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- Daussin, Frederic, et al.
(author)
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Training at high exercise intensity promotes qualitative adaptations of mitochondrial function in human skeletal muscle
- 2008
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In: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 104:5, s. 1436-1441
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Journal article (peer-reviewed)abstract
- This study explored mitochondrial capacities to oxidize carbohydrate and fatty acids and functional optimization of mitochondrial respiratory chain complexes in athletes who regularly train at high exercise intensity (ATH, n = 7) compared with sedentary (SED, n = 7). Peak O(2) uptake (Vo(2max)) was measured, and muscle biopsies of vastus lateralis were collected. Maximal O(2) uptake of saponin-skinned myofibers was evaluated with several metabolic substrates [glutamate-malate (V(GM)), pyruvate (V(Pyr)), palmitoyl carnitine (V(PC))], and the activity of the mitochondrial respiratory complexes II and IV were assessed using succinate (V(s)) and N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride (V(TMPD)), respectively. Vo(2max) was higher in ATH than in SED (57.8 +/- 2.2 vs. 31.4 +/- 1.3 ml.min(-1).kg(-1), P < 0.001). V(GM) was higher in ATH than in SED (8.6 +/- 0.5 vs. 3.3 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001). V(Pyr) was higher in ATH than in SED (8.7 +/- 1.0 vs. 5.5 +/- 0.2 micromol O(2).min(-1).g dry wt(-1), P < 0.05), whereas V(PC) was not significantly different (5.3 +/- 0.9 vs. 4.4 +/- 0.5 micromol O(2).min(-1).g dry wt(-1)). V(S) was higher in ATH than in SED (11.0 +/- 0.6 vs. 6.0 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001), as well as V(TMPD) (20.1 +/- 1.0 vs. 16.2 +/- 3.4 micromol O(2).min(-1).g dry wt(-1), P < 0.05). The ratios V(S)/V(GM) (1.3 +/- 0.1 vs. 2.0 +/- 0.1, P < 0.001) and V(TMPD)/V(GM) (2.4 +/- 1.0 vs. 5.2 +/- 1.8, P < 0.01) were lower in ATH than in SED. In conclusion, comparison of ATH vs. SED subjects suggests that regular endurance training at high intensity promotes the enhancement of maximal mitochondrial capacities to oxidize carbohydrate rather than fatty acid and induce specific adaptations of the mitochondrial respiratory chain at the level of complex I.
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- N'Guessan, Benoit, et al.
(author)
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Evaluation of quantitative and qualitative aspects of mitochondrial function in human skeletal and cardiac muscles
- 2004
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In: Molecular and Cellular Biochemistry. - Dordrecht, Netherlands : Kluwer Academic Publishers. - 0300-8177 .- 1573-4919. ; 256-257:1-2, s. 267-80
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Research review (peer-reviewed)abstract
- Techniques and protocols of assessment of mitochondrial properties are of physiological and physiopathological important significance. A precise knowledge of the advantages and limitations of the different protocols used to investigate the mitochondrial function, is therefore necessary. This report presents examples of how the skinned (or permeabilized) fibers technique could be applied for the polarographic determination of the actual quantitative and qualitative aspects of mitochondrial function in human muscle samples. We described and compared the main available respiration protocols in order to sort out which protocol seems more appropriate for the characterization of mitochondrial properties according to the questions under consideration: quantitative determination of oxidative capacities of a given muscle, characterization of the pattern of control of mitochondrial respiration, or assessment of a mitochondrial defect at the level of the respiratory chain complexes. We showed that while protocol A, using only two levels of the phosphate acceptor adenosine diphosphate (ADP) concentration and the adjunction of creatine, could be used for the determination of quantitative changes in very small amount of muscle samples, the ADP sensitivity of mitochondrial respiration was underestimated by this protocol in muscles with high oxidative capacities. The actual apparent Km for ADP and the role of functional activation of miCK in ATP production and energy transfer in oxidative muscles, are well-assessed by protocol B (in the absence of creatine) together with protocol C (in the presence of creatine) that use increasing concentrations of ADP ranging from 2.5-2000 microM. Protocol D is well-adapted to investigate the potential changes at different levels of the respiratory chain, by the use of specific substrates and inhibitors. As can be seen from the present data and the current review of previous reports in the literature, a standardization of the respiration protocols is needed for useful comparisons between studies.
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3. |
- Ponsot, Elodie, 1973-, et al.
(author)
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Exercise training in normobaric hypoxia in endurance runners. II. Improvement of mitochondrial properties in skeletal muscle
- 2006
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In: Journal of applied physiology. - Betsheda, USA : American Physiological Society. - 8750-7587 .- 1522-1601. ; 100:4, s. 1249-57
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Journal article (peer-reviewed)abstract
- This study investigates whether adaptations of mitochondrial function accompany the improvement of endurance performance capacity observed in well-trained athletes after an intermittent hypoxic training program. Fifteen endurance-trained athletes performed two weekly training sessions on treadmill at the velocity associated with the second ventilatory threshold (VT2) with inspired O2 fraction = 14.5% [hypoxic group (Hyp), n = 8] or with inspired O2 fraction = 21% [normoxic group (Nor), n = 7], integrated into their usual training, for 6 wk. Before and after training, oxygen uptake (VO2) and speed at VT2, maximal VO2 (VO2 max), and time to exhaustion at velocity of VO2 max (minimal speed associated with VO2 max) were measured, and muscle biopsies of vastus lateralis were harvested. Muscle oxidative capacities and sensitivity of mitochondrial respiration to ADP (Km) were evaluated on permeabilized muscle fibers. Time to exhaustion, VO2 at VT2, and VO2 max were significantly improved in Hyp (+42, +8, and +5%, respectively) but not in Nor. No increase in muscle oxidative capacity was obtained with either training protocol. However, mitochondrial regulation shifted to a more oxidative profile in Hyp only as shown by the increased Km for ADP (Nor: before 476 +/- 63, after 524 +/- 62 microM, not significant; Hyp: before 441 +/- 59, after 694 +/- 51 microM, P < 0.05). Thus including hypoxia sessions into the usual training of athletes qualitatively ameliorates mitochondrial function by increasing the respiratory control by creatine, providing a tighter integration between ATP demand and supply.
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4. |
- Ponsot, Elodie, 1973-, et al.
(author)
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Impairment of maximal aerobic power with moderate hypoxia in endurance athletes : do skeletal muscle mitochondria play a role?
- 2010
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In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 298:3, s. R558-R566
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Journal article (peer-reviewed)abstract
- This study investigates the role of central vs. peripheral factors in the limitation of maximal oxygen uptake ((V) over dot O-2max) with moderate hypoxia [inspired fraction (FIO2) = 14.5%]. Fifteen endurance-trained athletes performed maximal cycle incremental tests to assess (V) over dotO(2max), maximal cardiac output ((Q) over dot(max)), and maximal arteriovenous oxygen (a-vO(2)) difference in normoxia and hypoxia. Muscle biopsies of vastus lateralis were taken 1 wk before the cycling tests to evaluate maximal muscle oxidative capacity ((V) over dot(max)) and sensitivity of mitochondrial respiration to ADP (K-m) on permeabilized muscle fibers in situ. Those athletes exhibiting the largest reduction of (V) over dotO(2max) in moderate hypoxia (Severe Loss group: -18 +/- 2%) suffered from significant reductions in Q(max) (-4 +/- 1%) and maximal a-vO(2) difference (-14 +/- 2%). Athletes who well tolerated hypoxia, as attested by a significantly smaller drop of (V) over dotO(2max) with hypoxia (Moderate Loss group: -7 +/- 1%), also display a blunted (Q) over dot(max) (-9 +/- 2%) but, conversely, were able to maintain maximal a-vO(2) difference (+1 +/- 2%). Though (V) over dot(max) was similar in the two experimental groups, the smallest reduction of (V) over dotO(2max) with moderate hypoxia was observed in those athletes presenting the lowest apparent Km for ADP in the presence of creatine (K-m (+) (Cr)). In already-trained athletes with high muscular oxidative capacities, the qualitative, rather than quantitative, aspects of the mitochondrial function may constitute a limiting factor to aerobic ATP turnover when exercising at low FIO2, presumably through the functional coupling between the mitochondrial creatine kinase and ATP production. This study suggests a potential role for peripheral factors, including the alteration of cellular homeostasis in active muscles, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.
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5. |
- Zoll, Joffrey, et al.
(author)
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Exercise training in normobaric hypoxia in endurance runners. III. Muscular adjustments of selected gene transcripts
- 2006
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In: Journal of applied physiology. - Bethesda, USA : American Physiological Society. - 8750-7587 .- 1522-1601. ; 100:4, s. 1258-66
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Journal article (peer-reviewed)abstract
- We hypothesized that specific muscular transcript level adaptations participate in the improvement of endurance performances following intermittent hypoxia training in endurance-trained subjects. Fifteen male high-level, long-distance runners integrated a modified living low-training high program comprising two weekly controlled training sessions performed at the second ventilatory threshold for 6 wk into their normal training schedule. The athletes were randomly assigned to either a normoxic (Nor) (inspired O2 fraction = 20.9%, n = 6) or a hypoxic group exercising under normobaric hypoxia (Hyp) (inspired O2 fraction = 14.5%, n = 9). Oxygen uptake and speed at second ventilatory threshold, maximal oxygen uptake (VO2 max), and time to exhaustion (Tlim) at constant load at VO2 max velocity in normoxia and muscular levels of selected mRNAs in biopsies were determined before and after training. VO2 max (+5%) and Tlim (+35%) increased specifically in the Hyp group. At the molecular level, mRNA concentrations of the hypoxia-inducible factor 1alpha (+104%), glucose transporter-4 (+32%), phosphofructokinase (+32%), peroxisome proliferator-activated receptor gamma coactivator 1alpha (+60%), citrate synthase (+28%), cytochrome oxidase 1 (+74%) and 4 (+36%), carbonic anhydrase-3 (+74%), and manganese superoxide dismutase (+44%) were significantly augmented in muscle after exercise training in Hyp only. Significant correlations were noted between muscular mRNA levels of monocarboxylate transporter-1, carbonic anhydrase-3, glucose transporter-4, and Tlim only in the group of athletes who trained in hypoxia (P < 0.05). Accordingly, the addition of short hypoxic stress to the regular endurance training protocol induces transcriptional adaptations in skeletal muscle of athletic subjects. Expressional adaptations involving redox regulation and glucose uptake are being recognized as a potential molecular pathway, resulting in improved endurance performance in hypoxia-trained subjects.
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