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Limits to sustainable muscle performance: interaction between glycolysis and oxidative phosphorylation

Kevin E. Conley^1,2,3,*, William F. Kemper² and Gregory J. Crowther²

¹ Department of Radiology,
² Department of Physiology and Biophysics and
³ Department of Bioengineering, University of Washington Medical Center, Seattle, WA 98195-7115, USA

View larger version (18K): [in a new window]   Fig. 1. Maximal power output of human legs as a function of time during cycling. The symbols represent the highest power output that can be sustained for a given time (adapted from) (Wilkie, 1985). The upper left diagram illustrates that high power outputs cannot be sustained because the source of ATP (phosphocreatine, PCr) generates by-products that inhibit contraction (inorganic phosphate, Pi and H+). The upper right diagram illustrates that the continuous supply of ATP allows lower power outputs to be sustained.

View larger version (21K): [in a new window]   Fig. 2. ATP, H+ and O2 balances illustrating the integration of the major mass and energy fluxes in muscle.

View larger version (49K): [in a new window]   Fig. 3. Stack plot of magnetic resonance spectra showing inorganic phosphate (Pi), phosphocreatine (PCr) and ATP levels at rest, during exercise and through recovery in human quadriceps muscle. Reproduced with permission from The Physiological Society.

View larger version (16K): [in a new window]   Fig. 4. Diagram of the reciprocal changes in phosphocreatine level ([PCr]) and [ADP] that occur via the creatine kinase reaction during exercise (A) and the effect of the rise in [ADP] with exercise (red curve and arrowhead) on mitochondrial oxidative phosphorylation (B). Data in A are unpublished results from human ankle dorsiflexor muscles, and data in B are from isolated mammalian heart mitochondria (Mootha et al., 1997).

View larger version (23K): [in a new window]   Fig. 5. The central position of ADP in muscle energetics. The ADP level is the signal for oxidative phosphorylation, which reflects both the balance of ATP supply to demand via phosphocreatine ([PCr]) and the balance of H+ production versus efflux via pH in accord with the creatine kinase reaction (equation 2).

View larger version (12K): [in a new window]   Fig. 6. ADP levels during steady-state (A) and transient (B) exercise determined for mammalian muscle. The line is the normalized rate of oxidative phosphorylation versus [ADP] in isolated mitochondria (Mootha et al., 1997). The symbols in A represent the highest steady-state [ADP] reported in mammalian skeletal muscle (Harkema et al., 1997; Harkema and Meyer, 1997; Jeneson et al., 1996; Kushmerick et al., 1992; Paganini et al., 1997; Walter et al., 1997). The symbols in B represent measurements from the human quadriceps at each step of an exercise stress test (Richardson et al., 1995). These data are normalized to the maximal level and superimposed on the relationship for isolated mitochondria (solid line) (Mootha et al., 1997).

View larger version (17K): [in a new window]   Fig. 7. [ADP] calculated from the creatine kinase reaction (equation 2) as a function of phosphocreatine concentration, [PCr], at two pH levels. The solid arrow indicates the effect of a change in [PCr] at pH7.2 on [ADP]. The broken arrow indicates the change in [PCr] needed to maintain [ADP] with a reduction in pH from 7.2 to 6.5.

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