No evidence of mitochondrial abnormality in skeletal muscle of patients with iron‐deficient anaemia

Thompson, Campbell; Kemp, Graham J.; Taylor, Doris J.; Radda, George K.; Rajagopalan, B.

doi:10.1111/j.1365-2796.1993.tb00724.x

Cited by 11 publications

(9 citation statements)

References 27 publications

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“…Acute and chronic anemia are associated with increased arterial lactate concentrations for a given metabolic rate (18);and more specifically, graded reduction in [Hb] is associated with increased skeletal muscle lactate output during exercise (17). However, there are no differences in resting or exercise skeletal muscle pl-l, as a function of anemia in rat (19) or human (20). Finally, no relationship was found between [Hb] and either resting pl-l, or its threshold in the current study.…”

Section: Discussionmentioning

confidence: 96%

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

Evans

Al-Himyary²,

Hrovat³

et al. 1997

Am J Respir Crit Care Med

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Although lung transplantation improves exercise capacity by removal of a ventilatory limitation, recipients' postoperative maximum oxygen uptake (VO2max) remains markedly abnormal. To determine if abnormal skeletal muscle oxidative capacity contributes to this impaired aerobic capacity, nine lung transplant recipients and eight healthy volunteers performed incremental quadriceps exercise to exhaustion with simultaneous measurements of pulmonary gas exchange, minute ventilation, blood lactate, and quadriceps muscle pH and phosphorylation potential by 31P-magnetic resonance spectroscopy (31P-MRS). Five to 38 mo after lung transplantation, peak VO2 was decreased compared with that of normal control subjects (6.7 +/- 0.4 versus 12.3 +/- 1.0 ml/min/kg, p < 0.001), even after accounting for differences in age and lean body weight. Neither ventilation, arterial O2 saturation nor mild anemia could account for the decrease in aerobic capacity. Quadriceps muscle intracellular pH (pH(i)) was more acidic at rest (7.07 +/- 0.01 versus 7.12 +/- 0.01 units, p < 0.05) and fell during exercise from baseline values at a lower metabolic rate (282 +/- 21 versus 577 +/- 52 ml/min, p < 0.001). Regressions for pH(i) versus VO2, phosphocreatine/inorganic phosphate ratio (PCr/Pi) versus VO2, and blood lactate versus pH(i) were not different. Among transplant recipients, the metabolic rate at which pH(i) fell correlated closely with VO2max (r = 0.87, p < 0.01). The persistent decrease in VO2max after lung transplantation may be related to abnormalities of skeletal muscle oxidative capacity.

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Section: Discussionmentioning

confidence: 96%

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

Evans

Al-Himyary²,

Hrovat³

et al. 1997

Am J Respir Crit Care Med

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“…Conversely, some observational studies on IDA in humans have failed to confirm the associations between ID and muscle dysfunction. For example, Thompson et al investigated skeletal muscle bioenergetics in women with IDA using P magnetic resonance spectroscopy, and have not documented significant mitochondrial abnormality . Furthermore, Celsing et al investigated the biochemical properties of skeletal muscle samples obtained from subjects with chronic moderate to severe IDA and controls, and have demonstrated that the maximal activities of glycolytic and oxidative enzymes in these two groups were similar .…”

Section: Links Between Iron Deficiency Decreased Exercise Capacity mentioning

confidence: 99%

“…For example, Thompson et al investigated skeletal muscle bioenergetics in women with IDA using 31 P magnetic resonance spectroscopy, and have not documented significant mitochondrial abnormality. 77 Furthermore, Celsing et al investigated the biochemical properties of skeletal muscle samples obtained from subjects with chronic moderate to severe IDA and controls, and have demonstrated that the maximal activities of glycolytic and oxidative enzymes in these two groups were similar. 78 Importantly, the aforementioned studies were observational only and the study groups were relatively small.…”

Section: Iron Deficiency Global Exercise Capacity and Skeletal Muscmentioning

confidence: 99%

The influence of iron deficiency on the functioning of skeletal muscles: experimental evidence and clinical implications

Stugiewicz

Tkaczyszyn

Kasztura

et al. 2016

European J of Heart Fail

123

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Skeletal and respiratory myopathy not only constitutes an important pathophysiological feature of heart failure and chronic obstructive pulmonary disease, but also contributes to debilitating symptomatology and predicts worse outcomes in these patients. Accumulated evidence from laboratory experiments, animal models, and interventional studies in sports medicine suggests that undisturbed systemic iron homeostasis significantly contributes to the effective functioning of skeletal muscles. In this review, we discuss the role of iron status for the functioning of skeletal muscle tissue, and highlight iron deficiency as an emerging therapeutic target in chronic diseases accompanied by a marked muscle dysfunction.

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“…Iron homeostasis in mitochondria also differs from that in the cytoplasm. Iron deprivation affects mitochondrial iron enzymes less than cytosolic iron enzymes (21). By contrast, excess iron is not usually deposited in mitochondria but is deposited in the cytosol as ferritin.…”

mentioning

confidence: 98%

Human Mitochondrial Ferritin Expressed in HeLa Cells Incorporates Iron and Affects Cellular Iron Metabolism

Corsi¹,

Cozzi²,

Arosio³

et al. 2002

Journal of Biological Chemistry

147

176

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No evidence of mitochondrial abnormality in skeletal muscle of patients with iron‐deficient anaemia

Abstract: Mitochondrial ATP synthesis was not limited by oxygen supply or an intrinsic mitochondrial defect. Therefore, the reduced exercise capacity seen in iron deficiency could be due to central causes and not to skeletal muscle metabolic abnormalities.

Cited by 11 publications

References 27 publications

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

The influence of iron deficiency on the functioning of skeletal muscles: experimental evidence and clinical implications

Human Mitochondrial Ferritin Expressed in HeLa Cells Incorporates Iron and Affects Cellular Iron Metabolism

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