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Jeneson, J. A. L.

Publications and source records attributed to Jeneson, J. A. L..

2 recordsLinked to original sources

Correlates of exercise hyperemia and muscle energetics in the human upper arm

We employed interleaved dynamic 1H magnetic resonance imaging (MRI) and 31P MR spectroscopy in combination with arm-cycling to investigate correlations of exercise hyperemia and muscle energetics in the triceps brachii (TB) muscle of the upper arm of healthy individuals. The parameter hyperemic slope (HS) determined from MRI acquisitions immediately after exercise was used as primary index of maximal TB oxygenation level in response to exercise. We found that HS tended to be inversely correlated with TB acidification during exercise (P =0.06) as opposed to findings in leg muscle. The absolute increase in cardiac-output during exercise was found to be uncorrelated with HS (P =0.19) suggesting that the magnitude of the hyperemic response to exercise involving a minor muscle mass is governed by local rather than systemic factors. Post-exercise, the rate of metabolic recovery was fastest in the study subject with highest HS and slowest for the opposite case, although this correlation failed to reach significance in our small study cohort (P =0.14). This finding fits the conclusion of previous musculoskeletal 31P MRS studies that oxygen supply to working skeletal muscle exerts significant metabolic control over oxidative muscular energy balance even if the physical task only involves a minor muscle mass. New & NoteworthyThe use of interleaved dynamic 1H magnetic resonance imaging (MRI) and 31P MR spectroscopy uniquely afforded simultaneous interrogation of exercise hyperemia and muscle energetics in the human upper-arm. We found triceps muscle acidification during arm-cycling and readouts of hyperemia were, if anything, inversely correlated. Macrovascular and microvascular readouts of hyperemic response were uncorrelated. Post-exercise metabolic recovery rate tended to correlate with exercise hyperemia.

physiology↗

Dynamic balance of myoplasmic energetics and redox state in a fast-twitch oxidative glycolytic skeletal muscle fiber

In order to investigate the mechanisms governing energy and redox balance in skeletal muscle, we developed a computational model describing the coupled biochemical reaction network of glycolysis and mitochondrial oxidative phosphorylation (OxPhos) in fast-twitch oxidative glycolytic (FOG) muscle fibers. The model was identified against dynamic in vivo recordings of Phosphocreatine (PCr), inorganic Phosphate (Pi), and pH in rodent hindlimb muscle and verified against independent data from in vivo experiments and muscle biopsies. Step response testing revealed that mass action kinetics in combination with feedback control were sufficient to accomplish myoplasmic ATP homeostasis over a 100-fold range of ATP turnover rates. This vital emergent property of the metabolic model was associated with dynamic behaviour of intermediary metabolite concentrations similar to a second-order underdamped system that remains to be verified. The simulations additionally predicted that the lactate dehydrogenase (LDH) reaction makes substantial contributions to redox balance across the physiological range of ATP demands in this myofiber phenotype, while its role in slowing cellular acidification is minimal. Yet, LDH knock-out simulations revealed that oxidative recycling of myoplasmic NADH in and by itself sufficed to maintain redox balance over ATP turnover rates in the range of mitochondrial ATP synthesis. We conclude that aerobic lactate production in working muscles is a byproduct of the metabolic flexibility of FOG myofibers afforded by expression of high levels of LDH and OxPhos enzymes to support continual myoplasmic redox balance and ATP synthesis under conditions of high-intensity mechanical work. In the future, the presented simulation framework may be used to further enhance the understanding of how experimental observations in muscle emerge from the integrative behaviour of the metabolic network for carbohydrate metabolism in FOG myofibers.

physiology↗