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J Physiol. 2014 Dec 1;592(23):5287-300. doi: 10.1113/jphysiol.2014.279174. Epub 2014 Oct 3.

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

Author information

1
Rehabilitation Clinical Trials Center, Division of Respiratory & Critical Care Physiology & Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
2
Magnetic Resonance & Image Analysis Research Centre, University of Liverpool, Liverpool, UK.
3
School of Health Sciences, Liverpool Hope University, Liverpool, UK.
4
School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK Department of Internal Medicine and Cardiology, University of Leipzig - Heart Center, Leipzig, DE.
5
School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
6
Magnetic Resonance & Image Analysis Research Centre, University of Liverpool, Liverpool, UK Department of Musculoskeletal Biology, University of Liverpool, Liverpool, UK.
7
Rehabilitation Clinical Trials Center, Division of Respiratory & Critical Care Physiology & Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK hrossiter@ucla.edu.

Abstract

During constant-power high-intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2 sc ), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with (31)P magnetic resonance spectroscopy (MRS) and whole-body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension exercise in healthy participants (n = 14). Unlocalized (31)P spectra were collected from the quadriceps throughout using a dual-tuned ((1)H and (31)P) surface coil with a simple pulse-and-acquire sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable V̇O2 sc (mean ± SD, 0.06 ± 0.12 l min(-1)) or change in [PCr] (30 ± 8 vs. 32 ± 7 mm) or ATPtot (24 ± 14 vs. 17 ± 14 mm min(-1); each P = n.s.). During HVY, the V̇O2 sc was 0.37 ± 0.16 l min(-1) (22 ± 8%), [PCr] decreased (19 ± 7 vs. 18 ± 7 mm, or 12 ± 15%; P < 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mm min(-1), or 26 ± 30%; P < 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated with the V̇O2 sc during HVY (r(2) = 0.06; P = n.s.). This lack of relationship between ΔATPtot and V̇O2 sc , together with a steepening of the [PCr]-V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O2 cost of ATP resynthesis; P/O).

PMID:
25281731
PMCID:
PMC4262339
DOI:
10.1113/jphysiol.2014.279174
[Indexed for MEDLINE]
Free PMC Article

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