Adaptive changes in work capacity, skeletal muscle capillarization and enzyme levels during training and detraining

1981 ◽  
Vol 113 (1) ◽  
pp. 9-16 ◽  
Author(s):  
KLAUS KLAUSEN ◽  
LARS BO ANDERSEN ◽  
INGE PELLE
1988 ◽  
Vol 65 (1) ◽  
pp. 256-263 ◽  
Author(s):  
W. T. Willis ◽  
P. R. Dallman ◽  
G. A. Brooks

We investigated physiological and biochemical factors associated with the improved work capacity of trained iron-deficient rats. Female 21-day-old rats were assigned to one of four groups, two dietary groups (50 and 6 ppm dietary iron) subdivided into two levels of activity (sedentary and treadmill trained). Iron deficiency decreased hemoglobin (61%), maximal O2 uptake. (VO2max) (40%), skeletal muscle mitochondrial oxidase activities (59-90%), and running endurance (94%). In contrast, activities of tricarboxylic acid (TCA) cycle enzymes in skeletal muscle were largely unaffected. Four weeks of mild training in iron-deficient rats resulted in improved blood lactate homeostasis during exercise and increased VO2max (15%), TCA cycle enzymes of skeletal muscle (27-58%) and heart (29%), and liver NADH oxidase (34%) but did not affect any of these parameters in the iron-sufficient animals. In iron-deficient rats training affected neither the blood hemoglobin level nor any measured iron-dependent enzyme pathway of skeletal muscle but substantially increased endurance (230%). We conclude that the training-induced increase in endurance in iron-deficient rats may be related to cardiovascular improvements, elevations in liver oxidative capacity, and increases in the activities of oxidative enzymes that do not contain iron in skeletal and cardiac muscle.


1992 ◽  
Vol 73 (5) ◽  
pp. 2004-2010 ◽  
Author(s):  
R. Wibom ◽  
E. Hultman ◽  
M. Johansson ◽  
K. Matherei ◽  
D. Constantin-Teodosiu ◽  
...  

The adaptation of mitochondrial ATP production rate (MAPR) to training and detraining was evaluated in nine healthy men. Muscle samples (approximately 60 mg) were obtained before and after 6 wk of endurance training and after 3 wk of detraining. MAPR was measured in isolated mitochondria by a bioluminometric method. In addition, the activities of mitochondrial and glycolytic enzymes were determined in skeletal muscle. In response to training, MAPR increased by 70%, with a substrate combination of pyruvate + palmitoyl-L-carnitine + alpha-ketoglutarate + malate, by 50% with only pyruvate + malate, and by 92% with palmitoyl-L-carnitine + malate. With detraining MAPR decreased by 12–28% from the posttraining rate (although not significantly for all substrates). No differences were found when MAPR was related to the protein content in the mitochondrial fraction. The largest increase in mitochondrial enzyme activities induced by training was observed for cytochrome-c oxidase (78%), whereas succinate cytochrome c reductase showed only an 18% increase. The activity of citrate synthase increased by 40% and of glutamate dehydrogenase by 45%. Corresponding changes in maximal O2 uptake were a 9.6% increase by training and a 6.0% reversion after detraining. In conclusion, both MAPR and mitochondrial enzyme activities are shown to increase with endurance training and to decrease with detraining.


1997 ◽  
Vol 161 (4) ◽  
pp. 439-445 ◽  
Author(s):  
M.‐T. LINOSSIER ◽  
D. DORMOIS ◽  
C. PERIER ◽  
J. FREY ◽  
A. GEYSSANT ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Thomas Baasch‐Skytte ◽  
Thomas P. Gunnarsson ◽  
Matteo Fiorenza ◽  
Jens Bangsbo

2010 ◽  
Vol 298 (2) ◽  
pp. H375-H384 ◽  
Author(s):  
Lucile Vincent ◽  
Léonard Féasson ◽  
Samuel Oyono-Enguéllé ◽  
Viviane Banimbek ◽  
Christian Denis ◽  
...  

The influence of sickle cell trait and/or α-thalassemia on skeletal muscle microvascular network characteristics was assessed and compared with control subjects [hemoglobin (Hb) AA] in 30 Cameroonian residents [10 HbAA, 5 HbAA α-thalassemia (α-t), 6 HbAS, and 9 HbASα-t] matched for maximal work capacity and daily energy expenditure. Subjects performed an incremental exercise to exhaustion and underwent a muscle biopsy. Muscle fiber type and surface area were not different among groups. However, sickle cell trait (SCT) was associated with lower capillary density ( P < 0.05), lower capillary tortuosity ( P < 0.001), and enlarged microvessels ( P < 0.01). SCT carriers had reduced counts of microvessels <5-μm diameter, but a higher percentage of broader microvessels, i.e., diameter >10 μm ( P < 0.05). α-Thalassemia seemed to be characterized by a higher capillary tortuosity and unchanged capillary density and diameter. Thus, while SCT is a priori clinically benign, we demonstrate for the first time that significant remodeling of the microvasculature occurs in SCT carriers. These modifications may possibly reflect protective adaptations against hemorheological and microcirculatory dysfunction induced by the presence of HbS. The remodeling of the microvascular network occurs to a lesser extent in α-thalassemia. In α-thalassemic subjects, increased capillary tortuosity would promote oxygen supply to muscle tissues and might compensate for the lower Hb content often reported in those subjects.


Diabetes ◽  
2015 ◽  
Vol 64 (10) ◽  
pp. 3386-3395 ◽  
Author(s):  
Steven J. Prior ◽  
Andrew P. Goldberg ◽  
Heidi K. Ortmeyer ◽  
Eva R. Chin ◽  
Dapeng Chen ◽  
...  

2021 ◽  
Vol 11 (9) ◽  
pp. 3905
Author(s):  
Fuminori Kawano

Epigenetics is getting increased attention in the analysis of skeletal muscle adaptation to physiological stimuli. In this review, histone modifications in skeletal muscles and their role in the regulation of muscle characteristics and adaptive changes are highlighted. The distribution of active histone modifications, such as H3K4me3 and H3 acetylation, largely differs between fast- and slow-twitch muscles. It is also indicated that the transcriptional activity in response to exercise differs in these muscle types. Histone turnover activated by exercise training leads to loosening of nucleosomes, which drastically enhances gene responsiveness to exercise, indicating that the exercise training transforms the chromatin structure to an active status. Furthermore, histone modifications play a critical role in preserving the stem cell lineage in skeletal muscle. Lack of lysine-specific demethylase 1 in satellite cells promotes the differentiation into brown adipocytes during muscle regeneration after injury. H4K20me2, which promotes the formation of heterochromatin, is necessary to repress MyoD expression in the satellite cells. These observations indicate that histone modification is a platform that characterizes skeletal muscles and may be one of the factors regulating the range of adaptive changes in these muscles.


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