Influences of endurance training on the ultrastructural composition of the different muscle fiber types in humans

Howald, H.; Hoppeler, Hans; Claassen, Horst; Mathieu, Odile; Straub, R.

doi:10.1007/bf00589248

Cited by 354 publications

(279 citation statements)

References 32 publications

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“…In contrast, significantly less H ϩ transporter activation was found in mitochondria from the low respiration group. Fatty acid activation of the uncoupling protein 3 and adenine nucleotide translocator could also underlie the increased respiration and uncoupling in TA vs. FDI found in this study because higher intracellular lipid levels are reported in type I fibers of human muscle (32).…”

Section: Discussionmentioning

confidence: 68%

Mild mitochondrial uncoupling impacts cellular aging in human muscles in vivo

Amara¹,

Shankland²,

Jubrias³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

200

195

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Faster aging is predicted in more active tissues and animals because of greater reactive oxygen species generation. Yet age-related cell loss is greater in less active cell types, such as type II muscle fibers. Mitochondrial uncoupling has been proposed as a mechanism that reduces reactive oxygen species production and could account for this paradox between longevity and activity. We distinguished these hypotheses by using innovative optical and magnetic resonance spectroscopic methods applied to noninvasively measured ATP synthesis and O 2 uptake in vivo in human muscle. Here we show that mitochondrial function is unchanged with age in mildly uncoupled tibialis anterior muscle (75% type I) despite a high respiratory rate in adults. In contrast, substantial uncoupling and loss of cellular [ATP] indicative of mitochondrial dysfunction with age was found in the lower respiring and well coupled first dorsal interosseus (43-50% type II) of the same subjects. These results reject respiration rate as the sole factor impacting the tempo of cellular aging. Instead, they support mild uncoupling as a mechanism protecting mitochondrial function and contributing to the paradoxical longevity of the most active muscle fibers. magnetic resonance spectroscopy ͉ optical spectroscopy ͉ oxidative phosphorylation T he rate-of-living hypothesis proposes that higher rates of oxidative metabolism cause an increased production of reactive oxygen species (ROS) (1), leading to oxidative damage and mitochondrial dysfunction with age. However, mice with the lowest resting respiration rate have been shown to have the shortest longevity (2). Similarly, isolated muscle fibers show greater generation of ROS in type II fibers (3), which have the lowest oxidative capacity and chronic activity levels. This fiber type also has the shortest longevity and is the first to be lost with age (4). Thus, the tempo of aging appears to vary among mice and muscle fiber types but in an opposite manner than predicted by the rate-of-living hypothesis, with the least active having the shortest longevity.A physiological mechanism that could account for this paradox is mild mitochondrial uncoupling, which has been proposed to ameliorate ROS production by reducing reverse electron flow and superoxide generation (5). Consistent with this prediction are findings in mice with high respiration rates that showed elevated proton leak in isolated muscle mitochondria as a result of activation of the adenine nucleotide translocator and uncoupling protein 3. Mild uncoupling resulting from activation of these mitochondrial factors in type I muscle fibers could reduce ROS production, protect mitochondria from damage, and account for the longevity of this fiber type with age. A number of studies have provided evidence of mild uncoupling in human muscles (6, 7) but have not tested whether this uncoupling protects against mitochondrial dysfunction and cellular aging.New methods permit measurement of mitochondrial coupling in vivo by using a combination of noninvasive spectroscopi...

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Section: Discussionmentioning

confidence: 68%

Mild mitochondrial uncoupling impacts cellular aging in human muscles in vivo

Amara¹,

Shankland²,

Jubrias³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

200

195

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“…CS is involved in oxidative ATP production and is found in direct proportion to muscle mitochondrial content [30,31]. Kim et al [32] showed that CS activity was significantly reduced in the vastus lateralis of obese subjects, suggesting that the low mitochondrial content in the skeletal muscle of these subjects contributed to their decrease in muscle oxidative capacity.…”

Section: Discussionmentioning

confidence: 99%

Could the low level of expression of the gene encoding skeletal muscle mitofusin-2 account for the metabolic inflexibility of obesity?

et al. 2005

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Aims/hypothesis: In obesity the cellular capacity to switch from using lipid to carbohydrate and vice versa as the energy substrate, known as 'metabolic flexibility', is impaired. Mitofusin 2 (MFN2), a mitochondrial membrane protein, seems to contribute to the maintenance and operation of the mitochondrial network, and its expression is reduced in obesity. The aim of this study was to verify whether MFN2 might be implicated in the metabolic inflexibility of obesity. Materials and methods: Insulin sensitivity was measured in six morbidly obese women before and 2 years after malabsorptive bariatric surgery (BMI 53.3±10.5 vs 30.3±4.0 kg/m 2 ). Skeletal muscle MFN2, SLC2A4 (formerly known as GLUT4), COX3 (encoding cytochrome c oxidase subunit III) and CS (encoding citrate synthase) mRNA levels were measured by real-time PCR. Results: Following biliopancreatic surgery, significant increases in MFN2 mRNA (from 0.4±0.2 to 1.7±1.1 arbitrary units [AU], p=0.019) and SLC2A4 mRNA (0.38±0.12 to 0.76±0.24 AU, p=0.04) were observed, while increases in COX3 mRNA (from 14.2±6.4 to 20.2±12.5 AU) and CS mRNA (from 0.4±0.1 to 0.7±0.3 AU) failed to reach statistical significance. Insulin-mediated whole-body glucose uptake significantly (p<0.0001) increased from 21.2±4.1 to 52.8±5.9 μmol kg fat-free mass −1 min −1 and glucose oxidation rose from 11.1±2.1 to 37.7±4.7 μmol kg fat-free mass −1 min −1 (p<0.0001). Levels of MFN2 mRNA were strongly correlated with the absolute values for the glucose oxidation rate, both during fasting (glucose oxidation =3.55 MFN2 mRNA + 3.93; R 2 =0.92, p<0.0001) and during the clamp (glucose oxidation=18.8 MFN2 mRNA+34.7; R 2 =0.80, p<0.0001). The percentage changes in MFN2 mRNA were positively correlated with the percentage change in glucose oxidation during the clamp (glucose oxidation percent (%) change=0.3 MFN2 mRNA percent (%) change +153.2; R 2 =0.61, p<0.001). Conclusions/interpretation: We propose that the significant increase in MFN2 mRNA levels may explain the increase in glucose oxidation observed in morbid obesity following bariatric surgery.

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“…Furthermore, muscle hypertrophy by cycle training is frequently observed when cycle training has been performed for relatively long periods (24,58,62). Thus, it is plausible that cycle training does not increase muscle size during short periods (34,35) but that cycle training requires relatively long periods to induce significant muscle hypertrophy (5,58).…”

mentioning

confidence: 99%

Cycle training induces muscle hypertrophy and strength gain: strategies and mechanisms

Ozaki¹,

Loenneke²,

Thiebaud³

et al. 2015

Acta Physiologica Hungarica

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Cycle training is widely performed as a major part of any exercise program seeking to improve aerobic capacity and cardiovascular health. However, the effect of cycle training on muscle size and strength gain still requires further insight, even though it is known that professional cyclists display larger muscle size compared to controls. Therefore, the purpose of this review is to discuss the effects of cycle training on muscle size and strength of the lower extremity and the possible mechanisms for increasing muscle size with cycle training. It is plausible that cycle training requires a longer period to significantly increase muscle size compared to typical resistance training due to a much slower hypertrophy rate. Cycle training induces muscle hypertrophy similarly between young and older age groups, while strength gain seems to favor older adults, which suggests that the probability for improving in muscle quality appears to be higher in older adults compared to young adults. For young adults, higher-intensity intermittent cycling may be required to achieve strength gains. It also appears that muscle hypertrophy induced by cycle training results from the positive changes in muscle protein net balance.Keywords: aerobic exercise, muscular adaptation, lower body, cycling, ergometer Endurance training is a major part of any exercise program seeking to improve aerobic capacity and cardiovascular health. Another major part of exercise programming is strength/ resistance training, which improves muscle morphology. Thus to improve muscular strength and cardiovascular fitness in young, middle-aged and older populations, the American College of Sports Medicine recommends combining training intensity, volume, and frequency to optimize muscle hypertrophy and strength gain as well as aerobic capacity (V O 2 max) (23). However, the vigorous training intensity and/or high training frequency might hinder some older adults from participating in this type of training program. Interestingly, recent studies have reported concurrent improvements in V O 2 max and muscle hypertrophy in young and older populations after single exercise training (27,62,64,65). These single exercise modes include ambulatory exercise (walking, jogging, and running), cycling, and swimming.

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Influences of endurance training on the ultrastructural composition of the different muscle fiber types in humans

Cited by 354 publications

References 32 publications

Mild mitochondrial uncoupling impacts cellular aging in human muscles in vivo

Mild mitochondrial uncoupling impacts cellular aging in human muscles in vivo

Could the low level of expression of the gene encoding skeletal muscle mitofusin-2 account for the metabolic inflexibility of obesity?

Cycle training induces muscle hypertrophy and strength gain: strategies and mechanisms

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