Cellular Processes Integrating the Metabolic Response to Exercise

Meyer, Ronald A.; Foley, Jeanne M.

doi:10.1002/cphy.cp120118

Cited by 70 publications

(112 citation statements)

References 171 publications

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“…To assess the energy state of WT and AK1 Ϫ/Ϫ muscles, the ⌬GATP was calculated both from resting gastrocnemius, and from contracting muscles with the ⌬G°A TP of Ϫ32 kJ/mol (42). The free ADP was estimated either from the known stoichiometry with the CK reaction (57), or in contracting muscle the difference in total ADP from rested ADP was used.…”

Section: Methodsmentioning

confidence: 99%

“…AMP deaminase; tetanic contraction; muscle relaxation; calcium handling; cross-bridge cycling SKELETAL MUSCLE can maintain favorable energetic conditions in the face of great energetic demands. For example, the ATP consumption rate needed to support a tetanic contraction (ϳ10 mol/g per second) is ϳ200-fold above the resting rate in rat fast twitch fibers (28,42). The metabolic challenge this represents is highlighted by the fact that the ATP content of mammalian skeletal muscle is only 6 -7 mol/g.…”

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confidence: 99%

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Skeletal muscle contractile performance and ADP accumulation in adenylate kinase-deficient mice

Hancock¹,

Janssen²,

Terjung³

2005

American Journal of Physiology-Cell Physiology

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The production of AMP by adenylate kinase (AK) and subsequent deamination by AMP deaminase limits ADP accumulation during conditions of high-energy demand in skeletal muscle. The goal of this study was to investigate the consequences of AK deficiency (Ϫ/Ϫ) on adenine nucleotide management and whole muscle function at high-energy demands. To do this, we examined isometric tetanic contractile performance of the gastrocnemius-plantaris-soleus (GPS) muscle group in situ in AK1 Ϫ/Ϫ mice and wild-type (WT) controls over a range of contraction frequencies (30 -120 tetani/min). We found that AK1 Ϫ/Ϫ muscle exhibited a diminished inosine 5Ј-monophosphate formation rate (14% of WT) and an inordinate accumulation of ADP (ϳ1.5 mM) at the highest energy demands, compared with WT controls. AK-deficient muscle exhibited similar initial contractile performance (521 Ϯ 9 and 521 Ϯ 10 g tension in WT and AK1 Ϫ/Ϫ muscle, respectively), followed by a significant slowing of relaxation kinetics at the highest energy demands relative to WT controls. This is consistent with a depressed capacity to sequester calcium in the presence of high ADP. However, the overall pattern of fatigue in AK1 Ϫ/Ϫ mice was similar to WT control muscle. Our findings directly demonstrate the importance of AMP formation and subsequent deamination in limiting ADP accumulation. Whole muscle contractile performance was, however, remarkably tolerant of ADP accumulation markedly in excess of what normally occurs in skeletal muscle. AMP deaminase; tetanic contraction; muscle relaxation; calcium handling; cross-bridge cycling SKELETAL MUSCLE can maintain favorable energetic conditions in the face of great energetic demands. For example, the ATP consumption rate needed to support a tetanic contraction (ϳ10 mol/g per second) is ϳ200-fold above the resting rate in rat fast twitch fibers (28, 42). The metabolic challenge this represents is highlighted by the fact that the ATP content of mammalian skeletal muscle is only 6 -7 mol/g. Therefore, without compensation, the entire ATP pool would be completely depleted in Ͻ1 s at this rate. Obviously, this does not occur due to the ATP synthetic processes of oxidative phosphorylation, glycolysis, the creatine kinase (CK) reaction, and the adenylate kinase (AK) reaction. Moreover, the free energy available from ATP hydrolysis (⌬G ATP ) is a function of the ATP content relative to the products of ATP hydrolysis, namely ADP and inorganic phosphate (P i )where ⌬G°A TP is the conventional expression for the free engery of ATP at standard conditions, R is the ideal gas constant at 0.0083143 kJ/mol⅐K, and T is the temperature in Kelvin. Furthermore, the accumulation of ADP and P i direct physiological consequences independent of an impaired ⌬G ATP . Thus, the metabolic challenge when ATP turnover is high, is to preserve ATP content and limit inordinate accumulation of ADP and P i .When the rate of ATP hydrolysis is out of balance with the rate of ATP synthesis, the need to limit the accumulation of ADP and P i is the greatest. The rea...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Skeletal muscle contractile performance and ADP accumulation in adenylate kinase-deficient mice

Hancock¹,

Janssen²,

Terjung³

2005

American Journal of Physiology-Cell Physiology

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“…This would result in an increase in V O 2 at the end of phase II, even though the external power output requirement has not changed, by virtue of an increase in cross-bridge turnover and Ca 2+ pump activity required to sustain the additional fibre recruitment, both of which are ATPase dependent (Meyer & Foley, 1996). This would necessitate an increase in the bulk O 2 supply to meet the increased O 2 demand, without necessarily altering the rate of adjustment of V O 2 toward A 1 fi.…”

Section: Figurementioning

confidence: 99%

Effects of Prior Exercise and Recovery Duration on Oxygen Uptake Kinetics During Heavy Exercise in Humans

Burnley

Doust

Carter

et al. 2001

Experimental Physiology

102

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The pulmonary oxygen uptake (V O 2 ) response to constant intensity exercise reflects the time course of the adjustment of muscle O 2 consumption towards a steady state, following a short delay reflecting the transit time of blood flow from the exercising muscle to the lung (Barstow et al. 1990;Grassi, 2000). It has been reported that a prior bout of heavy exercise (above the lactate threshold, LT) speeds the V O 2 kinetics during subsequent heavy exercise (Gerbino et al. 1996;MacDonald et al. 1997). Both of these studies characterised the heavy exercise V O 2 response using a single dynamic parameter ('effective' time constant or mean response time). Although these monoexponential approximations may be reasonable for the interpretation of V O 2 kinetics during moderate intensity exercise (below the LT), where a steady state V O 2 is normally attained within 2-3 min, they may not be appropriate for the determination of the V O 2 kinetics of heavy exercise (Whipp & Wasserman, 1972;Linnarsson, 1974). The delayed emergence of the V O 2 slow component during heavy exercise (Barstow & Mole, 1991;Paterson & Whipp, 1991) significantly distorts the monoexponential description of the V O 2 response (Linnarsson, 1974; Barstow et al. 1993;Burnley et al. 2000).In a recent study from our laboratory (Burnley et al. 2000), we used a model which characterised the three identifiable phases of the V O 2 response with separate independent exponential functions ( Fig. 1; Barstow et al. 1996). Using this modelling approach, we showed that the 'speeding' of monoexponential V O 2 kinetics noted previously was caused by a reduction in the amplitude of the V O 2 slow component, and not by a speeding of phase II kinetics, because the associated time constant (r 1 ) was unaltered in the second exercise bout. These results indicate that if convective and/or diffusive oxygen delivery is increased by prior heavy exercise (Gerbino et al. 1996), then this has no discernible effect on the time course of the phase II V O 2 response during subsequent heavy exercise.In our previous study (Burnley et al. 2000), in addition to the reduction in the amplitude of the V O 2 slow component, we found that prior heavy exercise increased the absolute amplitude of the V O 2 response at the end of phase II. Further, in all 10 of the subjects tested, baseline V O 2 was elevated at the onset of the second bout of heavy exercise. However, because the parameter A 1 fi (the net amplitude of the phase II response, Fig. 1

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“…The role of PCr appears critical, whether the molecule is considered mainly as an energy buffer or as a "driving force" for muscle respiration (11,15). The monoexponential increase in V O 2 m during the "primary component" of the V O 2 on-kinetics, as described in canine muscle after convective and diffusive O 2 constraints were eliminated or reduced, appears in agreement with metabolic models of muscle respiratory control during contractions, according to which a single reaction with first-order kinetics controls V O 2 m during the transition.…”

Section: Metabolic Control Of Muscle Respirationmentioning

confidence: 99%

Regulation of Oxygen Consumption at Exercise Onset: Is It Really Controversial?

Grassi

2001

Exercise and Sport Sciences Reviews

100

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Cellular Processes Integrating the Metabolic Response to Exercise

Abstract: The sections in this article are: The Central Role of Adenine Nucleotides Components of the High‐Energy Phosphate System Phosphate Metabolites are a Linked Network Approaches to Understanding Metabolic Control Classic Enzyme Kinetics Nonequilibrium Thermodynamics Regulat… Show more

Cited by 70 publications

References 171 publications

Skeletal muscle contractile performance and ADP accumulation in adenylate kinase-deficient mice

Skeletal muscle contractile performance and ADP accumulation in adenylate kinase-deficient mice

Effects of Prior Exercise and Recovery Duration on Oxygen Uptake Kinetics During Heavy Exercise in Humans

Regulation of Oxygen Consumption at Exercise Onset: Is It Really Controversial?

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