scholarly journals Aerobic Metabolic Adaptations in Endurance Eccentric Exercise and Training: From Whole Body to Mitochondria

2021 ◽  
Vol 11 ◽  
Author(s):  
Julianne Touron ◽  
Frédéric Costes ◽  
Emmanuel Coudeyre ◽  
Hélène Perrault ◽  
Ruddy Richard

A characteristic feature of eccentric as compared with concentric exercise is the ability to generate greater mechanical loads for lower cardiopulmonary demands. Current evidence concurs to show that eccentric training translates into considerable gains in muscle mass and strength. Less is known, however, regarding its impact on oxygen transport and on factors to be considered for optimizing its prescription and monitoring. This article reviews the existing evidence for endurance eccentric exercise effects on the components of the oxygen transport system from systemic to mitochondria in both humans and animals. In the studies reviewed, specially designed cycle-ergometers or downhill treadmill running were used to generate eccentric contractions. Observations to date indicate that overall, the aerobic demand associated with the eccentric training load was too low to significantly increase peak maximal oxygen consumption. By extension, it can be inferred that the very high eccentric power output that would have been required to solicit a metabolic demand sufficient to enhance peak aerobic power could not be tolerated or sustained by participants. The impact of endurance eccentric training on peripheral flow distribution remains largely undocumented. Given the high damage susceptibility of eccentric exercise, the extent to which skeletal muscle oxygen utilization adaptations would be seen depends on the balance of adverse and positive signals on mitochondrial integrity. The article examines the protection provided by repeated bouts of acute eccentric exercise and reports on the impact of eccentric cycling and downhill running training programs on markers of mitochondrial function and of mitochondrial biogenesis using mostly from animal studies. The summary of findings does not reveal an impact of training on skeletal muscle mitochondrial respiration nor on selected mitochondrial messenger RNA transcripts. The implications of observations to date are discussed within future perspectives for advancing research on endurance eccentric exercise physiological impacts and using a combined eccentric and concentric exercise approach to optimize functional capacity.

2013 ◽  
Vol 38 (4) ◽  
pp. 401-409 ◽  
Author(s):  
José Magalhães ◽  
Marta Fraga ◽  
José Lumini-Oliveira ◽  
Inês Gonçalves ◽  
Manoel Costa ◽  
...  

Eccentric exercise (EE) is known to induce damage and dysfunction in skeletal muscle. However, the possible role of mitochondrial (dys)function, including the vulnerability to mitochondrial permeability transition pore (MPTP) opening, is unclear. Therefore, this study aimed to analyze the impact of a single acute bout of downhill running on skeletal muscle mitochondrial function. Thirty 12-week-old Charles River CD1 male mice were randomly assigned into control (C) or exercised groups. EE consisted of 120 min of downhill treadmill running at a –16° gradient. Exercised animals were sacrificed immediately (Ecc0h) and 48 h (Ecc48h) after the end of the running bout. Plasma and skeletal muscles were then obtained. Muscle mitochondrial function, including oxygen consumption prior to and after anoxia and reoxygenation, membrane potential, and MPTP opening, were evaluated. Respiratory chain complexI, II, and V activities were determined. EE significantly increased plasma creatine kinase activity (119.4 ± 5.6 vs. 1061.3 ± 46.3 vs. 256.8 ± 15.3 U·L–1, C, Ecc0h and Ecc48h, respectively) and myoglobin and interleukin-6 content. Impaired state 3 and respiratory control ratio (8.4 ± 0.4 vs. 5.6 ± 0.9 vs. 8.4 ± 0.5, C, Ecc0h and Ecc48h, respectively), as well as increased susceptibility to MPTP opening, seen by cyclosporin A-sensitive high swelling amplitude, lower time to maximal swelling velocity (313.8 ± 17.7 vs. 244.5 ± 19.4 vs. 298.5 ± 8.7 s, C, Ecc0h and Ecc48h, respectively), and calcium release immediately after the end of exercise (C vs. Ecc0h) were observed. EE induced a transient impairment in the activity of complex V (C vs. Ecc0h). No significant changes from the C group were observed 48 h after the end of EE (C vs. Ecc48h) in any analyzed parameters. In conclusion, prolonged EE transiently impaired mice skeletal muscle mitochondrial function and increased susceptibility to calcium-induced MPTP opening.


Author(s):  
Cécile Bétry ◽  
Aline V. Nixon ◽  
Paul L. Greenhaff ◽  
Elizabeth J. Simpson

Abstract Introduction Skeletal muscle is a major site for whole-body glucose disposal, and determination of skeletal muscle glucose uptake is an important metabolic measurement, particularly in research focussed on interventions that impact muscle insulin sensitivity. Calculating arterial-venous difference in blood glucose can be used as an indirect measure for assessing glucose uptake. However, the possibility of multiple tissues contributing to the composition of venous blood, and the differential in glucose uptake kinetics between tissue types, suggests that sampling from different vein sites could influence the estimation of glucose uptake. This study aimed to determine the impact of venous cannula position on calculated forearm glucose uptake following an oral glucose challenge in resting and post-exercise states. Materials and Methods In 9 young, lean, males, the impact of sampling blood from two antecubital vein positions; the perforating vein (‘perforating’ visit) and, at the bifurcation of superficial and perforating veins (‘bifurcation’ visit), was assessed. Brachial artery blood flow and arterialised-venous and venous blood glucose concentrations were measured in 3 physiological states; resting-fasted, resting-fed, and fed following intermittent forearm muscle contraction (fed-exercise). Results Following glucose ingestion, forearm glucose uptake area under the curve was greater for the ‘perforating’ than for the ‘bifurcation’ visit in the resting-fed (5.92±1.56 vs. 3.69±1.35 mmol/60 min, P<0.01) and fed-exercise (17.38±7.73 vs. 11.40±7.31 mmol/75 min, P<0.05) states. Discussion Antecubital vein cannula position impacts calculated postprandial forearm glucose uptake. These findings have implications for longitudinal intervention studies where serial determination of forearm glucose uptake is required.


2003 ◽  
Vol 285 (6) ◽  
pp. H2382-H2391 ◽  
Author(s):  
B. J. McGuire ◽  
T. W. Secomb

A previously developed Krogh-type theoretical model was used to estimate capillary density in human skeletal muscle based on published measurements of oxygen consumption, arterial partial pressure of oxygen, and blood flow during maximal exercise. The model assumes that oxygen consumption in maximal exercise is limited by the ability of capillaries to deliver oxygen to tissue and is therefore strongly dependent on capillary density, defined as the number of capillaries per unit cross-sectional area of muscle. Based on an analysis of oxygen transport processes occurring at the microvascular level, the model allows estimation of the minimum number of straight, evenly spaced capillaries required to achieve a given oxygen consumption rate. Estimated capillary density values were determined from measurements of maximal oxygen consumption during knee extensor exercise and during whole body cycling, and they range from 459 to 1,468 capillaries/mm2. Measured capillary densities, obtained with either histochemical staining techniques or electron microscopy on quadriceps muscle biopsies from healthy subjects, are generally lower, ranging from 123 to 515 capillaries/mm2. This discrepancy is partly accounted for by the fact that capillary density decreases with muscle contraction and muscle biopsy samples typically are strongly contracted. The results imply that estimates of maximal oxygen transport rates based on capillary density values obtained from biopsy samples do not fully reflect the oxygen transport capacity of the capillaries in skeletal muscle.


1983 ◽  
Vol 61 (2) ◽  
pp. 178-182 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius–plantaris muscle group was isolated. Cardiac output [Formula: see text], muscle blood flow [Formula: see text], total body and muscle oxygen uptake [Formula: see text] were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle [Formula: see text], [Formula: see text], and [Formula: see text] were increased in both groups at 30 min of anemia. By 60 min, [Formula: see text] and [Formula: see text] declined to preanemic control values in the moderate anemia group; whole body [Formula: see text] was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle [Formula: see text] showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle [Formula: see text] during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle [Formula: see text] response was related to the decrease in arterial oxygen transport.


2021 ◽  
Vol 12 ◽  
Author(s):  
Gagandeep Mann ◽  
Stephen Mora ◽  
Glory Madu ◽  
Olasunkanmi A. J. Adegoke

Branched-chain amino acids (BCAAs) are critical for skeletal muscle and whole-body anabolism and energy homeostasis. They also serve as signaling molecules, for example, being able to activate mammalian/mechanistic target of rapamycin complex 1 (mTORC1). This has implication for macronutrient metabolism. However, elevated circulating levels of BCAAs and of their ketoacids as well as impaired catabolism of these amino acids (AAs) are implicated in the development of insulin resistance and its sequelae, including type 2 diabetes, cardiovascular disease, and of some cancers, although other studies indicate supplements of these AAs may help in the management of some chronic diseases. Here, we first reviewed the catabolism of these AAs especially in skeletal muscle as this tissue contributes the most to whole body disposal of the BCAA. We then reviewed emerging mechanisms of control of enzymes involved in regulating BCAA catabolism. Such mechanisms include regulation of their abundance by microRNA and by post translational modifications such as phosphorylation, acetylation, and ubiquitination. We also reviewed implications of impaired metabolism of BCAA for muscle and whole-body metabolism. We comment on outstanding questions in the regulation of catabolism of these AAs, including regulation of the abundance and post-transcriptional/post-translational modification of enzymes that regulate BCAA catabolism, as well the impact of circadian rhythm, age and mTORC1 on these enzymes. Answers to such questions may facilitate emergence of treatment/management options that can help patients suffering from chronic diseases linked to impaired metabolism of the BCAAs.


1987 ◽  
Vol 63 (1) ◽  
pp. 257-261 ◽  
Author(s):  
G. D. Cartee ◽  
R. P. Farrar

Old rats have a decreased hindlimb muscle respiratory capacity and whole-body maximal O2 consumption (VO2 max). The decline in spontaneous physical activity in old rats might contribute to these age-related changes. The magnitude of the age-related decline is not uniform in all skeletal muscle respiratory enzymes, and the decrease in palmitate oxidation is particularly great. This study was designed to determine if young and old rats subjected to the same exercise-training protocol would attain similar values for VO2 max and several markers of muscle respiratory capacity. Four- and 18-mo-old Fischer 344 rats underwent an identical 6-mo program of treadmill running. After training, both age groups had increased VO2 max above sedentary age-matched controls. However, the old trained rats had a lower VO2 max than identically trained young rats. In contrast to VO2 max, the two trained groups attained similar values for gastrocnemius citrate synthase, cytochrome oxidase, 3-hydroxyacyl-CoA dehydrogenase, palmitate oxidation, and total carnitine concentration. Thus, when the young and old rats performed an identical exercise protocol within the capacity of the old animals, differences in skeletal muscle respiratory capacity were eliminated. The dissimilarity in VO2 max between the identically trained groups was apparently caused by age-related differences in factors other than muscle respiratory capacity.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 656-656
Author(s):  
Amadeo Salvador ◽  
Colleen McKenna ◽  
Andrew Askow ◽  
Hsin-Yu Fang ◽  
Sarah Burke ◽  
...  

Abstract Objectives Yes-Associated Protein (YAP) is implicated as a regulator of the post-exercise skeletal muscle response through mechanical transduction. We recently observed that resistance exercise (RE) increased both total (t) and phosphorylated (p) muscle YAP content, which correlated with extracellular signal-regulated kinase 1/2 (Erk1/2). Other anabolic signaling pathways (i.e., mTORC1) are known to be potentiated by the combined stimuli of RE and protein ingestion during post-exercise recovery. However, the impact of protein ingestion on t- and p-muscle YAP content during recovery from RE is unknown. Therefore, we aimed to determine the nutrient sensitivity of YAP in both an acute and chronic exercise setting in aging skeletal muscle. Methods Acute study: 13 untrained older women (59.8 ± 0.5 y) were randomized to perform an acute bout of unilateral RE (3 sets × 12 repetitions at 65% of one repetition maximum) followed by the ingestion of whey protein (0.3 g/kg lean body mass) or water. Muscle biopsies of both the rested and exercised legs were collected before and during the postprandial period. Chronic study: 20 untrained middle-aged men and women (47.5 ± 0.3 y) performed 3 weeks of whole body RE (3 d/wk) with moderate or high protein intake set at 1.2 g/kg/d or 1.6 g/kg/d, respectively. Muscle biopsies were taken weekly in the rested state. Total and phosphorylated YAPSer127 and Erk1/2Thr202/Tyr204 were examined by western blotting. Results Acute study: Protein ingestion decreased t- and p-YAP compared to the water condition in the non-exercised leg (main effect: P &lt; 0.04). There was no change in t- or p-YAP, regardless of condition, in the exercised-leg throughout recovery (P = 0.88). There was no change in p/t ratio of Erk1/2 in the exercised or non-exercised leg.  Chronic study: There was no change in either p- or t-YAP in moderate and high protein conditions throughout training (both, P &gt; 0.05). There was a decrease in t-Erk1/2 irrespective of condition (P = 0.04). There was no change in p/t ratio of Erk1/2 throughout training. There was a significant correlation between t-Erk1/2 and t-YAP (r = 0.741 and P &lt; 0.001). Conclusions Protein ingestion mediated an acute down-regulation of YAP in the postprandial-state. However, resistance training did not modulate YAP content in aged skeletal muscle tissue. Funding Sources Funded by Beef Checkoff. AFS is supported by CAPES-Brazil.


2017 ◽  
Vol 42 (3) ◽  
pp. 319-325 ◽  
Author(s):  
Roksana B. Zak ◽  
Robert J. Shute ◽  
Matthew W.S. Heesch ◽  
D. Taylor La Salle ◽  
Matthew P. Bubak ◽  
...  

Many human diseases lead to a loss of skeletal muscle metabolic function and mass. Local and environmental temperature can modulate the exercise-stimulated response of several genes involved in mitochondrial biogenesis and skeletal muscle function in a human model. However, the impact of environmental temperature, independent of exercise, has not been addressed in a human model. Thus, the purpose of this study was to compare the effects of exposure to hot, cold, and room temperature conditions on skeletal muscle gene expression related to mitochondrial biogenesis and muscle mass. Recreationally trained male subjects (n = 12) had muscle biopsies taken from the vastus lateralis before and after 3 h of exposure to hot (33 °C), cold (7 °C), or room temperature (20 °C) conditions. Temperature had no effect on most of the genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Core temperature was significantly higher in hot and cold environments compared with room temperature (37.2 ± 0.1 °C, p = 0.001; 37.1 ± 0.1 °C, p = 0.013; 36.9 ± 0.1 °C, respectively). Whole-body oxygen consumption was also significantly higher in hot and cold compared with room temperature (0.38 ± 0.01 L·min−1, p < 0.001; 0.52 ± 0.03 L·min−1, p < 0.001; 0.35 ± 0.01 L·min−1, respectively). In conclusion, these data show that acute temperature exposure alone does not elicit significant changes in skeletal muscle gene expression. When considered in conjunction with previous research, exercise appears to be a necessary component to observe gene expression alterations between different environmental temperatures in humans.


1984 ◽  
Vol 223 (3) ◽  
pp. 815-821 ◽  
Author(s):  
A J M Wagenmakers ◽  
J T G Schepens ◽  
J H Veerkamp

Starvation does not change the actual activity per g of tissue of the branched-chain 2-oxo acid dehydrogenase in skeletal muscles, but affects the total activity to a different extent, depending on the muscle type. The activity state (proportion of the enzyme present in the active state) does not change in diaphragm and decreases in quadriceps muscle. Liver and kidney show an increase of both activities, without a change of the activity state. In heart and brain no changes were observed. Related to organ wet weights, the actual activity present in the whole-body muscle mass decreases on starvation, whereas the activities present in liver and kidney do not change, or increase slightly. Exercise (treadmill-running) of untrained rats for 15 and 60 min causes a small increase of the actual activity and the activity state of the branched-chain 2-oxo acid dehydrogenase complex in heart and skeletal muscle. Exercise for 1 h, furthermore, increased the actual and the total activity in liver and kidney, without a change of the activity state. In brain no changes were observed. The actual activity per g of tissue in skeletal muscle was less than 2% of that in liver and kidney, both before and after exercise and starvation. Our data indicate that the degradation of branched-chain 2-oxo acids predominantly occurs in liver and to a smaller extent in kidney and skeletal muscle in fed, starved and exercised rats.


2018 ◽  
Vol 62 (1) ◽  
pp. 81-90 ◽  
Author(s):  
Mateusz Radojewski ◽  
Tomasz Podgórski ◽  
Barbara Pospieszna ◽  
Jakub Kryściak ◽  
Ewa Śliwicka ◽  
...  

Abstract The aim of the study was to evaluate the impact of the competitive phase on physiological and metabolic indices and selected markers of skeletal muscle damage in male volleyball players. The study group consisted of 24 young male volleyball players. During the study, participants underwent two series of measurements, before and after the competitive phase of the annual training cycle. In both study terms, players performed an incremental treadmill running test to determine their ventilatory threshold and maximal oxygen uptake. Venous and capillary blood samples were taken for biochemical analysis. There was no significant difference in the physical fitness level, values of biochemical variables and the level of antioxidant status in the surveyed athletes between the two study terms. Significant changes within skeletal muscle damage markers were observed between the beginning and the end of the competitive period: an increase in the concentration of cellular DNA damage products (8-hydroxy-2′-deoxyguanosine; p < 0.0001) and a decrease in muscle activity of creatine kinase (p<0.05). In spite of the increment in cell damage markers, the unaffected level of physiological and biochemical markers may indicate that the experienced cell destruction did not negatively affect the level of physical fitness. When designing the annual training plan, coaches and athletes need to take into consideration that temporary physiological states – oxidative stress and inflammation – may be required to attain training adaptation.


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