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Iron Deficiency without Anemia Decreases Physical Endurance and Mitochondrial Complex I Activity of Oxidative Skeletal Muscle in the Mouse.

ABSTRACT: Iron deficiency (ID), with or without anemia, is responsible for physical fatigue. This effect may be linked to an alteration of mitochondrial metabolism. Our aim was to assess the impact of ID on skeletal striated muscle mitochondrial metabolism. Iron-deficient non-anemic mice, obtained using a bloodletting followed by a low-iron diet for three weeks, were compared to control mice. Endurance was assessed using a one-hour submaximal exercise on a Rotarod device and activities of mitochondrial complexes I and IV were measured by spectrophotometry on two types of skeletal striated muscles, the soleus and the quadriceps. As expected, ID mice displayed hematologic markers of ID and reduced iron stores, although none of them were anemic. In ID mice, endurance was significantly reduced and activity of the respiratory chain complex I, normalized to citrate synthase activity, was significantly reduced in the soleus muscle but not in the quadriceps. Complex IV activities were not significantly different, neither in the soleus nor in the quadriceps. We conclude that ID without anemia is responsible for impaired mitochondrial complex I activity in skeletal muscles with predominant oxidative metabolism. These results bring pathophysiological support to explain the improved physical activity observed when correcting ID in human. Further studies are needed to explore the mechanisms underlying this decrease in complex I activity and to assess the role of iron therapy on muscle mitochondrial metabolism.

SUBMITTER: Rineau E

PROVIDER: S-EPMC8064065 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionPortugal underwent significant political, demographic and epidemiological transitions during the 20th century resulting in migration to urban areas with subsequent overcrowding and issues with water sanitation. This study investigates population health during these transitions and interprets results within a framework of recent history and present-day public health information. We investigate skeletal evidence for anemia (cribra orbitalia and porotic hyperostosis) as indicators of stress and frailty-i.e., whether the lesions contribute to susceptibility for disease or increased risk of death.MethodsThe presence and severity of skeletal lesions were compared against known sex and cause of death data to investigate potential heterogeneity in frailty and the relationship between lesions and risk of dying over time. Additionally, we tested for the presence of selective mortality in our data (i.e., whether or not the sample is biased for individuals with higher frailty). Our sample derives from a large, documented, modern Portuguese collection from Lisbon and is the first study of its kind using a documented collection. The collection represents primarily middle-class individuals.Results and conclusionsAnalyses indicated that porotic hyperostosis became more common and severe over time, while cribra orbitalia severity increased over time. Neither process was linked to cause of death. However, there was a significant relationship to sex; males exhibited a higher prevalence and severity of lesions and increased mortality. A Gompertz function showed decreased survivorship in early life but increased survivorship over age 60. Using comorbidities of anemia, we were unable to detect selective mortality-i.e., in our sample, lesions do not represent a sign of poor health or increased frailty and are not significantly linked with a decreased mean age-at-death. However, lesion prevalence and severity do reflect the socioeconomic processes in urban Lisbon during the 1800s and 1900s and the possibility of water-borne parasites as the contributing factor for iron deficiency anemia.

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Iron Deficiency without Anemia Decreases Physical Endurance and Mitochondrial Complex I Activity of Oxidative Skeletal Muscle in the Mouse.

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