Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee-extension

Physiology 2014 (London, UK) (2014) Proc Physiol Soc 31, PCA143

Poster Communications: Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee-extension

D. T. Cannon1,2, W. E. Bimson3, S. A. Hampson4, T. S. Bowen2,5, S. R. Murgatroyd2, S. Marwood4, G. J. Kemp3,6, H. B. Rossiter1,2

1. Division of Respiratory & Critical Care Physiology & Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States. 2. School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom. 3. Magnetic Resonance and Image Analysis Research Centre, University of Liverpool, Liverpool, United Kingdom. 4. School of Health Sciences, Liverpool Hope University, Liverpool, United Kingdom. 5. Department of Internal Medicine and Cardiolgoy, University of Leipzig - Heart Center, Leipzig, Germany. 6. Department of Musculoskeletal Biology, University of Liverpool, Liverpool, United Kingdom.

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During constant power exercise above the lactate threshold (LT), the kinetics of oxygen uptake (VO2) are supplemented by the VO2 slow component (VO2sc), reflecting reduced work efficiency occurring predominately within the locomotor muscles (Poole et al., 1991). The intracellular source of inefficiency is postulated to originate from an increase in the ATP cost of power production (P/W), rather than an increase in the O2 cost of ATP resynthesis (decrease in P/O) (Rossiter et al., 2002). To test this hypothesis, we measured intramuscular ATP turnover with 31P magnetic resonance spectroscopy (MRS) during moderate and heavy bilateral knee-extension exercise. Fourteen healthy participants completed a series of rest-exercise-rest protocols using a computer-controlled ergometer (Lode BV, Groningen, NL) in an MR scanner (Trio, SIEMENS AG, Erlangen, DE). 31P spectra were collected from the quadriceps throughout using a dual-tuned (1H and 31P) surface coil (RAPID Biomedical GmbH, Rimpar, DE). Pre-determined moderate (MOD; sub-LT) and heavy (HVY; supra-LT) constant power exercise was completed for 3 and 8 min, allowing total ATP turnover rate (ATPtot) to be estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling (Kemp et al., 2001 & 2007). During MOD there was no discernable VO2sc (0.06±0.12 L.min-1). Conversely, during HVY the VO2sc was 0.37±0.16 L.min-1, or 29±10% of the fundamental VO2. Similarly, there was no difference (p>0.05) in [PCr] between 3 and 8 min of MOD (30.2±8.4 vs. 31.8±7.0 mM), whereas the reduction in [PCr] was significant (p<0.05) during HVY (19.4±6.6 vs. 17.5±7.3 mM or 12±15%). ATPtot was not different between 3 and 8 min of MOD (24±14 vs. 17±13 mM.min-1; p>0.05), but increased during HVY (37±16 vs. 44±13 mM.min-1; p<0.05; 27±25%). However, this increase in ATPtot was not related to the VO2sc during HVY (p>0.05; r2=-0.06). The transit-delay-corrected [PCr]-VO2 relationship (r2=0.94) was linear for the entirety of moderate exercise and the first 3 min of heavy exercise. However, by 8 min of heavy exercise, the slope of the [PCr]-VO2 relationship was steepened by 12±10% (p<0.05), indicative of reduced P/O.The rate of ATP turnover increased between 3 and 8 min of supra-LT, but not sub-LT, exercise. Importantly, this conclusion was reached using direct measurement of [PCr] kinetics to determine ATPtot, and without relying on assumptions of intramuscular [PCr]-VO2 or [ADP]-VO2 relationships. However, the poor correlation between individual increases in ATPtot and the VO2sc, together with the steepening of the [PCr]-VO2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial (P/O) sources.



Where applicable, experiments conform with Society ethical requirements.

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