| 1. |
- Li, Xiao, et al.
(författare)
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The A55T and K153R polymorphisms of MSTN gene are associated with the strength training-induced muscle hypertrophy among Han Chinese men.
- 2014
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Ingår i: Journal of Sports Sciences. - : Informa UK Limited. - 0264-0414 .- 1466-447X. ; 32:9, s. 883-91
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Tidskriftsartikel (refereegranskat)abstract
- Myostatin, encoded by the MSTN gene, is a strong regulator of skeletal muscle growth. The present study aimed to investigate whether the A55T and K153R polymorphisms of MSTN were associated with the strength training-induced muscle hypertrophy among Han Chinese men. A total of 94 healthy, untrained men were recruited for an 8-week strength training programme. The thicknesses of biceps and quadriceps, along with anthropometric measurements of the participants, were assessed before and after the programme. The MSTN polymorphisms were subsequently genotyped employing polymerase chain reaction-restriction fragment length polymorphism technique and confirmed by DNA sequencing. One-way analysis of variance was used to compare the pre- and post-training measurements between carriers of different polymorphic genotypes. Our results indicated that individuals with AT + TT genotype of the A55T polymorphism showed a significant increase in the thickness of biceps (0.292 ± 0.210 cm, P = 0.03), but not quadriceps (0.254 ± 0.198 cm, P = 0.07), compared to carriers of AA genotype. For the K153R polymorphism, the increases in the thicknesses of both biceps (0.300 ± 0.131 cm) and quadriceps (0.421 ± 0.281 cm) were significantly higher among individuals with KR than those with KK genotypes (P < 0.01 for both muscles). The results obtained therefore suggested a possible association between the two polymorphisms and the strength training-induced muscle hypertrophy among men of Han Chinese ethnicity.
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| 2. |
- Tonkonogi, Michail, et al.
(författare)
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Reduced oxidative power but unchanged antioxidative capacity in skeletal muscle from aged humans.
- 2003
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Ingår i: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 446:2, s. 261-9
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Tidskriftsartikel (refereegranskat)abstract
- The hypothesis that the aging process is associated with mitochondrial dysfunction and oxidative stress has been investigated in human skeletal muscle. Muscle biopsy samples were taken from seven old male subjects [OS; 75 (range 61-86) years] and eight young male subjects [YS; 25 (22-31) years]. Oxidative function was measured both in permeabilised muscle fibres and isolated mitochondria. Despite matching the degree of physical activity, OS had a lower training status than YS as judged from pulmonary maximal O(2) consumption ( Vdot;O(2)max, -36%) and handgrip strength (-20%). Both maximal respiration and creatine-stimulated respiration were reduced in muscle fibres from OS (-32 and -34%, respectively). In contrast, respiration in isolated mitochondria was similar in OS and YS. The discrepancy might be explained by a biased harvest of "healthy" mitochondria and/or disruption of structural components during the process of isolation. Cytochrome C oxidase was reduced (-40%, P<0.01), whereas UCP3 protein tended to be elevated in OS ( P=0.09). Generation of reactive oxygen species by isolated mitochondria and measures of antioxidative defence (muscle content of glutathione, glutathione redox status, antioxidative enzymes activity) were not significantly different between OS and YS. It is concluded that aging is associated with mitochondrial dysfunction, which appears to be unrelated to reduced physical activity. The hypothesis of increased oxidative stress in aged muscle could not be confirmed in this study.
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| 3. |
- Apró, William, 1980-, et al.
(författare)
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Endurance Exercise Does Not Impair mTOR Signalling After Resistance Exercise : D-58 Thematic Poster - Skeletal Muscle Cell Signaling: JUNE 2, 2011 3:15 PM - 5:15 PM: ROOM: 304
- 2011
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Ingår i: Medicine & Science in Sports & Exercise. - 0195-9131 .- 1530-0315. ; 43:5, s. 52-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Resistance exercise is known to stimulate muscle hypertrophy and this effect is mainly mediated by the mammalian target of rapamycin (mTOR) pathway. In contrast, endurance exercise results in a divergent phenotypic response which to a large extent is mediated by adenosine monophosphate-activated protein kinase (AMPK). Research indicates that molecular interference may exist, possibly through an inhibitory effect on mTOR signalling by AMPK, when these two modes of exercise are combined. PURPOSE: To investigate the impact of subsequent endurance exercise on resistance exercise induced mTOR signalling. METHODS: In a randomized and cross-over fashion, ten male subjects performed either heavy resistance exercise (R) or heavy resistance exercise followed by endurance exercise (RE) on two separate occasions. The R protocol consisted of thirteen sets of leg press exercise with 3 minutes of recovery allowed between each set. In the RE session, resistance exercise was followed by 15 minutes recovery after which 30 min of cycling was initiated at an intensity equal to 70 % of the subjects' maximal oxygen consumption. Muscle biopsies were collected before, 1 and 3 hours after resistance exercise in both trials. Samples were analyzed for several signalling proteins in the mTOR pathway using western blot technique. RESULTS: Phosphorylation of mTOR increased approx. twofold at 1 h post resistance exercise and remained elevated at the 3 h time point (p< 0.01) with no difference between the two trials. Phosphorylation of p70S6k, a downstream target of mTOR, was increased about 6-and18-fold at 1 h and 3 h post resistance exercise (p< 0.01). There was no difference in p70S6k phosphorylation at any time point between the two trials. Phosphorylation of the eukaryotic elongation factor eEF2 was decreased 3- to 4-fold at both time points post resistance exercise (p< 0.01) with no difference between trials. Phosphorylation of AMPK was unchanged at the 1 h time point but decreased approximately 30 % from pre-exercise values in both trials at 3 h post resistance exercise (p< 0.01). CONCLUSIONS: The signalling response following heavy resistance exercise is not blunted by subsequent endurance exercise. Supported by the Swedish National Centre for Research in Sports.
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| 4. |
- Apró, William, et al.
(författare)
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Resistance exercise induced mTORC1 signaling is not impaired by subsequent endurance exercise in human skeletal muscle.
- 2013
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Ingår i: American Journal of Physiology. Endocrinology and Metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 305:1, s. E22-32
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Tidskriftsartikel (refereegranskat)abstract
- The current dogma is that the muscle adaptation to resistance exercise is blunted when combined with endurance exercise. The suggested mechanism (based on rodent experiments) is that activation of adenosine monophosphate-activated protein kinase (AMPK) during endurance exercise impairs muscle growth through inhibition of the mechanistic target of rapamycin complex 1 (mTORC1). The purpose of this study was to investigate potential interference of endurance training on the signaling pathway of resistance training [mTORC1 phosphorylation of ribosomal protein S6 kinase 1 (S6K1)] in human muscle. Ten healthy and moderately trained male subjects performed on two separate occasions either acute high-intensity and high-volume resistance exercise (leg press, R) or R followed by 30 min of cycling (RE). Muscle biopsies were collected before and 1 and 3 h post resistance exercise. Phosphorylation of mTOR (Ser(2448)) increased 2-fold (P < 0.05) and that of S6K1 (Thr(389)) 14-fold (P < 0.05), with no difference between R and RE. Phosphorylation of eukaryotic elongation factor 2 (eEF2, Thr(56)) was reduced ∼70% during recovery in both trials (P < 0.05). An interesting finding was that phosphorylation of AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC, Ser(79)) decreased ∼30% and ∼50%, respectively, 3 h postexercise (P < 0.05). Proliferator-activated receptor-γ coactivator-1 (PGC-1α) mRNA increased more after RE (6.5-fold) than after R (4-fold) (RE vs. R: P < 0.01) and was the only gene expressed differently between trials. These data show that the signaling of muscle growth through the mTORC1-S6K1 axis after heavy resistance exercise is not inhibited by subsequent endurance exercise. It is also suggested that prior activation of mTORC1 signaling may repress subsequent phosphorylation of AMPK.
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| 5. |
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| 6. |
- Ding, Mozhu, et al.
(författare)
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Cerebral Small Vessel Disease Associated With Atrial Fibrillation Among Older Adults : A Population-Based Study.
- 2021
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Ingår i: Stroke. - : American Heart Association. - 0039-2499 .- 1524-4628. ; 52:8, s. 2685-2689
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: Cerebral small vessel disease, as a potential mechanism underlying the association between atrial fibrillation (AF) and dementia, remains poorly investigated. In this cohort study, we sought to examine the association between AF and cerebral small vessel disease markers among older adults.METHODS: Data on 336 participants (age ≥60 years, mean 70.2 years; 60.2% women) free of dementia, disability, and cerebral infarcts were derived from the population-based Swedish National Study on Aging and Care in Kungsholmen. Structural brain magnetic resonance imaging examinations were performed at baseline (2001-2004) and follow-ups (2004-2007 and 2007-2010). Magnetic resonance imaging markers of cerebral small vessel disease included perivascular spaces, lacunes, and volumes of white matter hyperintensities, lateral ventricles, and total brain tissue. AF was assessed at baseline and follow-ups through clinical examinations, electrocardiogram, and medical records. Data were analyzed using linear mixed-effects models.RESULTS: At baseline, 18 persons (5.4%) were identified to have prevalent AF and 17 (5.6%) developed incident AF over the 6-year follow-up. After multivariable adjustment, AF was significantly associated with a faster annual increase in white matter hyperintensities volume (β coefficient=0.45 [95% CI, 0.04-0.86]) and lateral ventricular volume (0.58 [0.13-1.02]). There was no significant association of AF with annual changes in perivascular spaces number (β coefficient=0.53 [95% CI, -0.27 to 1.34]) or lacune number (-0.01 [-0.07 to 0.05]).CONCLUSIONS: Independent of cerebral infarcts, AF is associated with accelerated progression of white matter lesions and ventricular enlargement among older adults.
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| 7. |
- Hey-Mogensen, M, et al.
(författare)
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Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes.
- 2010
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 53:9, s. 1976-85
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Tidskriftsartikel (refereegranskat)abstract
- AIM/HYPOTHESIS: Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. METHODS: Type 2 diabetic men (n = 13) and control (n = 14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic-hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. RESULTS: Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. CONCLUSIONS/INTERPRETATION: Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.
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| 8. |
- Li, Jing, 1973-, et al.
(författare)
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The meaning of the Chinese cultural keyword xin
- 2013
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Ingår i: Journal of Languages and Culture. - Lagos, Nigeria : Academic Journals. - 2141-6540. ; 4:5, s. 75-89
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Tidskriftsartikel (refereegranskat)abstract
- In China, the word, xin 心 (often translated as ‘heart’) is frequently used and its concept is central to Chinese culture. However, its meaning is not exactly the same as ‘heart’ in English. Using qigong as the context, this article aims to explore the meaning of xin as a cultural keyword in order to gain an in-depth understanding of Chinese culture and knowledge within that cultural system. Qigong is a Chinese health maintenance system and healing tradition which integrates physical activity with training of the mind and self-cultivation. One of qigong’s basic components is xin adjustment. It is impossible to convey the full meaning of this concept without understanding the meaning of xin. In Chinese culture, xin is the root of physical and mental life. It is the seat of all emotions, and embodies the inherent goodness of human nature and wisdom. Xin helps to guide the individual’s way of life and attitude, and can lead one to deep contentment.
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| 9. |
- Ma, Chuanwei, et al.
(författare)
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Global trends in the prevalence of secondhand smoke exposure among adolescents aged 12-16 years from 1999 to 2018 : an analysis of repeated cross-sectional surveys.
- 2021
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Ingår i: The Lancet Global Health. - : Elsevier. - 2214-109X. ; 9:12, s. E1667-E1678
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Secondhand smoke exposure can cause morbidity and premature mortality. However, the global prevalence of, and trends in, secondhand smoke exposure among adolescents are poorly documented. We aimed to assess the prevalence of, and trends in, secondhand smoke exposure among adolescents from 1999 to 2018.METHODS: We did an analysis of the most recent data from the Global Youth Tobacco Survey (GYTS), a nationally representative, self-administered, school-based cross-sectional survey of tobacco use and related factors among adolescents aged 12-16 years worldwide. Data from 142 countries and territories that had done a GYTS between 2010 and 2018, comprising 711 366 participants, were used to assess the prevalence of secondhand smoke exposure. Data from 131 countries and territories that had done two or more surveys between 1999 and 2018, comprising 1 405 458 participants, were used to assess trends in secondhand smoke exposure. The frequency of secondhand smoke exposure at home, in public places, or in any place was defined as follows, based on students' responses: 1 or more days, 3 or more days, 5 or more days, or daily during the past 7 days.FINDINGS: Based on the most recent surveys done in 142 countries between Jan 1, 2010, and Dec 31, 2018, the global prevalence of secondhand smoke exposure in any place was 62·9% (95% CI 61·7-64·1) on 1 or more days, 51·0% (49·8-52·1) on 3 or more days, 40·1% (38·9-41·2) on 5 or more days, and 32·5% (31·5-33·6) daily during the past 7 days. The prevalence of secondhand smoke exposure at home was 33·1% (95% CI 32·1-34·1) on 1 or more days, 20·1% (19·3-20·9) on 3 or more days, 14·9% (14·2-15·7) on 5 or more days, and 12·3% (11·7-13·0) daily during the past 7 days; and in public places the prevalence of secondhand smoke exposure was 57·6% (56·4-58·8) on 1 or more days, 43·4% (42·2-44·6) on 3 or more days, 30·3% (29·2-31·5) on 5 or more days, and 23·5% (22·5-24·5) daily during the past 7 days. Between Jan 1, 1999, and Dec 31, 2018, the prevalence of secondhand smoke exposure (on ≥1 day during the past 7 days) in any place decreased in 57 (43·5%) of 131 countries, increased in 27 (20·6%), and remained unchanged in 47 (35·9%). Although the prevalence of secondhand smoke exposure at home decreased in 86 (65·6%) countries, the prevalence in public places did not change in 46 (35·1%) countries and increased in 40 (30·5%).INTERPRETATION: Secondhand smoke exposure among adolescents remains a serious public health challenge worldwide. Although the prevalence of secondhand smoke exposure at home decreased in most countries, the prevalence in public places increased or remained unchanged in most countries between 1999 and 2018. These findings emphasise the need to strengthen smoke-free policies, especially in public places.FUNDING: Youth Team of Humanistic and Social Science of Shandong University, Jinan, China.TRANSLATION: For the Chinese translation of the abstract see Supplementary Materials section.
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| 10. |
- Psilander, Niklas, et al.
(författare)
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Mitochondrial gene expression in elite cyclists : effects of high-intensity interval exercise.
- 2010
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Ingår i: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 110:3, s. 597-606
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Tidskriftsartikel (refereegranskat)abstract
- Little is known about the effect of training on genetic markers for mitochondrial biogenesis in elite athletes. We tested the hypothesis that low-volume sprint interval exercise (SIE) would be as effective as high-volume interval exercise (IE). Ten male cyclists competing on national elite level (W (max) 403 ± 13 W, VO(2peak) 68 ± 1 mL kg(-1) min(-1)) performed two interval exercise protocols: 7 × 30-s "all-out" bouts (SIE) and 3 × 20-min bouts at ~87% of VO(2peak) (IE). During IE, the work was eightfold larger (1,095 ± 43 vs. 135 ± 5 kJ) and the exercise duration 17 times longer (60 vs. 3.5 min) than during SIE. Muscle samples were taken before and 3 h after exercise. The mRNA of upstream markers of mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1α), PGC-1α-related coactivator (PRC) and peroxisome proliferator-activated receptor δ (PPARδ)] increased to the same extent after SIE and IE (6-, 1.5- and 1.5-fold increase, respectively). Of the downstream targets of PGC-1α, mitochondrial transcription factor A (Tfam) increased only after SIE and was significantly different from that after IE (P < 0.05), whereas others increased to the same extent (pyruvate dehydrogenase kinase, PDK4) or was unchanged (nuclear respiratory factor 2, NRF2). We conclude that upstream genetic markers of mitochondrial biogenesis increase in a similar way in elite athletes after one exercise session of SIE and IE. However, since the volume and duration of work was considerably lower during SIE and since Tfam, the downstream target of PGC-1α, increased only after SIE, we conclude that SIE might be a time-efficient training strategy for highly trained individuals.
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