I think that, in general, more work, heat, kinetic energy equals more fission. Rest, sleep, cold exposure during rest, would promote fusion. I'm thinking it's limiting considering only the effects of the frequency. A FIR sauna induces deep level heat which goes on to push body processes towards fission just at exercise with its heat, acid, and atp depletion does. Of course maybe after an adaptation period sauna no longer does this enough on its own and that's why detox with niacin and sauna became popular -- though ribose and niacinamide seems better and safer.
We're free to believe what we like, of course, whether those beliefs fit demonstrated study facts, or not. But if we aren't willing to adapt / transform our beliefs to fit evidence, what's the point of spending time purporting to be informed, when we're not, on a site like Longecity?
Please stop promoting beliefs you hold that, per available evidence, are false and that you make no effort to back up with evidence. ! . ! . !
2019, Exercise training remodels human skeletal muscle mitochondrial fission and fusion machinery towards a pro-elongation phenotype
AIMS:
Mitochondria exist as a morphologically plastic network driven by cellular bioenergetic demand. Induction of fusion and fission machinery allows the organelle to regulate quality control and substrate flux. Physiological stressors promote fragmentation of the mitochondrial network, a process implicated in the onset of metabolic disease, including type 2 diabetes and obesity. It is well-known that exercise training improves skeletal muscle mitochondrial volume, number, and density. However, the effect of exercise training on muscle mitochondrial dynamics remains unclear.
METHODS:
Ten sedentary adults (65.8 ± 4.6 years; 34.3 ± 2.4 kg/m2 ) underwent 12 weeks of supervised aerobic exercise training (5 day/wk, 85% of HRMAX ). Body composition, cardio-metabolic testing, hyperinsulinaemic-euglycaemic clamps, and skeletal muscle biopsies were performed before and after training. MFN1, MFN2, OPA1, OMA1, FIS1, Parkin, PGC-1α, and HSC70 protein expression was assessed via Western blot.
RESULTS:
Exercise training led to improvements in insulin sensitivity, aerobic capacity, and fat oxidation (all P < 0.01), as well as reductions in body weight, BMI, fat mass and fasting glucose (all P < 0.001). When normalized for changes in mitochondrial content, exercise reduced skeletal muscle FIS1 and Parkin (P < 0.05), while having no significant effect on MFN1, MFN2, OPA1, and OMA1 expression. Exercise also improved the ratio of fusion to fission proteins (P < 0.05), which positively correlated with improvements in glucose disposal (r2 = 0.59, P < 0.05).
CONCLUSIONS:
Exercise training alters the expression of mitochondrial fusion and fission proteins, promoting a more fused, tubular network. These changes may contribute to the improvements in insulin sensitivity and substrate utilization that are observed after exercise training.
2019, Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training
AIM:
Healthy ageing interventions encompass regular exercise to prevent mitochondrial dysfunction, key player in sarcopenia pathogenesis. Mitochondrial biogenesis has been well documented, but mitochondrial remodelling in response to exercise training is poorly understood. Here we investigated fusion, fission and mitophagy before and after an exercise intervention in older adults.
METHODS:
Skeletal muscle biopsies were collected from 22 healthy sedentary men and women before and after 4 months of supervised training. Eight lifelong trained age- and gender-matched volunteers served as positive controls. Transmission electron microscopy was used to estimate mitochondrial content. Western blotting and qRT-PCR were used to detect changes in specific proteins and transcripts.
RESULTS:
After intervention, mitochondrial content increased to levels of controls. While enhancement of fusion was prevalent after intervention, inhibition of fission and increased mitophagy were dominant in controls. Similarly to PARKIN, BCL2L13 content was higher in controls. The observed molecular adaptations paralleled long-term effects of training on physical fitness, exercise efficiency and oxidative capacity.
CONCLUSIONS:
This study describes distinct patterns of molecular adaptations in human skeletal muscle under chronic exercise training. After 16 weeks of exercise, the pattern was dominated by fusion to increase mitochondrial content to the metabolic demands of exercise. In lifelong exercise, the pattern was dominated by mitophagy synchronized with increased fusion and decreased fission, indicating an increased mitochondrial turnover. In addition to these temporally distinct adaptive mechanisms, this study suggests for the first time a specific role of BCL2L13 in chronic exercise that requires constant maintenance of mitochondrial quality.
Edited by HighDesertWizard, 21 May 2019 - 04:20 AM.
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