Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans

Abstract

Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training "specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia [fraction of inspired oxygen (Fi(O(2))) = 21% or 13.5%]. Biopsies were taken from the musculus vastus lateralis, and cycle-ergometric incremental maximum oxygen uptake (VO(2max)) exercise tests were performed under normoxia, before and after the 10-wk training program. The main finding was a significant increase (P < 0.05) of fatty acid oxidation capacity per muscle mass, after endurance and strength training under normoxia [2.6- and 2.4-fold for endurance training normoxia group (ET(N)) and strength training normoxia group (ST(N)); n = 8 and 3] and hypoxia [2.0-fold for the endurance training hypoxia group (ET(H)) and strength training hypoxia group (ST(H)); n = 7 and 7], and higher coupling control of oxidative phosphorylation. The enhanced lipid oxidative phosphorylation (OXPHOS) capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P < 0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in muscle mass-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, and octanoylcarnitine). No significant increase was observed in mitochondrial DNA (mtDNA) content. Physiological OXPHOS capacity increased significantly in ET(N) (P < 0.01), with the same trend in ET(H) and ST(H) (P < 0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active lifestyle induced muscular changes of mitochondrial quality representative of mitochondrial health.

Tau protein aggregation is associated with cellular senescence in the brain

“…Two milligram of brain homogenate was loaded into the chamber, and experiments were carried out when oxygen concentration in each well was saturated under atmospheric conditions (~190 nM/ml O 2 ). All reagents and SUIT protocol were described previously (Pesta et al, 2011) with small modifications. Briefly, 1.25 mM ADP was sufficient for saturation in brain homogenate, rotenone was added at a concentration of 1 µM, and FCCP was added in a single injection at a concentration of 0.5 µM.…”

Skeletal muscle mitochondrial density, gene expression, and enzyme activities in human heart failure: minimal effects of the disease and resistance training

“…Recent studies, however, have challenged this notion (44,62). In elderly individuals, in particular, beneficial effects of resistance training on mitochondrial content, enzyme activity, and the expression of genes regulating mitochondrial size and function (23,31,43), as well as improvements in aerobic fitness (15), have been found.…”

Once-weekly muscle endurance and strength training prevents deterioration of muscle oxidative function and attenuates the degree of strength decline during 3-week forearm immobilization

“…Wang et al (2011) reported that resistance exercises, performed after endurance exercises, resulted in enhanced expression of the genes involved in the signalling cascade of mitochondrial biogenesis/oxidative metabolism. Additionally, in sedentary subjects, Pesta et al (2011) reported that the effect of thrice-weekly lower limb strength training on mitochondrial adaptation was similar to that induced by thrice-weekly endurance training using a cycle ergometer. Therefore, there is a possibility that once-weekly strength training with endurance training performed on the same day generates a synergistic effect on mitochondrial adaptation.…”