Article
Control of respiration and bioenergetics during muscle contraction.
Department of Biological Chemistry, University of California, Davis, Davis, CA 95616-8635, USA.
AJP Cell Physiology (impact factor:
3.54).
03/2005;
288(3):C730-8.
DOI:10.1152/ajpcell.00138.2004
pp.C730-8
Source: PubMed
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Citations (0)
- Cited In (2)
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Article: A computational model of skeletal muscle metabolism linking cellular adaptations induced by altered loading states to metabolic responses during exercise.
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ABSTRACT: The alterations in skeletal muscle structure and function after prolonged periods of unloading are initiated by the chronic lack of mechanical stimulus of sufficient intensity, which is the result of a series of biochemical and metabolic interactions spanning from cellular to tissue/organ level. Reduced activation of skeletal muscle alters the gene expression of myosin heavy chain isoforms to meet the functional demands of reduced mechanical load, which results in muscle atrophy and reduced capacity to process fatty acids. In contrast, chronic loading results in the opposite pattern of adaptations. To quantify interactions among cellular and skeletal muscle metabolic adaptations, and to predict metabolic responses to exercise after periods of altered loading states, we develop a computational model of skeletal muscle metabolism. The governing model equations - with parameters characterizing chronic loading/unloading states- were solved numerically to simulate metabolic responses to moderate intensity exercise (WR < or = 40% VO2 max). Model simulations showed that carbohydrate oxidation was 8.5% greater in chronically unloaded muscle compared with the loaded muscle (0.69 vs. 0.63 mmol/min), while fat oxidation was 7% higher in chronically loaded muscle (0.14 vs. 0.13 mmol/min), during exercise. Muscle oxygen uptake (VO2) and blood flow (Q) response times were 29% and 44% shorter in chronically loaded muscle (0.4 vs. 0.56 min for VO2 and 0.25 vs. 0.45 min for Q). The present model can be applied to test complex hypotheses during exercise involving the integration and control of metabolic processes at various organizational levels (cellular to tissue) in individuals who have undergone periods of chronic loading or unloading.BioMedical Engineering OnLine 01/2007; 6:14. · 1.40 Impact Factor -
Article: NIRS measurement of O(2) dynamics in contracting blood and buffer perfused hindlimb muscle.
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ABSTRACT: In order to obtain evidence that Mb releases O(2) during muscle contraction, we have set up a buffer-perfused hindlimb rat model and applied NIRS to detect the dynamics of tissue deoxygenation during contraction. The NIRS signal was monitored on hindlimb muscle during twitch contractions at 1 Hz, evoked via electrostimulator at different submaximal levels. The hindlimb perfusion was carried out by perfusion of Krebs Bicarbonate buffer. The NIRS still detected a strong signal even under Hb-free contractions. The deoxygenation signal (Delta[deoxy]) was progressively increased at onset of the contraction and reached the plateau under both blood- and buffer-perfused conditions. However, the amplitude of Delta[deoxy] during steady state continued to significantly increase as tension increased. The tension-matched comparison of the Delta[deoxy] level under buffer-perfused and blood perfused conditions indicate that Mb can contribute approximately 50% to the NIRS signal. These results clarify the Mb contribution to the NIRS signal and show a falling intracellular PO(2) as workload increases.Advances in experimental medicine and biology 01/2010; 662:323-8. · 1.09 Impact Factor
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Keywords
1)H-NMR experiments
31% nonoxidative component
ADP-independent phase
constant load
desaturation rate constant
dynamic energy utilization-restoration cycle
energy cost
energy flux
final steady-state cellular Po(2)
final steady-state level
human calf muscle
Mb desaturates
Mb desaturation
Mb function
muscle contraction
plantar flexion exercise
present report
similar time constant
steady state
workload levels