mRNAs of enzymes involved in energy metabolism and mtDNA are increased in endurance-trained athletes

Puntschart, A; Claassen, Horst; Jostarndt, K; Hoppeler, Hans; Billeter, R.

doi:10.1152/ajpcell.1995.269.3.c619

Cited by 99 publications

(78 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Improvements in VO 2peak and oxidative enzymes in response to aerobic exercise have been previously shown in older people (56,57). Earlier studies also showed that vigorous training results in higher muscle mRNA content of TFAM and other mitochondrial genes in young men (58,59). The present study is the first to show that aerobic training stimulates expression of mitochondrial genes and transcription factors in muscle from older and younger people.…”

Section: Discussionsupporting

confidence: 80%

Impact of Aerobic Exercise Training on Age-Related Changes in Insulin Sensitivity and Muscle Oxidative Capacity

et al. 2003

View full text Add to dashboard Cite

1Insulin resistance increases and muscle oxidative capacity decreases during aging, but lifestyle changesespecially physical activity-may reverse these trends. Here we report the effect of a 16-week aerobic exercise program (n ‫؍‬ 65) or control activity (n ‫؍‬ 37) performed by men and women aged 21-87 years on insulin sensitivity and muscle mitochondria. Insulin sensitivity, measured by intravenous glucose tolerance test, decreased with age (r ‫؍‬ ؊0.32) and was related to abdominal fat content (r ‫؍‬ ؊0.65). Exercise increased peak oxygen uptake (VO 2peak ; 10%), activity of muscle mitochondrial enzymes (citrate synthase and cytochrome c oxidase, 45-76%) and mRNA levels of mitochondrial genes (COX4, ND4, both 66%) and genes involved in mitochondrial biogenesis (PGC-1␣, 55%; NRF-1, 15%; TFAM, 85%). Exercise also increased muscle GLUT4 mRNA and protein (30 -52%) and reduced abdominal fat (5%) and plasma triglycerides (25%). None of these changes were affected by age. In contrast, insulin sensitivity improved in younger people but not in middle-aged or older groups. Thus, the muscle mitochondrial response to 4 months of aerobic exercise training was similar in all age-groups, although the older people did not have an improvement in insulin sensitivity. Diabetes 52: 1888 -1896, 2003 T he number of people with type 2 diabetes and impaired glucose tolerance is rapidly increasing (1,2). Key factors contributing to this increase in diabetes include age, obesity, and sedentary lifestyle (3-8). Exercise is a readily available intervention that can increase insulin action (9 -14) and prevent the onset of diabetes (15-18). An important question is whether the effects of aerobic exercise on insulin action are diminished with advancing age. A recent study reported that a vigorous 7-day exercise program increased insulin sensitivity and muscle glucose transporter (GLUT4) content by a similar amount in younger (22 years) and older (61 years) people (12). However, current health and fitness guidelines for healthy adults recommend exercising at more moderate intensities at least 3 days per week over long periods (19). Thus, the first purpose of the current study was to determine whether a 4-month program of bicycle training that could be readily followed by most elderly individuals would lead to a similar improvement in insulin sensitivity in men and women across a wide age span.Skeletal muscle is the major site of insulin-mediated glucose disposal and is implicated in the pathogenesis of insulin resistance and diabetes (20,21). Several pieces of evidence suggest that insulin action may be related to the oxidative capacity of skeletal muscle. First, aerobic exercise training improves both insulin sensitivity and activity of oxidative enzymes in muscle (22,23). Second, people who are obese and insulin resistant or have type 2 diabetes tend to have lower activity of muscle oxidative enzymes (24,25). Third, insulin infusion preferentially stimulates the synthesis rate of mitochondrial proteins in skeletal muscle (26) and increa...

show abstract

Section: Discussionsupporting

confidence: 80%

Impact of Aerobic Exercise Training on Age-Related Changes in Insulin Sensitivity and Muscle Oxidative Capacity

et al. 2003

View full text Add to dashboard Cite

show abstract

“…We therefore expressed the mRNA levels of UCP2a3 relative to the mitochondrial mRNA level of cytochrome-b. It has previously been shown that mitochondrial mRNAs for enzymes involved in energy metabolism are increased in direct proportion to the increase in mitochondrial content in response to training, 23 which allows us to use cytochrome-b mRNA as an indicator of mitochondrial content. When expressed relative to cytochrome-b, UCP3L and UCP3S expression was signi®cantly lower in trained compared to untrained subjects.…”

Section: Discussionmentioning

confidence: 99%

“…In response to training, the expression of mitochondrial mRNAs is increased in direct proportion to total mitochondrial content. 23 All ratios were corrected for the size of the products.…”

Section: Muscle Biopsy and Rna Analysismentioning

confidence: 99%

Skeletal muscle UCP2 and UCP3 expression in trained and untrained male subjects

et al. 1999

View full text Add to dashboard Cite

OBJECTIVE:The new uncoupling proteins, UCP2 and UCP3, are thought to play a role in energy ef®ciency in humans. Endurance training has been suggested to have effects on resting metabolic rate and energy ef®ciency. We therefore determined UCP2 and UCP3 mRNA levels in skeletal muscle of trained and untrained male subjects. METHODS: Using reverse transcription-polymerase chain reaction (RT-PCR), expression of UCP2, UCP3L and UCP3S mRNA were measured in muscle biopsies from the quadriceps femoris in eight trained (23.9 AE 1.6 y; 70.6 AE 3.1 kg; 14 AE 3% body fat; maximal power output (W max ): 5.6 AE 0.4 Wakg; mean AE s.d.) and 10 lean, untrained (22.1 AE 2.9 y; 72.0 AE 7.9 kg; 18 AE 4% body fat; W max : 3.9 AE 0.4 Wakg; mean AE s.d.) subjects. In six of the trained subjects, UCP2 and UCP3 mRNA were measured before and after an exercise bout to exhaustion. To correct for differences in mitochondrial content, levels of UCP2 and UCP3 mRNA were expressed relative to cytochrome-b, a marker of mitochondrial content. RESULTS: Acute exercise had no effect on the expression of UCP3L or UCP3S, but in ®ve out of six subjects UCP2 expression decreased after exercise, although the difference was not statistically signi®cant (P 0.11). Trained subjects had signi®cantly reduced mRNA levels of UCP3L (P 0.028) and UCP3S (P 0.031). VO 2max expressed per kg of fat-free mass was negatively correlated with UCP3L (r 7 0.61, P 0.009) and UCP3S (r 7 0.52, P 0.028). Mechanical ef®ciency correlated negatively with UCP3L (r 7 0.56, P 0.019), UCP3S (r 7 0.47, P 0.048) and tended to correlate with UCP2 (r 7 0.46, P 0.06). CONCLUSION: The lower levels of UCP3 mRNA in trained subjects and the inverse relationship of UCP3 expression and mechanical ef®ciency suggest that exercise training produces an adaptive physiological response in skeletal muscle improving mechanical ef®ciency.

show abstract

“…Last but not least, modifications of protein degradation could also affect the size of the muscle cell's protein complement. Previous research showed that the concentration of nuclear and mitochondrial coded mRNAs was almost double in highly trained endurance runners and in proportion to the mitochondrial content in the vastus lateralis muscle (Puntschart et al, 1995). Pilegaard et al (2003) demonstrated that peroxysome-proliferator-activated receptor-γ coactivator 1 (PGC-1α) transcription and mRNA was transiently elevated after a bout of endurance exercise in humans.…”

Section: Sensing Muscle Stressmentioning

confidence: 99%

Molecular networks in skeletal muscle plasticity

Hoppeler

2016

Journal of Experimental Biology

153

117

View full text Add to dashboard Cite

The skeletal muscle phenotype is subject to considerable malleability depending on use as well as internal and external cues. In humans, low-load endurance-type exercise leads to qualitative changes of muscle tissue characterized by an increase in structures supporting oxygen delivery and consumption, such as capillaries and mitochondria. High-load strength-type exercise leads to growth of muscle fibers dominated by an increase in contractile proteins. In endurance exercise, stress-induced signaling leads to transcriptional upregulation of genes, with Ca 2+ signaling and the energy status of the muscle cells sensed through AMPK being major input determinants. Several interrelated signaling pathways converge on the transcriptional co-activator PGC-1α, perceived to be the coordinator of much of the transcriptional and post-transcriptional processes. Strength training is dominated by a translational upregulation controlled by mTORC1. mTORC1 is mainly regulated by an insulin-and/or growth-factor-dependent signaling cascade as well as mechanical and nutritional cues. Muscle growth is further supported by DNA recruitment through activation and incorporation of satellite cells. In addition, there are several negative regulators of muscle mass. We currently have a good descriptive understanding of the molecular mechanisms controlling the muscle phenotype. The topology of signaling networks seems highly conserved among species, with the signaling outcome being dependent on the particular way individual species make use of the options offered by the multi-nodal networks. As a consequence, muscle structural and functional modifications can be achieved by an almost unlimited combination of inputs and downstream signaling events.

show abstract

mRNAs of enzymes involved in energy metabolism and mtDNA are increased in endurance-trained athletes

Cited by 99 publications

References 6 publications

Impact of Aerobic Exercise Training on Age-Related Changes in Insulin Sensitivity and Muscle Oxidative Capacity

Impact of Aerobic Exercise Training on Age-Related Changes in Insulin Sensitivity and Muscle Oxidative Capacity

Skeletal muscle UCP2 and UCP3 expression in trained and untrained male subjects

Molecular networks in skeletal muscle plasticity

Contact Info

Product

Resources

About