Proton efflux in human skeletal muscle during recovery from exercise

Kemp, Graham J.; Thompson, Campbell; Taylor, D. J.; Radda, George K.

doi:10.1007/s004210050276

Cited by 46 publications

(58 citation statements)

References 37 publications

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“…The initial PCr recovery rate (V mM/min) was used as a measure of end-exercise rate of oxidative ATP synthesis. Although details of the relationship between V and oxidative ATP synthesis are a matter of debate, 13,15,18 the initial PCr recovery rate can be regarded as regulated by cytosolic free [ADP]. The mitochondrial capacity, i.e., the inferred maximum rate of oxidative synthesis, 14 is calculated from V and the end of exercise [ADP] as:…”

Section: Methodsmentioning

confidence: 99%

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy

et al. 2005

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Exercise therapy improves mitochondrial function in patients with mitochondrial myopathy (MM). We undertook this study to determine the metabolic abnormalities that are improved by exercise therapy. This study identified metabolic pathology using (31)P-magnetic resonance spectroscopy and magnetic resonance imaging (MRI) in a group of patients with MM compared to a control group matched for age, gender, and physical activity. We also observed the effect of exercise therapy for 12 weeks on muscle metabolism and physical function in the MM group. During muscle activity, there was impaired responsiveness of the mitochondria to changes in cytosolic adenosine diphosphate concentration, increased dependence on anaerobic energy pathways, and an adaptive increase in proton efflux in patients with MM. Following exercise therapy, mitochondrial function and muscle mass improved without any change in proton efflux rate. These metabolic findings were accompanied by improvements in functional ability. We conclude that there are significant metabolic differences between patients with MM and a control population, independent of age, gender, and physical activity. Exercise therapy can assist in improving mitochondrial function in MM patients.

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Section: Methodsmentioning

confidence: 99%

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy

et al. 2005

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“…To improve precision, we use a modified version of this calculation (60) in which the total proton disappearance (i.e., ͐Edt) is estimated cumulatively from the start of recovery, then fitted to an exponential function to obtain the initial recovery rate E. This is approximately proportional to the end-of-exercise fall in pH below resting values (60), and as end-of-exercise pH covers a substantial range in all groups, dE/dpH was calculated by linear regression across each group, which quantifies the capacity of the proton efflux system.…”

Section: Atp Production From Anaerobic Glycolysis (L)mentioning

confidence: 99%

Reproducibility assessment of metabolic variables characterizing muscle energetics in Vivo: A ³¹P‐MRS study

Layec

Bringard²,

Fur

et al. 2009

Magnetic Resonance in Med

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The purpose of the present study was to assess the reliability of metabolic parameters measured using 31 P magnetic resonance spectroscopy ( 31 P MRS) during two standardized rest-exerciserecovery protocols. Twelve healthy subjects performed the standardized protocols at two different intensities; i.e., a moderate intensity (MOD) repeated over a two-month period and heavy intensity (HEAVY) repeated over a year's time. Test-retest reliability was analyzed using coefficient of variation ( Key words: magnetic resonance spectroscopy; reliability; oxidative capacity; PCr kinetics; exercise Phosphorus-31 nuclear magnetic resonance spectroscopy ( 31 P-MRS) is now widely accepted as the "gold standard" method for noninvasive measurements of energy metabolism in exercising muscle. The analysis of changes in phosphorylated compounds concentrations and intracellular pH during rest-exercise-recovery protocols has provided significant advance in the understanding of underlying mechanisms of muscle energy production (1-4). Given the noninvasiveness of the method, 31 P-MRS enables repeated measurements and has been successfully used in a wide range of situations such as the assessment of therapeutic interventions in patients with metabolic disorders (5-7) and the characterization of training-induced metabolic changes (8 -11). More recently, the dynamics of phosphocreatine (PCr) has been used to evaluate the control of mitochondrial respiration in skeletal muscle (12) or the mechanism underlying the V O 2p slow component (13) typically observed during a high-intensity exercise; i.e., above the lactate threshold. In addition, the rate constant of postexercise recovery kinetics of [PCr] has been used as an index of mitochondrial function (14 -17). In addition to these traditional variables, more sophisticated analyses have been put forth in order to quantify the contribution of oxidative and anaerobic pathways to energy production in exercising muscle (2,18,19).Despite the widespread use of 31 P MRS for muscle energetics investigation, the reproducibility of the corresponding variables has been scarcely investigated. It has actually been investigated through repeated measurements performed 1 week (5) and 4 weeks apart (20). Bendahan et al. (5) reported a good reliability in metabolic parameters when investigated using analysis of variance (ANOVA). However, detection of systematic bias might have been affected by large random error between tests as suggested previously (21). observed large test-retest variability in metabolic parameters measured during steady state phases of moderate isometric plantar flexion exercise. However, kinetics parameters of recovery exhibited a small coefficient of variation (CV Ͻ 9%). In this line, van den Broek et al. (22) reported a low variability (CV Ͻ 11.5%) for the parameters describing the recovery kinetics of PCr and adenosine diphosphate (ADP) in a single subject who repeated the same exercise protocol 10 times. Based on a visual inspection of the kinetics of phosphorylated compounds and pH i...

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“…Quantification of phosphocreatine (PCr), inorganic phosphate (Pi), and pH was performed using the AMARES time domain fit routine in the jMRUI processing software (version 3.0) (7,8). Standard methods were used to calculate the parameters of oxidative metabolism and pH handling (6).…”

Section: Mrs Protocolmentioning

confidence: 99%

Improving the Vitamin D Status of Vitamin D Deficient Adults Is Associated With Improved Mitochondrial Oxidative Function in Skeletal Muscle

Sinha

Hollingsworth

Ball

et al. 2013

The Journal of Clinical Endocrinology &Amp; Metabolism

200

171

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Objective: Suboptimal mitochondrial function has been implicated in several disorders in which fatigue is a prominent feature. Vitamin D deficiency is a well-recognized cause of fatigue and myopathy. The aim of this study was to examine the effects of cholecalciferol therapy on skeletal mitochondrial oxidative function in symptomatic, vitamin D-deficient individuals.Design: This longitudinal study assessed mitochondrial oxidative phosphorylation in the gastrosoleus compartment using phosphorus-31 magnetic resonance spectroscopy measurements of phosphocreatine recovery kinetics in 12 symptomatic, severely vitamin D-deficient subjects before and after treatment with cholecalciferol. All subjects had serum assays before and after cholecalciferol therapy to document serum 25-hydroxyvitamin D (25OHD) and bone profiles. Fifteen healthy controls also underwent 31 P-magnetic resonance spectroscopy and serum 25OHD assessment. Results:The phosphocreatine recovery half-time ( 1/2 PCr) was significantly reduced after cholecalciferol therapy in the subjects indicating an improvement in maximal oxidative phosphorylation (34.44 Ϯ 8.18 sec to 27.84 Ϯ 9.54 sec, P Ͻ .001). This was associated with an improvement in mean serum 25OHD levels (8.8 Ϯ 4.2 nmol/L to 113.8 Ϯ 51.5 nmol/L, P Ͻ .001). There was no difference in phosphate metabolites at rest. A linear regression model showed that decreasing serum 25OHD levels was associated with increasing 1/2 PCr (r ϭ Ϫ0.41, P ϭ .009). All patients reported an improvement in fatigue after cholecalciferol therapy. Conclusions:Cholecalciferol therapy augments muscle mitochondrial maximal oxidative phosphorylation after exercise in symptomatic, vitamin D-deficient individuals. This finding suggests that changes in mitochondrial oxidative phosphorylation in skeletal muscle could at least be partly responsible for the fatigue experienced by these patients.

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Proton efflux in human skeletal muscle during recovery from exercise

Cited by 46 publications

References 37 publications

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy

Reproducibility assessment of metabolic variables characterizing muscle energetics in Vivo: A ³¹P‐MRS study

Improving the Vitamin D Status of Vitamin D Deficient Adults Is Associated With Improved Mitochondrial Oxidative Function in Skeletal Muscle

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Proton efflux in human skeletal muscle during recovery from exercise

Cited by 46 publications

References 37 publications

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy

Reproducibility assessment of metabolic variables characterizing muscle energetics in Vivo: A 31P‐MRS study

Improving the Vitamin D Status of Vitamin D Deficient Adults Is Associated With Improved Mitochondrial Oxidative Function in Skeletal Muscle

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Reproducibility assessment of metabolic variables characterizing muscle energetics in Vivo: A ³¹P‐MRS study