scholarly journals Endurance Is Improved in Female Rats After Living High-Training High Despite Alterations in Skeletal Muscle

2021 ◽  
Vol 3 ◽  
Author(s):  
Alexandra Malgoyre ◽  
Alexandre Prola ◽  
Adelie Meunier ◽  
Rachel Chapot ◽  
Bernard Serrurier ◽  
...  

Altitude camps are used during the preparation of endurance athletes to improve performance based on the stimulation of erythropoiesis by living at high altitude. In addition to such whole-body adaptations, studies have suggested that high-altitude training increases mitochondrial mass, but this has been challenged by later studies. Here, we hypothesized that living and training at high altitude (LHTH) improves mitochondrial efficiency and/or substrate utilization. Female rats were exposed and trained in hypoxia (simulated 3,200 m) for 5 weeks (LHTH) and compared to sedentary rats living in hypoxia (LH) or normoxia (LL) or those that trained in normoxia (LLTL). Maximal aerobic velocity (MAV) improved with training, independently of hypoxia, whereas the time to exhaustion, performed at 65% of MAV, increased both with training (P = 0.009) and hypoxia (P = 0.015), with an additive effect of the two conditions. The distance run was 7.98 ± 0.57 km in LHTH vs. 6.94 ± 0.51 in LLTL (+15%, ns). The hematocrit increased >20% with hypoxia (P < 0.001). The increases in mitochondrial mass and maximal oxidative capacity with endurance training were blunted by combination with hypoxia (−30% for citrate synthase, P < 0.01, and −23% for Vmax glut−succ, P < 0.001 between LHTH and LLTL). A similar reduction between the LHTH and LLTL groups was found for maximal respiration with pyruvate (−29%, P < 0.001), for acceptor-control ratio (−36%, hypoxia effect, P < 0.001), and for creatine kinase efficiency (−48%, P < 0.01). 3-hydroxyl acyl coenzyme A dehydrogenase was not altered by hypoxia, whereas maximal respiration with Palmitoyl-CoA specifically decreased. Overall, our results show that mitochondrial adaptations are not involved in the improvement of submaximal aerobic performance after LHTH, suggesting that the benefits of altitude camps in females relies essentially on other factors, such as the transitory elevation of hematocrit, and should be planned a few weeks before competition and not several months.

2010 ◽  
Vol 299 (2) ◽  
pp. E225-E233 ◽  
Author(s):  
David J. Bishop ◽  
Claire Thomas ◽  
Tom Moore-Morris ◽  
Michail Tonkonogi ◽  
Kent Sahlin ◽  
...  

We tested the hypothesis that reducing hydrogen ion accumulation during training would result in greater improvements in muscle oxidative capacity and time to exhaustion (TTE). Male Wistar rats were randomly assigned to one of three groups (CON, PLA, and BIC). CON served as a sedentary control, whereas PLA ingested water and BIC ingested sodium bicarbonate 30 min prior to every training session. Training consisted of seven to twelve 2-min intervals performed five times/wk for 5 wk. Following training, TTE was significantly greater in BIC (81.2 ± 24.7 min) compared with PLA (53.5 ± 30.4 min), and TTE for both groups was greater than CON (6.5 ± 2.5 min). Fiber respiration was determined in the soleus (SOL) and extensor digitorum longus (EDL), with either pyruvate (Pyr) or palmitoyl carnitine (PC) as substrates. Compared with CON (14.3 ± 2.6 nmol O2·min−1·mg dry wt−1), there was a significantly greater SOL-Pyr state 3 respiration in both PLA (19.6 ± 3.0 nmol O2·min−1·mg dry wt−1) and BIC (24.4 ± 2.8 nmol O2·min−1·mg dry wt−1), with a significantly greater value in BIC. However, state 3 respiration was significantly lower in the EDL from both trained groups compared with CON. These differences remained significant in the SOL, but not the EDL, when respiration was corrected for citrate synthase activity (an indicator of mitochondrial mass). These novel findings suggest that reducing muscle hydrogen ion accumulation during running training is associated with greater improvements in both mitochondrial mass and mitochondrial respiration in the soleus.


1989 ◽  
Vol 256 (4) ◽  
pp. H1110-H1116 ◽  
Author(s):  
D. C. Poole ◽  
O. Mathieu-Costello ◽  
J. B. West

The total capillary length available for blood-tissue transfer is determined by the number and orientation of the capillaries. Therefore, whether capillary tortuosity changes with exercise training has important implications for peripheral gas exchange. To determine the effects of exercise training on capillary orientation and capillary length per volume of muscle fiber [Jv(c,f)] female rats were trained by treadmill running (30 m/min, up to 60 min/day, 5 days/wk) for 4 wk. Muscles from control and trained rats were perfusion fixed at sarcomere lengths (l) ranging from 1.59 to 2.15 microns, and morphometric techniques were used to estimate capillary orientation and Jv(c,f). Training increased (P less than 0.05) musculus soleus oxidative capacity 35% [as estimated from citrate synthase activity: 24.7 +/- 1.4 to 34.7 +/- 1.0 (SE) mumol.g-1.min-1], capillary-to-fiber ratio 30% (2.17 +/- 0.06 to 2.83 +/- 0.05), and Jv(c,f) 32% (1,886 +/- 73 to 2,496 +/- 180 mm-2). Capillary tortuosity (as determined from comparisons of transverse and longitudinal sections) was a direct function of l in control and trained rats and contributed 17-73% of capillary length above that estimated from capillary counts on transverse sections. We conclude that capillary tortuosity in m. soleus is unchanged by training. Therefore, Jv(c,f) increases as a consequence of increased capillary number. M. soleus citrate synthase activity is best correlated with Jv(c,f) and not with capillary counts on transverse sections. We hypothesize that training-induced muscle changes of capillary geometry improve O2 delivery to skeletal muscle and may therefore alter the metabolic response (e.g., lactate accumulation) to exercise after training.(ABSTRACT TRUNCATED AT 250 WORDS)


2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 284
Author(s):  
Brady D. Andersen ◽  
Daniel E. Turk ◽  
Robert W. Gotshall ◽  
Matthew S. Hickey ◽  
Richard G. Israel ◽  
...  

2007 ◽  
Vol 102 (1) ◽  
pp. 412-416 ◽  
Author(s):  
S. A. Hahn ◽  
L. F. Ferreira ◽  
J. B. Williams ◽  
K. P. Jansson ◽  
B. J. Behnke ◽  
...  

There are currently no models of exercise that recruit and train muscles, such as the rat spinotrapezius, that are suitable for transmission intravital microscopic investigation of the microcirculation. Recent experimental evidence supports the concept that running downhill on a motorized treadmill recruits the spinotrapezius muscle of the rat. Based on these results, we tested the hypothesis that 6 wk of downhill running (−14° grade) for 1 h/day, 5 days/wk, at a speed of up to 35 m/min, would 1) increase whole body peak oxygen uptake (V̇o2 peak), 2) increase spinotrapezius citrate synthase activity, and 3) reduce the fatigability of the spinotrapezius during electrically induced 1-Hz submaximal tetanic contractions. Trained rats ( n = 6) elicited a 24% higher V̇o2 peak (in ml·min−1·kg−1: sedentary 58.5 ± 2.0, trained 72.7 ± 2.0; P < 0.001) and a 41% greater spinotrapezius citrate synthase activity (in μmol·min−1·g−1: sedentary 14.1 ± 0.7, trained 19.9 ± 0.9; P < 0.001) compared with sedentary controls ( n = 6). In addition, at the end of 15 min of electrical stimulation, trained rats sustained a greater percentage of the initial tension than their sedentary counterparts (control 34.3 ± 3.1%, trained 59.0 ± 7.2%; P < 0.05). These results demonstrate that downhill running is successful in promoting training adaptations in the spinotrapezius muscle, including increased oxidative capacity and resistance to fatigue. Since the spinotrapezius muscle is commonly used in studies using intravital microscopy to examine microcirculatory function at rest and during contractions, our results suggest that downhill running is an effective training paradigm that can be used to investigate the mechanisms for improved microcirculatory function following exercise training in health and disease.


2003 ◽  
Vol 88 (11) ◽  
pp. 5444-5451 ◽  
Author(s):  
Clinton R. Bruce ◽  
Mitchell J. Anderson ◽  
Andrew L. Carey ◽  
David G. Newman ◽  
Arend Bonen ◽  
...  

Abstract We determined whole-body insulin sensitivity, long-chain fatty acyl coenzyme A (LCACoA) content, skeletal muscle triglyceride (TGm) concentration, fatty acid transporter protein content, and oxidative enzyme activity in eight patients with type 2 diabetes (TYPE 2); six healthy control subjects matched for age (OLD), body mass index, percentage of body fat, and maximum pulmonary O2 uptake; nine well-trained athletes (TRAINED); and four age-matched controls (YOUNG). Muscle biopsies from the vastus lateralis were taken before and after a 2-h euglycemic-hyperinsulinemic clamp. Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TGm were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P &lt; 0.05) than in OLD, YOUNG, and TRAINED. TGm was elevated in TYPE 2 compared with all other groups (P &lt; 0.05). However, both basal and insulin-stimulated skeletal muscle LCACoA content were similar. Basal citrate synthase activity was higher in TRAINED (P &lt; 0.01), whereas β-hydroxyacyl CoA dehydrogenase activity was higher in TRAINED compared with TYPE 2 and OLD. There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r = 0.71, P &lt; 0.001; β-hydroxyacyl CoA dehydrogenase, r = 0.61, P = 0.001). No differences were found in FAT/CD36 protein content between groups. In contrast, FABPpm protein was lower in OLD compared with TYPE 2 and YOUNG (P &lt; 0.05). In conclusion, despite markedly elevated skeletal muscle TGm in type 2 diabetic patients and strikingly different levels of whole-body glucose disposal, both basal and insulin-stimulated LCACoA content were similar across groups. Furthermore, skeletal muscle oxidative capacity was a better predictor of insulin sensitivity than either TGm concentration or long-chain fatty acyl CoA content.


2009 ◽  
Vol 107 (1) ◽  
pp. 346-353 ◽  
Author(s):  
Estelle Habouzit ◽  
Hélène Richard ◽  
Hervé Sanchez ◽  
Nathalie Koulmann ◽  
Bernard Serrurier ◽  
...  

In the present study, we tested the hypothesis that chronic ANG I-converting enzyme (ACE) inhibition could improve the training-induced improvement in endurance exercise performance and that this could be related to enhanced skeletal muscle metabolic efficiency. Female Wistar rats were assigned to four groups comprising animals either maintained sedentary or endurance trained (Sed and Tr, respectively), and treated or not for 10 wk with an ACE inhibitor, perindopril (2 mg·kg−1·day−1) (Per and Ct, respectively) ( n = 8 each). Trained rats underwent an 8-wk treadmill training protocol that consisted of 2 h/day running at 30 m/min on a 8% decline. Before the start of and 1 wk before the end of experimental conditioning, the running time to exhaustion of rats was measured on a treadmill. The training program led to an increase in endurance time, higher in Tr-Per than in Tr-Ct group (125% in Tr-Ct vs. 183% in Tr-Per groups, P < 0.05). Oxidative capacity, measured in saponin-permeabilized fibers of slow soleus and fast plantaris muscles, increased with training, but less in Tr-Per than in Tr-Ct rats. The training-induced increase in citrate synthase activity also was less in soleus from Tr-Per than Tr-Ct rats. The training-induced increase in the percentage of the type IIa isoform of myosin heavy chain (MHC) (45%, P < 0.05) and type IIx MHC (25%, P < 0.05) associated with decreased type IIb MHC (34%, P < 0.05) was minimized by perindopril administration. These findings demonstrate that the enhancement in physical performance observed in perindopril-treated animals cannot be explained by changes in mitochondrial respiration and/or MHC distribution within muscles involved in running exercise.


2002 ◽  
Vol 282 (3) ◽  
pp. E574-E579 ◽  
Author(s):  
Pascal Imbeault ◽  
Angelo Tremblay ◽  
Jean-Aimé Simoneau ◽  
Denis R. Joanisse

In this study, we examined whether weight loss-induced changes in plasma organochlorine compounds (OC) were associated with those in skeletal muscle markers of glycolytic and oxidative metabolism. Vastus lateralis skeletal muscle enzyme activities and plasma OC (Aroclor 1260, polychlorinated biphenyl 153, p,p′-DDE, β-hexachlorocyclohexane, and hexachlorobenzene) were measured before and after a weight loss program in 17 men and 20 women. Both sexes showed a similar reduction in body weight (∼11 kg) in response to treatment, although men lost significantly more fat mass than women ( P < 0.05). Enzymatic markers of glycolysis, phosphofructokinase (PFK) activity, and oxidative metabolism, β-hydroxyacyl-CoA dehydrogenase (HADH), citrate synthase (CS), and cytochrome c oxidase (COX) activities, remained unchanged after weight loss. A significant increase in plasma OC levels was observed in response to weight loss, an effect that was more pronounced in men. No relationship was observed between changes in OC and those in PFK activity in either sex [−0.31 < r < 0.12, not significant (NS)]. However, the greater the increase in plasma OC levels, the greater the reduction in oxidative enzyme (HADH, CS, COX) activities was in response to weight loss in men (−0.75 < r < −0.50, P < 0.05) but not in women (−0.33 < r < 0.33, NS). These results suggest that the weight loss-induced increase in plasma pollutant levels is likely to be associated with reduced skeletal muscle oxidative metabolism in men but not in women.


Author(s):  
Nicolas Wirtz ◽  
André Filipovic ◽  
Sebastian Gehlert ◽  
Markus de Marées ◽  
Thorsten Schiffer ◽  
...  

Intramuscular density of monocarboxylate-transporter (MCT) could affect the ability to perform high amounts of fast and explosive actions during a soccer game. MCTs have been proven to be essential for lactate shuttling and pH regulation during exercise and can undergo notable adaptational changes depending on training. The aim of this study was to evaluate the occurrence and direction of potential effects of a 7-weeks training period of jumps with superimposed whole-body electromyostimulation on soccer relevant performance surrogates and MCT density in soccer players. For this purpose, 30 amateur soccer players were randomly assigned to three groups. One group performed dynamic whole-body strength training including 3 x 10 squat jumps with WB-EMS (EG, n = 10) twice a week in addition to their daily soccer training routine. A jump training group (TG, n = 10) performed the same training routine without EMS, whereas a control group (CG, n = 8) merely performed their daily soccer routine. 2 (Time: pre vs. post) x 3 (group: EG, TG, CG) repeated measures analyses of variance (rANOVA) revealed neither a significant time, group nor interaction effect for VO2peak, Total Time to Exhaustion and Lamax as well as MCT-1 density. Due to a lack of task-specificity of the underlying training stimuli, we conclude that seven weeks of WB-EMS superimposed to jump exercise twice a week does not relevantly influence aerobic performance or MCT density.


2001 ◽  
Vol 90 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Sarah L. Kennedy ◽  
William C. Stanley ◽  
Ashish R. Panchal ◽  
Robert S. Mazzeo

The purpose of this study was to examine the effect of acute (24 h) and chronic (5 wk) hypobaric hypoxic exposure equivalent to a simulated altitude of 4,300 m (446 mmHg) on the enzymes of fat metabolism. Heart, liver, and skeletal muscle were taken from 32 male Sprague-Dawley rats. Altitude exposure did not affect the activity of citrate synthase in any of the tissues, suggesting that mitochondrial content was unchanged. Carnitine palmitoyltransferase-I (CPT-I) activity was significantly reduced in the heart by both acute and chronic high altitude exposure compared with controls. A similar reduction was found for CPT-I activity in extensor digitorum longus after acute and chronic exposure compared with control animals. CPT-I activity was not affected by altitude exposure in the soleus muscle or the liver. 3-Hydroxyacyl-CoA dehydrogenase (β-HAD) activity was significantly depressed in the hearts of chronically exposed animals compared with controls. No difference between acute and control animals was found in the heart for β-HAD activity. Liver β-HAD activity was also significantly decreased in the acclimatized as well as in the acute animals compared with the control group. Quadriceps β-HAD activity was reduced for the chronic animals only compared with controls. These data suggest that acclimatization to high altitude selectively decreases key enzymes in fat utilization and oxidation in the heart, liver, and select skeletal muscles.


1995 ◽  
Vol 79 (6) ◽  
pp. 1914-1920 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. J. MacDonald ◽  
R. L. Hughson

The rates of increase in O2 uptake (VO2) after step changes in work rate from 25 W to 60% of pretraining peak VO2 (VO2 peak) were measured at various times during an endurance training program (2 h/day at 60% pretraining VO2 peak). Seven untrained males [23 +/- 1 (SE) yr] performed a series of repeated step changes in work rate before training (PRE) and after 4 days (4D), 9 days (9D), and 30 days (30D) of training. VO2 kinetic responses were determined from breath-by-breath data averaged across four repetitions and analyzed using a two-component exponential model. Mean response time (time taken to reach 63% of steady-state VO2) was faster (P < 0.01) than PRE (38.1 +/- 2.6 s) at both 4D (34.9 +/- 2.4 s) and 9D (32.5 +/- 1.8 s) and was faster (P < 0.01) at 30D than at all other times (28.3 +/- 1.0 s). Blood lactate concentrations (after 6 min of cycling) were also lower at 4D and 9D than PRE (P < 0.01) and were lower at 30D than at all other times (P < 0.01). VO2 peak was unchanged from PRE (3.52 +/- 0.20 l/min) at 8D (3.55 +/- 0.20 l/min) but was increased (P < 0.01) at 30D (3.89 +/- 0.18 l/min). Muscle oxidative capacity (maximal citrate synthase activity) was not significantly increased until 30D (P < 0.01). It is concluded that at least part of the acceleration of whole body VO2 kinetics with endurance training is a rapid phenomenon, occurring before changes in VO2 peak and/or muscle oxidative potential.


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