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1.
J Appl Biomech ; 28(5): 599-607, 2012 Nov.
Article in English | MEDLINE | ID: mdl-22694808

ABSTRACT

We aimed to analyze the effects of fatigue on kinematical parameters during submaximal and maximal butterfly. Seven female swimmers performed two randomized 100-m butterfly bouts, at submaximal velocity and at maximal velocity in 25-m pool. During the 1st and 4th laps of each 100 m, kinematic data were recorded by two video cameras (above and below water) on the sagittal plane. Velocity, stroke length, stroke frequency, intracyclic horizontal velocity variation, horizontal and vertical displacements of the hand and foot and stroke phases' duration were computed for each stroke cycle. Velocity, stroke length, stroke frequency were lower for 4th than 1st lap, at both intensities. Dropped elbow and foot vertical amplitude of 1st and 2nd downbeats were higher for 4th than 1st lap, at both intensities. At submaximal and maximal intensity, swimmers spent more time during push and recovery phases. At submaximal intensity, swimmers experienced fewer difficulties to cope with fatigue between 1st and 4th lap, which allowed the maintenance of intracyclic velocity variation. However, at maximal intensity, swimmers were probably more fatigued and, as a consequence, less mechanically efficient, showing an increase in intracyclic velocity variation.


Subject(s)
Fatigue/physiopathology , Swimming/physiology , Adolescent , Adult , Biomechanical Phenomena , Female , Humans , Physical Endurance/physiology , Young Adult
2.
Age (Dordr) ; 32(3): 337-46, 2010 Sep.
Article in English | MEDLINE | ID: mdl-20640548

ABSTRACT

The aim of this study was to analyze the influence of aerobic fitness (AF) on age-related lymphocyte DNA damage in humans, giving special attention to the role of the mitochondrial respiratory chain and hydrogen peroxide production. Considering age and AF (as assessed by VO(2)max), 66 males (19-59 years old) were classified as high fitness (HF) or low fitness (LF) and distributed into one of the following groups: young adults (19-29 years old), adults (30-39 years old), and middle-aged adults (over 40 years old). Peripheral lymphocytes obtained at rest were used to assess DNA damage (strand breaks and formamidopyrimidine DNA glycosylase (FPG) sites through the comet assay), activity of mitochondrial complexes I and II (polarographically measured), and the hydrogen peroxide production rate (assayed by fluorescence). Results revealed a significant interaction between age groups and AF for DNA strand breaks (F = 8.415, p = .000), FPG sites (F = 11.766, p = .000), mitochondrial complex I activity (F = 7.555, p = .000), and H(2)O(2) production (F = 7.500, p = .000). Except for mitochondrial complex II activity, the age variation of the remaining parameters was significantly attenuated by HF. Considering each AF level, an increase in DNA strand breaks and FPG sites with age (r = 0.655, p = 0.000, and r = 0.738, p = 0.000, respectively) was only observed in LF. Moreover, decreased mitochondrial complex I activity with age (r = -.470, p = .009) was reported in LF. These results allow the conclusion that high AF seems to play a key role in attenuating the biological aging process.


Subject(s)
Aging/physiology , DNA Damage , Leukocytes/physiology , Mitochondria/physiology , Physical Fitness/physiology , Adult , Age Factors , Electron Transport/physiology , Exercise , Female , Humans , Hydrogen Peroxide/toxicity , Male , Middle Aged
3.
J Gerontol A Biol Sci Med Sci ; 64(9): 927-39, 2009 Sep.
Article in English | MEDLINE | ID: mdl-19465709

ABSTRACT

This study investigated the impact of lifelong sedentariness on skeletal muscle mass and mitochondrial function. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young-Y; old sedentary-OS; old active-OA). Young animals were sacrificed after 1 week of quarantine, and OS and OA groups were individually placed into standard cages and in cages with running wheels, respectively, until sacrifice (25 months). Body weights and hind-limb skeletal muscle wet weights were obtained from all groups. Mitochondrial respiratory functional measures (i.e., state 3 and 4 respiration, respiratory control ratio, and ratio of nanomoles of ADP phosphorylated by nanomoles of O2 consumed [ADP/O]) and biochemical markers of oxidative damage (aconitase activity, protein carbonyl derivatives, sulfhydryl groups) were measured in isolated mitochondrial suspensions. Our results reveal that lifelong sedentary behavior has a negative impact on the age-related loss of skeletal muscle mass and on the isolated mitochondrial function of mixed skeletal muscle of mice, which is associated with an increased oxidative damage to mitochondrial biomolecules.


Subject(s)
Aging/physiology , Mitochondria, Muscle/physiology , Muscle, Skeletal/physiology , Physical Conditioning, Animal , Aconitate Hydratase/metabolism , Adenosine Diphosphate/pharmacology , Animals , Citrate (si)-Synthase/metabolism , Mice , Mice, Inbred C57BL , Oxidative Stress , Oxygen Consumption , Phosphorylation
4.
J Gerontol A Biol Sci Med Sci ; 64(1): 21-33, 2009 Jan.
Article in English | MEDLINE | ID: mdl-19196905

ABSTRACT

This study investigated the influence of age on the functional status of mitochondria isolated from skeletal muscle of C57BL/6 mice aged 3 and 18 months. We hypothesized that skeletal muscle mitochondria isolated from aged animals will exhibit a decreased respiratory function. Mitochondrial respiratory functional measures (ie, State 3 and 4 respiration, respiratory control ratio and number of nanomoles of ADP phosphorylated by nanomoles of O(2) consumed per mitochondrion) and biochemical markers of oxidative damage (aconitase activity, protein carbonyl derivatives, sulfhydryl groups, and malondialdehyde) were measured in isolated mitochondrial suspensions. Along with traditional tests of mitochondrial function, an in vitro repetitive ADP-stimulation test was used to evaluate the mitochondrial capacity to reestablish the homeostatic balance between successive ADP stimulations. The number of mitochondria per mitochondrial suspension, calculated by transmission electron microscopy, was used to normalize functional and biochemical data. Our results confirm the existence of an age-associated decline in mitochondrial function of mixed skeletal muscle, which is significantly correlated with higher levels of mitochondrial oxidative damage.


Subject(s)
Aging/metabolism , Energy Metabolism/physiology , Mitochondria, Muscle/metabolism , Muscle, Skeletal/metabolism , Oxidative Stress/physiology , Animals , Citrate (si)-Synthase/metabolism , Cytochromes c/metabolism , Electrophoresis, Polyacrylamide Gel , Lipid Peroxidation , Male , Mice , Mice, Inbred C57BL , Microscopy, Electron, Transmission , Mitochondria, Muscle/ultrastructure , Muscle Proteins/metabolism , Muscle, Skeletal/ultrastructure
5.
J Gerontol A Biol Sci Med Sci ; 63(4): 350-9, 2008 Apr.
Article in English | MEDLINE | ID: mdl-18426958

ABSTRACT

Several in vitro studies about age-associated skeletal muscle mitochondrial dysfunction are somewhat conflicting, and this might be related to different normalization procedures. The objective of this study was to normalize the functional and biochemical data per number of mitochondria present in a mitochondrial suspension. Functional and biochemical parameters were obtained in mitochondrial suspensions from murine skeletal muscle of different ages. Mitochondrial respiratory function was polarographically measured using a Clark-type oxygen electrode. Biochemical analyses included determination of citrate synthase (CS) activity and total protein content in the mitochondrial suspension. Electron microscopy analysis of the suspensions allowed calculation of the number of mitochondria per milligram of protein. Our results conclude that advanced age is associated with mitochondrial dysfunction; moreover, from the correlation between morphological and biochemical data, it is evident that CS activity in the mitochondrial suspensions is a more accurate marker of mitochondrial mass than is total protein content.


Subject(s)
Aging/metabolism , Aging/pathology , Mitochondria, Muscle/metabolism , Mitochondria, Muscle/ultrastructure , Muscle, Skeletal/physiopathology , Animals , Biomarkers , Citrate (si)-Synthase/metabolism , Citrate (si)-Synthase/ultrastructure , Energy Metabolism , Male , Mice , Mice, Inbred C57BL , Mitochondrial Proteins/metabolism , Mitochondrial Proteins/ultrastructure , Muscle, Skeletal/ultrastructure , Oxygen Consumption
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