Wohlwend 2014 Abstract MiP2014

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Exercise modality specific mitochondrial adaptations in skeletal muscle of elderly people.
Link:
Wohlwend M
Mitochondr Physiol Network 19.13 - MiP2014

Wohlwend M, Andeaes K, Shahab A, Moreira JB, Hassel E, Bye A, Rognmo O (2014)

Event: MiP2014

In aged subjects, mitochondrial function is impaired, characterized by diminished oxidative capacity, reduced oxidative phosphorylation [1] and mitochondrial uncoupling [2]. Exercise training has previously been indicated to increase mitochondrial content in untrained [3] and elderly subjects [4]. Despite the consensus in the literature: that high intensity training (HIT) is superior to moderate intensity training (MIT) with regards to health effects [5], it is unclear how these training modalities affect mitochondrial function, particularly in elderly people.

To address this issue, subjects (N=20), aged between 70-75 y were randomized to eight weeks, three times a week, supervised, isocalorically matched sessions of either HIT, consisting of 4x4 intervals at 90% HRmax with 3 min active breaks in between, MIT, consisting of 50 min continuous running on 70% HRmax, or a control group that remained sedentary. Muscle biopsies were taken from the vastus lateralis before and after the intervention and high-resolution respirometry in saponin permeabilized muscle fibers was performed. Addition of various substrates and inhibitors allowed evaluation of TCA cycle and electron transfer-pathway function.

Results indicated that combined Complex I- and Complex II-linked oxidative phosphorylation capacity (CI&II) increased after both MIT and HIT (P<0.05). Complex I-linked oxidative phosphorylation (CI) increased only after HIT (P<0.05) and this coincided with a relative increase of CI/CI&II (P<0.05), suggesting qualitative improvements within CI, independent of mitochondrial density. HIT also improved mitochondrial coupling efficiency during fatty acid oxidation (P<0.05). There were no changes in mitochondrial function in the control group.

The findings of the current study show that both MIT and HIT improve CI+II-linked oxidative phosphorylation in elderly people. However, mitochondria seem to adapt differently to the respective training modalities. While MIT gains seemed to rely on mitochondrial density, HIT seemed to additionally improve mitochondrial quality.


O2k-Network Lab: NO Trondheim Rognmo O


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style  Pathology: Aging;senescence 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized cells 


Coupling state: OXPHOS  Pathway: N, NS  HRR: Oxygraph-2k  Event: A3, Oral  MiP2014 

Affiliation

KG Jebsen Center Exercise Medicine, Dep Circulation Medical Imaging, Norwegian Univ Sc Tech, Trondheim, Norway. – martin.wohlwend@ntnu.no

References

  1. Chistiakov DA, Sobenin IA, Revin VV, Orekhov AN, Bobryshev YV (2014) Mitochondrial aging and age-related dysfunction of mitochondria. Biomed Res Int doi: 10.1155/238463.
  2. Conley KE, Jubrias SA, Cress ME, Esselman P (2013) Exercise efficiency is reduced by mitochondrial uncoupling in the elderly. Exp Physiol 98: 768-77.
  3. Jacobs RA, Flück D, Bonne TC, Bürgi S, Christensen PM, Toigo M, Lundby C (2013) Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function. J Appl Physiol 115: 785-93.
  4. Broskey NT, Greggio C, Boss A, Boutant M, Dwyer A, Schlueter L, Hans D, Gremion G, Kreis R, Boesch C, Canto C, Amati F (2014) Skeletal muscle mitochondria in the elderly: effects of physical fitness and exercise training. J Clin Endocrinol Metab 99: 1852-61.
  5. Wen CP, Wai JPM, Tsai MK, Yang YC, Cheng TYD, Lee M-C, Chan HT, Tsao CK, Tsai SP, Wu X (2011) Minimum amount of physical activity for reduced mortality and extended life expectancy: a prospective cohort study. Lancet 378: 1244-53.