were separated by 3 min and 54 s of complete rest. Muscle ATP did not change during the four bouts. Phosphocreatine (PCr) degradation during EX1 (13.3 ± 2.4 mmol/kg wet weight) was higher ( P < 0.01) compared with EX3- 4(9.7 ± 1.6 and 9.6 ± 1.8 mmol/kg wet weight, respectively). The intramyocellular pH at the end of EX1 (6.87 ± 0.05) was significantly lower ( P < 0.001) than those of EX2 (6.97 ± 0.02), EX3 (7.02 ± 0.01), and EX4 (7.02 ± 0.02). Total Pi and diprotonated Pi were significantly higher ( P < 0.001) at the end of EX1 (17.3 ± 2.7 and 7.8 ± 1.6 mmol/kg wet weight, respectively) compared with the values at the end of EX3 and EX4. The monoprotonated Pi at the end of EX1 (9.5 ± 1.2 mmol/kg wet weight) was also significantly higher ( P < 0.001) than that after EX4 (7.5 ± 1.1 mmol/kg wet weight). Subjects' rating of perceived exertion increased ( P < 0.001) toward exhaustion as the number of exercises progressed (7.1 ± 0.4, EX1; 8.0 ± 0.3, EX2; 8.5 ± 0.3, EX3; and 9.0 ± 0.4, EX4; scale from 0 to 10). The present results indicate that human muscle fatigue during repeated intense isotonic exercise is not due to progressive depletion of high energy phosphates nor to intracellular accumulation of hydrogen ions, total, mono-, or diprotonated Pi.

Interrelationship of oxidative metabolism and local perfusion demonstrated by NMR in human skeletal muscle

1996 ◽  
Vol 81 (5) ◽  
pp. 2221-2228 ◽  
Author(s):  
Jean-François Toussaint ◽  
Kenneth K. Kwong ◽  
Fidelis M’Kparu ◽  
Robert M. Weisskoff ◽  
Paul J. Laraia ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Magnetic Resonance ◽  
Time Constant ◽  
Oxidative Metabolism ◽  
Human Skeletal Muscle ◽  
Plantar Flexion ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Mean Flow ◽  
Normal Volunteers

Toussaint, Jean-François, Kenneth K. Kwong, Fidelis M’Kparu, Robert M. Weisskoff, Paul J. LaRaia, and Howard L. Kantor.Interrelationship of oxidative metabolism and local perfusion demonstrated by NMR in human skeletal muscle. J. Appl. Physiol. 81(5): 2221–2228, 1996.—Using nuclear magnetic resonance (NMR), we have examined the relationship of high-energy phosphate metabolism and perfusion in human soleus and gastrocnemius muscles. With31P-NMR spectroscopy, we monitored phosphocreatine (PCr) decay and recovery in eight normal volunteers and four heart failure patients performing ischemic plantar flexion. By using echo-planar imaging, perfusion was independently measured by a local [inversion-recovery (T1-flow)] and a regional technique (NMR-plethysmography). After correction for its pH dependence, PCr recovery time constant is 27.5 ± 8.0 s in normal volunteers, with mean flow 118 ± 75 (soleus and gastrocnemius T1-flow) and 30.2 ± 9.7 ml ⋅ 100 ml−1 ⋅ min−1(NMR-plethysmography-flow). We demonstrate a positive correlation between PCr time constant and local perfusion given by y = 50 − 0.15 x( r 2 = 0.68, P = 0.01) for the 8 normal subjects, and y = 64 − 0.24 x( r 2 = 0.83, P = 0.0001) for the 12 subjects recruited in the study. Regional perfusion techniques also show a significant but weaker correlation. Using this totally noninvasive method, we conclude that aerobic ATP resynthesis is related to the magnitude of perfusion, i.e., O2availability, and demonstrate that magnetic resonance imaging and magnetic resonance spectroscopy together can accurately assess muscle functional status.

scholarly journals Phosphocreatine hydrolysis during submaximal exercise: the effect of F I O 2

1998 ◽  
Vol 85 (4) ◽  
pp. 1457-1463 ◽  
Author(s):  
Luke J. Haseler ◽  
Russell S. Richardson ◽  
John S. Videen ◽  
Michael C. Hogan
Keyword(s):  
Steady State ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Plantar Flexion ◽  
High Energy ◽  
Constant Load ◽  
Submaximal Exercise ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Work Intensity

There is evidence that the concentration of the high-energy phosphate metabolites may be altered during steady-state submaximal exercise by the breathing of different fractions of inspired O2([Formula: see text]). Whereas it has been suggested that these changes may be the result of differences in time taken to achieve steady-state O2 uptake (V˙o 2) at different[Formula: see text] values, we postulated that they are due to a direct effect of O2 tension. We used31P-magnetic resonance spectroscopy during constant-load, steady-state submaximal exercise to determine 1) whether changes in high-energy phosphates do occur at the sameV˙o 2 with varied[Formula: see text] and 2) that these changes are not due to differences in V˙o 2onset kinetics. Six male subjects performed steady-state submaximal plantar flexion exercise [7.2 ± 0.6 (SE) W] for 10 min while lying supine in a 1.5-T clinical scanner. Magnetic resonance spectroscopy data were collected continuously for 2 min before exercise, 10 min during exercise, and 6 min during recovery. Subjects performed three different exercise bouts at constant load with the[Formula: see text] switched after 5 min of the 10-min exercise bout. The three exercise treatments were 1)[Formula: see text] of 0.1 switched to 0.21, 2)[Formula: see text] of 0.1 switched to 1.00, and 3)[Formula: see text] of 1.00 switched to 0.1. For all three treatments, the[Formula: see text] switch significantly ( P ≤ 0.05) altered phosphocreatine: 1) 55.5 ± 4.8 to 67.8 ± 4.9% (%rest); 2) 59.0 ± 4.3 to 72.3 ± 5.1%; and 3) 72.6 ± 3.1 to 64.2 ± 3.4%, respectively. There were no significant differences in intracellular pH for the three treatments. The results demonstrate that the differences in phosphocreatine concentration with varied [Formula: see text] are not the result of different V˙o 2onset kinetics, as this was eliminated by the experimental design. These data also demonstrate that changes in intracellular oxygenation, at the same work intensity, result in significant changes in cell homeostasis and thereby suggest a role for metabolic control by O2 even during submaximal exercise.

Human muscle fatigue after glycogen depletion: a 31P magnetic resonance study

1992 ◽  
Vol 73 (1) ◽  
pp. 75-81 ◽  
Author(s):  
L. A. Bertocci ◽  
J. L. Fleckenstein ◽  
J. Antonio
Keyword(s):  
Skeletal Muscle ◽  
Magnetic Resonance ◽  
Muscle Fatigue ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Handgrip Exercise ◽  
Glycogen Depletion ◽  
Skeletal Muscle Fatigue ◽  
Exercise Induced

To differentiate the effects of high energy phosphates, pH, and [H2PO4-] on skeletal muscle fatigue, intracellular acidosis during handgrip exercise was attenuated by prolonged submaximal exercise. Healthy human subjects (n = 6) performed 5-min bouts of maximal rhythmic handgrip (RHG) before (CONTROL) and after prolonged (60-min) handgrip exercise (ATTEN-EX) designed to attenuate lactic acidosis in active muscle by partially depleting muscle glycogen. Concentrations of free intracellular phosphocreatine ([PCr]), adenosine triphosphate ([ATP]), and orthophosphate ([P(i)]) and pH were measured by 31P nuclear magnetic resonance spectroscopy and used to calculate adenosine diphosphate [ADP], [H2PO4-], and [HPO4(2-)]. Handgrip force output was measured with a dynamometer, and fatigue was determined by loss of maximal contractile force. After ATTEN-EX, the normal exercise-induced muscle acidosis was reduced. At peak CONTROL RHG, pH fell to 6.3 +/- 0.1 (SE) and muscle fatigue was correlated with [PCr] (r = 0.83), [P(i)] (r = 0.82), and [H2PO4-] (r = 0.81); [ADP] was 22.0 +/- 5.7 mumol/kg. At peak RHG after ATTEN-EX, pH was 6.9 +/- 0.1 and [ADP] was 116.1 +/- 18.2 mumol/kg, although [PCr] and [P(i)] were not different from CONTROL RHG (P greater than 0.05). After ATTEN-EX, fatigue correlated most closely with [ADP] (r = 0.84). The data indicate that skeletal muscle fatigue 1) is multifactorial, 2) can occur without decreased pH or increased [H2PO4-], and 3) is correlated with [ADP] after exercise-induced glycogen depletion.

scholarly journals Intracellular energetics and critical Po2 in resting ischemic human skeletal muscle in vivo

2010 ◽  
Vol 299 (5) ◽  
pp. R1415-R1422 ◽  
Author(s):  
Ian R. Lanza ◽  
Michael A. Tevald ◽  
Douglas E. Befroy ◽  
Jane A. Kent-Braun
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Ex Vivo ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Atp Production ◽  
Resting Muscle

During ischemia and some types of muscular contractions, oxygen tension (Po2) declines to the point that mitochondrial ATP synthesis becomes limited by oxygen availability. Although this critical Po2 has been determined in animal tissue in vitro and in situ, there remains controversy concerning potential disparities between values measured in vivo and ex vivo. To address this issue, we used concurrent heteronuclear magnetic resonance spectroscopy (MRS) to determine the critical intracellular Po2 in resting human skeletal muscle in vivo. We interleaved measurements of deoxymyoglobin using 1H-MRS with measures of high-energy phosphates and pH using 31P-MRS, during 15 min of ischemia in the tibialis anterior muscles of 6 young men. ATP production and intramyocellular Po2 were quantified throughout ischemia. Critical Po2, determined as the Po2 corresponding to the point where PCr begins to decline (PCrip) in resting muscle during ischemia, was 0.35 ± 0.20 Torr, means ± SD. This in vivo value is consistent with reported values ex vivo and does not support the notion that critical Po2 in resting muscle is higher when measured in vivo. Furthermore, we observed a 4.5-fold range of critical Po2 values among the individuals studied. Regression analyses revealed that time to PCrip was associated with critical Po2 and the rate of myoglobin desaturation ( r = 0.83, P = 0.04) but not the rate of ATP consumption during ischemia. The apparent dissociation between ATP demand and myoglobin deoxygenation during ischemia suggests that some degree of uncoupling between intracellular energetics and oxygenation is a potentially important factor that influences critical Po2 in vivo.

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.

Magnetic resonance spectroscopy of high-energy phosphates and lactate immediately after coronary artery bypass surgery

Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 328-333 ◽  
Author(s):  
D NF Harris ◽  
J A Wilson ◽  
S D Taylor-Robinson ◽  
K M Taylor
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Cerebral Ischaemia ◽  
Artery Bypass ◽  
High Energy ◽  
Jugular Bulb ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Intracellular Acidosis ◽  
High Incidence

Hypothermic cardiopulmonary bypass (CPB) is associated with a high incidence of neuropsychological defects, marked cerebral swelling immediately after surgery and jugular bulb desaturation during rewarming. This suggests cerebral ischaemia may occur, but evidence is indirect. We studied four patients with 31P magnetic resonance spectroscopy (MRS) and four with 1H MRS before and immediately after coronary surgery. There was no visible lactate in 1H MR spectra. In 31P MR spectra, the ratio of phosphocreatine to adenosine triphosphate was maintained (before: 2.13 ± 0.86 vs after: 2.57 ± 1.31; mean ± 1 SD) and there was no intracellular acidosis (intracellular pH: 7.1 ± 0.04 vs 7.16 ± 0.08), while phosphocreatine/inorganic phosphate was increased immediately after the operation (2.92 ± 0.37 vs 6.39 ± 2.67, p = 0.03). This suggests rebound replacement of energy stores following recovery from temporary cerebral ischaemia during CPB: intra-operative studies would be needed to test this hypothesis further.

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.

Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans

2008 ◽  
Vol 294 (1) ◽  
pp. R12-R16 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Uwe H. Melchert ◽  
Harald G. Scholand-Engler ◽  
Maria C. Howitz ◽  
Bernd Schultes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Underlying Mechanism ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
High Energy Phosphate ◽  
Available Energy ◽  
Healthy Humans ◽  
High Energy Phosphate Metabolism ◽  
The Brain

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using 31P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by 31P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain ( P = 0.013), while there was a similar trend in the hypopglycemic condition ( P = 0.055). Skeletal muscle content remained constant in both conditions ( P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to −4%) revealed clear divergent effects in both conditions ( P < 0.05). These effects were reflected by PCr/Pi ratio ( P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia ( P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.

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