Muscle metabolic responses to exercise above and below the “critical power” assessed using 31P-MRS

2008 ◽  
Vol 294 (2) ◽  
pp. R585-R593 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Fred DiMenna ◽  
Jonathan Fulford ◽  
David C. Poole
Keyword(s):  
Critical Power ◽  
Quadriceps Muscle ◽  
High Energy ◽  
Knee Extension ◽  
Work Rate ◽  
Metabolic Responses ◽  
Time To Exhaustion ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Constant Work Rate

We tested the hypothesis that the asymptote of the hyperbolic relationship between work rate and time to exhaustion during muscular exercise, the “critical power” (CP), represents the highest constant work rate that can be sustained without a progressive loss of homeostasis [as assessed using 31P magnetic resonance spectroscopy (MRS) measurements of muscle metabolites]. Six healthy male subjects initially completed single-leg knee-extension exercise at three to four different constant work rates to the limit of tolerance (range 3–18 min) for estimation of the CP (mean ± SD, 20 ± 2 W). Subsequently, the subjects exercised at work rates 10% below CP (<CP) for 20 min and 10% above CP (>CP) for as long as possible, while the metabolic responses in the contracting quadriceps muscle, i.e., phosphorylcreatine concentration ([PCr]), Pi concentration ([Pi]), and pH, were estimated using 31P-MRS. All subjects completed 20 min of <CP exercise without duress, whereas the limit of tolerance during >CP exercise was 14.7 ± 7.1 min. During <CP exercise, stable values for [PCr], [Pi], and pH were attained within 3 min after the onset of exercise, and there were no further significant changes in these variables (end-exercise values = 68 ± 11% of baseline [PCr], 314 ± 216% of baseline [Pi], and pH 7.01 ± 0.03). During >CP exercise, however, [PCr] continued to fall to the point of exhaustion and [Pi] and pH changed precipitously to values that are typically observed at the termination of high-intensity exhaustive exercise (end-exercise values = 26 ± 16% of baseline [PCr], 564 ± 167% of baseline [Pi], and pH 6.87 ± 0.10, all P < 0.05 vs. <CP exercise). These data support the hypothesis that the CP represents the highest constant work rate that can be sustained without a progressive depletion of muscle high-energy phosphates and a rapid accumulation of metabolites (i.e., H+ concentration and [Pi]), which have been associated with the fatigue process.

Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia

1996 ◽  
Vol 81 (5) ◽  
pp. 1891-1900 ◽  
Author(s):  
Charles S. Fulco ◽  
Steven F. Lewis ◽  
Peter N. Frykman ◽  
Robert Boushel ◽  
Sinclair Smith ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Hypobaric Hypoxia ◽  
Knee Extension ◽  
Work Rate ◽  
Dynamic Exercise ◽  
Time To Exhaustion ◽  
Electromyographic Activity ◽  
Constant Work Rate ◽  
Generating Capacity ◽  
Leg Exercise

Fulco, Charles S., Steven F. Lewis, Peter N. Frykman, Robert Boushel, Sinclair Smith, Everett A. Harman, Allen Cymerman, and Kent B. Pandolf. Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia. J. Appl. Physiol. 81(5): 1891–1900, 1996.—Using an exercise device that integrates maximal voluntary static contraction (MVC) of knee extensor muscles with dynamic knee extension, we compared progressive muscle fatigue, i.e., rate of decline in force-generating capacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr). Eight healthy men performed exhaustive constant work rate knee extension (21 ± 3 W, 79 ± 2 and 87 ± 2% of 1-leg knee extension O2 peak uptake for normoxia and hypobaria, respectively) from knee angles of 90–150° at a rate of 1 Hz. MVC (90° knee angle) was performed before dynamic exercise and during ≤5-s pauses every 2 min of dynamic exercise. MVC force was 578 ± 29 N in normoxia and 569 ± 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 ± 10 and 284 ± 20 N for normoxia and hypobaria, respectively; P > 0.05) that were higher ( P < 0.01) than peak force of constant work rate knee extension (98 ± 10 N, 18 ± 3% of MVC). Time to exhaustion was 56% shorter for hypobaria than for normoxia (19 ± 5 vs. 43 ± 7 min, respectively; P < 0.01), and rate of right leg MVC fall was nearly twofold greater for hypobaria than for normoxia (mean slope = −22.3 vs. −11.9 N/min, respectively; P < 0.05). With increasing duration of dynamic exercise for normoxia and hypobaria, integrated electromyographic activity during MVC fell progressively with MVC force, implying attenuated maximal muscle excitation. Exhaustion, per se, was postulated to relate more closely to impaired shortening velocity than to failure of force-generating capacity.

Muscle metabolic determinants of exercise tolerance following exhaustion: relationship to the “critical power”

2013 ◽  
Vol 115 (2) ◽  
pp. 243-250 ◽  
Author(s):  
Weerapong Chidnok ◽  
Jonathan Fulford ◽  
Stephen J. Bailey ◽  
Fred J. DiMenna ◽  
Philip F. Skiba ◽  
...  
Keyword(s):  
Critical Power ◽  
Recovery Period ◽  
Random Order ◽  
Exercise Duration ◽  
High Energy ◽  
Knee Extension ◽  
Resonance Spectroscopy ◽  
Passive Recovery ◽  
Significant Difference ◽  
Recovery Exercise

We tested the hypothesis that muscle high-energy phosphate compounds and metabolites related to the fatigue process would be recovered after exhaustion during recovery exercise performed below but not above critical power (CP) and that these changes would influence the capacity to continue exercise. Eight male subjects completed single-leg, knee-extension exercise to exhaustion (for ∼180 s) on three occasions, followed by a work-rate reduction to severe-intensity exercise, heavy-intensity exercise (<CP), or a 10-min passive recovery period, in random order. The muscle metabolic responses to exercise were assessed using 31P magnetic resonance spectroscopy. There was a significant difference between the sustainable exercise duration during the recovery from exhaustive exercise between the <CP and >CP conditions (at least 10 min and 39 ± 31 s, respectively; P < 0.05). During passive recovery and <CP recovery exercise, muscle phosphocreatine concentration ([PCr]) increased rapidly after the exhaustion point, reaching ∼96% and ∼76% of baseline values, respectively, after 10 min ( P < 0.05). Moreover, pH increased abruptly, reaching 7.0 ± 0.0 and 7.0 ± 0.2, respectively, after 10 min recovery ( P < 0.05). However, during >CP recovery exercise, neither muscle [PCr] nor pH recovered, reaching ∼37% of the initial baseline and 6.6 ± 0.2, respectively. These results indicate that the muscle metabolic dynamics in recovery from exhaustive >CP differ according to whether the recovery exercise is performed below or above the CP. These findings confirm the importance of the CP as an intramuscular metabolic threshold that dictates the accumulation of fatigue-related metabolites and the capacity to tolerate high-intensity exercise.

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 Establishing the V̇o2 versus constant-work-rate relationship from ramp-incremental exercise: simple strategies for an unsolved problem

2019 ◽  
Vol 127 (6) ◽  
pp. 1519-1527 ◽  
Author(s):  
Danilo Iannetta ◽  
Rafael de Almeida Azevedo ◽  
Daniel A. Keir ◽  
Juan M. Murias
Keyword(s):  
Lactate Threshold ◽  
Unsolved Problem ◽  
Critical Power ◽  
Work Rate ◽  
Incremental Exercise ◽  
Mean Response Time ◽  
Constant Work Rate ◽  
Ramp Exercise ◽  
The Mean ◽  
Highly Correlated

The dissociation between constant work rate of O2 uptake (V̇o2) and ramp V̇o2 at a given work rate might be mitigated during slowly increasing ramp protocols. This study characterized the V̇o2 dynamics in response to five different ramp protocols and constant-work-rate trials at the maximal metabolic steady state (MMSS) to characterize 1) the V̇o2 gain (G) in the moderate, heavy, and severe domains, 2) the mean response time of V̇o2 (MRT), and 3) the work rates at lactate threshold (LT) and respiratory compensation point (RCP). Eleven young individuals performed five ramp tests (5, 10, 15, 25, and 30 W/min), four to five time-to-exhaustions for critical power estimation, and two to three constant-work-rate trials for confirmation of the work rate at MMSS. G was greatest during the slowest ramp and progressively decreased with increasing ramp slopes (from ~12 to ~8 ml·min−1·W−1, P < 0.05). The MRT was smallest during the slowest ramp slopes and progressively increased with faster ramp slopes (1 ± 1, 2 ± 1, 5 ± 3, and 10 ± 4, 15 ± 6 W, P < 0.05). After “left shifting” the ramp V̇o2 by the MRT, the work rate at LT was constant regardless of the ramp slope (~150 W, P > 0.05). The work rate at MMSS was 215 ± 55 W and was similar and highly correlated with the work rate at RCP during the 5 W/min ramp ( P > 0.05, r = 0.99; Lin’s concordance coefficient = 0.99; bias = −3 W; root mean square error = 6 W). Findings showed that the dynamics of V̇o2 (i.e., G) during ramp exercise explain the apparent dichotomy existing with constant-work-rate exercise. When these dynamics are appropriately “resolved”, LT is constant regardless of the ramp slope of choice, and RCP and MMSS display minimal variations between each other. NEW & NOTEWORTHY This study demonstrates that the dynamics of V̇o2 during ramp-incremental exercise are dependent on the characteristics of the increments in work rate, such that during slow-incrementing ramp protocols the magnitude of the dissociation between ramp V̇o2 and constant V̇o2 at a given work rate is reduced. Accurately accounting for these dynamics ensures correct characterizations of the V̇o2 kinetics at ramp onset and allows appropriate comparisons between ramp and constant-work-rate exercise-derived indexes of exercise intensity.

Influence of intracellular acidosis on contractile function in the working rat heart

1987 ◽  
Vol 253 (6) ◽  
pp. H1499-H1505 ◽  
Author(s):  
F. M. Jeffrey ◽  
C. R. Malloy ◽  
G. K. Radda
Keyword(s):  
Stroke Volume ◽  
Intracellular Ph ◽  
Rat Heart ◽  
Contractile Function ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Intracellular Acidosis ◽  
Tension Development ◽  
O2 Delivery

The decrease in myocardial contractility during ischemia, hypoxia, and extracellular acidosis has been attributed to intracellular acidosis. Previous studies of the relationship between pH and contractile state have utilized respiratory or metabolic acidosis to alter intracellular pH. We developed a model in the working perfused rat heart to study the effects of intracellular acidosis with normal external pH and optimal O2 delivery. Intracellular pH and high-energy phosphates were monitored by 31P nuclear magnetic resonance spectroscopy. Hearts were perfused to a steady state with a medium containing 10 mM NH4Cl (extracellular pH, 7.4). The subsequent washout of NH3 from the cytosol generated a slight acidosis (from intracellular pH 7.0 to 6.8) which was associated with little change in the determinants of O2 consumption (rate-pressure product) and O2 delivery (coronary flow). Acidosis induced a substantial decrease in aortic flow and stroke volume which was associated with little change in peak systolic pressure. Results were qualitatively similar at different external [Ca2+] (1.75, 2.5, 3.15 mM) and preload (12 or 21 cmH2O) but were most prominent at the lowest external [Ca2+] and left atrial pressure. In contrast to this model of isolated intracellular acidosis, hearts subject to a respiratory (extracellular plus intracellular) acidosis showed a marked reduction in pressure development. It was concluded that 1) for the same intracellular acidosis the influence on tension development was more pronounced with a combined extra- and intracellular acidosis than with an isolated intracellular acidosis, and 2) stroke volume at constant preload was impaired by intracellular acidosis even though changes in developed pressure were minimal. These observations suggest that isolated intracellular acidosis has adverse effects on diastolic compliance and/or relaxation.

scholarly journals Tirilazad Pretreatment Improves Early Cerebral Metabolic and Blood Flow Recovery from Hyperglycemic Ischemia

1995 ◽  
Vol 15 (1) ◽  
pp. 88-96 ◽  
Author(s):  
Yuichi Maruki ◽  
Raymond C. Koehler ◽  
Jeffrey R. Kirsch ◽  
Kathleen K. Blizzard ◽  
Richard J. Traystman
Keyword(s):  
Lipid Peroxidation ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Intracellular Ph ◽  
High Energy ◽  
Vehicle Group ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Early Reperfusion ◽  
Tirilazad Mesylate

Acidosis may augment cerebral ischemic injury by promoting lipid peroxidation. We tested the hypothesis that when acidosis is augmented by hyperglycemia, pretreatment with the 21-aminosteroid tirilazad mesylate (U74006F), a potent inhibitor of lipid peroxidation in vitro, improves early cerebral metabolic recovery. In a randomized, blinded study, anesthetized dogs received either tirilazad mesylate (1 mg/kg plus 0.2 mg/kg/h; n = 8) or vehicle (n = 8). Hyperglycemia (400–500 mg/dl) was produced prior to 30 min of global incomplete cerebral ischemia. Intracellular pH and high energy phosphates were measured by phosphorus magnetic resonance spectroscopy. During ischemia, microsphere-determined CBF decreased to 8 ± 4 ml min−1 100 g−1 and intracellular pH decreased to 5.6 ± 0.2 in both groups. During the first 20 min of reperfusion, ATP partially recovered in the vehicle group to 57 ± 21% of baseline, but then declined progressively in association with elevated intracranial pressure. By 30 min, ATP recovery was greater in the tirilazad group (77 ± 35 vs. 36 ± 19%), although postischemic hyperemia was similar. By 45 min, the tirilazad group had a higher intracellular pH (6.5 ± 0.5 vs. 5.9 ± 0.6) and a lower intracranial pressure (18 ± 6 vs. 52 ± 24 mm Hg). By 180 min, blood flow and ATP were undetectable in seven of eight vehicle-treated dogs, whereas ATP was >67% and pH was >6.7 in six of eight tirilazad-treated dogs. Thus, tirilazad acts during early reperfusion to prevent secondary metabolic decay associated with severe acidotic ischemia. If tirilazad acts by inhibiting lipid peroxidation, then these data are consistent with extreme acidosis limiting recovery by a mechanism involving lipid peroxidation.

Regional blood flow and skeletal muscle energy status in endotoxemic rats

1987 ◽  
Vol 252 (5) ◽  
pp. E581-E587 ◽  
Author(s):  
M. M. Jepson ◽  
M. Cox ◽  
P. C. Bates ◽  
N. J. Rothwell ◽  
M. J. Stock ◽  
...  
Keyword(s):  
Blood Flow ◽  
Protein Synthesis ◽  
Regional Blood Flow ◽  
High Energy ◽  
Whole Body ◽  
Sublethal Dose ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Energy Status ◽  
Brown Adipose

Endotoxins induce muscle wasting in part as a result of depressed protein synthesis. To investigate whether these changes reflect impaired energy transduction, blood flow, O2 extraction, and high-energy phosphates in muscle and whole-body O2 consumption (VO2) have been measured. VO2 was measured for 6h after an initial sublethal dose of endotoxin (Escherichia coli lipopolysaccharide 0.3 mg/100 g body wt sc) or saline and during 6h after a second dose 24 h later. In fed or fasted rats, VO2 was either increased or better maintained after endotoxin. In anesthetized fed rats 3-4 after the second dose of endotoxin VO2 was increased, and this was accompanied by increased blood flow to liver (hepatic arterial supply), kidney, and perirenal brown adipose tissue and a 57 and 64% decrease in flow to back and hindlimb muscle, respectively, with no change in any other organ. Hindlimb arteriovenous O2 was unchanged, indicating markedly decreased aerobic metabolism in muscle, and the contribution of the hindlimb to whole-body VO2 decreased by 46%. Adenosine 5'-triphosphate levels in muscle were unchanged in endotoxin-treated rats, and this was confirmed by topical nuclear magnetic resonance spectroscopy, which also showed muscle pH to be unchanged. These results show that although there is decreased blood flow and aerobic oxidation in muscle, adenosine 5'-triphosphate availability does not appear to be compromised so that the endotoxin-induced muscle catabolism and decreased protein synthesis must reflex some other mechanism.

scholarly journals Noninvasive Monitoring of Training Induced Muscle Adaptation with -MRS: Fibre Type Shifts Correlate with Metabolic Changes

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Eike Hoff ◽  
Lars Brechtel ◽  
Patrick Strube ◽  
Paul Konstanczak ◽  
Gisela Stoltenburg-Didinger ◽  
...  
Keyword(s):  
Fibre Type ◽  
Gastrocnemius Muscle ◽  
Noninvasive Monitoring ◽  
High Energy ◽  
Metabolic Changes ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Type Ii ◽  
Fibre Type Composition ◽  
Fast Twitch

Purpose. To evaluate training induced metabolic changes noninvasively with magnetic resonance spectroscopy (-MRS) for measuring muscle fibre type adaptation.Methods. Eleven volunteers underwent a 24-week training, consisting of speed-strength, endurance, and detraining (each 8 weeks). Prior to and following each training period, needle biopsies and -MRS of the resting gastrocnemius muscle were performed. Fibre type distribution was analyzed histologically and tested for correlation with the ratios of high energy phosphates ([PCr]/[], [PCr]/[βATP] and [PCr + ]/[βATP]). The correlation between the changes of the -MRS parameters during training and the resulting changes in fibre composition were also analysed.Results. We observed an increased type-II-fibre proportion after speed-strength and detraining. After endurance training the percentage of fast-twitch fibres was reduced. The progression of the [PCr]/[]-ratio was similar to that of the fast-twitch fibres during the training. We found a correlation between the type-II-fibre proportion and [PCr]/[] (, ) or [PCr]/[βATP] (, ); the correlations between its changes (delta) and the fibre-shift were significant as well (delta[PCr]/[] , delta[PCr]/[βATP] , ).Conclusion. Shifts in fibre type composition and high energy phosphate metabolite content covary in human gastrocnemius muscle. Therefore -MRS might be a feasible method for noninvasive monitoring of exercise-induced fibre type transformation.

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