Endurance exercise training decreases capillary basement membrane width in older nondiabetic and diabetic adults

1996 ◽  
Vol 80 (3) ◽  
pp. 747-753 ◽  
Author(s):  
J. R. Williamson ◽  
P. L. Hoffmann ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
A. R. Coggan ◽  
...  

The objectives of these studies were to 1) evaluate the relationships among age, glucose intolerance, and skeletal muscle capillary basement membrane (CBM) width (CBMW) and 2) determine the effects of exercise training on CBMW by comparing values of young (28 +/- 4 yr) and older (63 +/- 7 yr) athletes with those of age-matched sedentary control subjects and by measuring CBMW in older men and women before and after a 9-mo endurance-exercise training program. CBMW was measured in tissue samples obtained from the gastrocnemius muscle. CBMW in sedentary 64 +/- 3-yr-old subjects was 25% thicker than in sedentary 24 +/- 3-yr-old subjects. CBMW was similar in young and older athletes and was thinner than the CBMW of age-matched sedentary control subjects. There were no differences in CBMW among older sedentary individuals with normal or impaired glucose tolerance or mild non-insulin-dependent diabetes mellitus. Nine months of endurance exercise training reduced CBMW in older men and women by 30-40%, to widths that were not different from those of the young subjects; this response was independent of glucose tolerance status. These findings suggest that habitual exercise prevents the thickening of the skeletal muscle CBM that is characteristic of advancing age. Moreover, the thickening of the CBM appears to be readily reversed as a result of exercise training, even in older individuals.

1993 ◽  
Vol 75 (2) ◽  
pp. 849-855 ◽  
Author(s):  
R. J. Spina ◽  
T. Ogawa ◽  
W. M. Kohrt ◽  
W. H. Martin ◽  
J. O. Holloszy ◽  
...  

Recent studies have shown that people in their seventh decade are able to adapt to exercise training with an increase in maximal O2 uptake (VO2max) similar in relative magnitude to that observed in young people. The purpose of this study was to determine the relative contributions of increases in stroke volume and O2 extraction to the training-induced increase in VO2max in older men and women. Fifteen men [63 +/- 3 (SE) yr] and 16 women (64 +/- 3 yr), in good health, participated in 9–12 mo of endurance exercise training at 70 to 85% of maximal heart rate for 45 min/day, 4 days/wk. VO2max increased 19% (2.35 +/- 0.1 to 2.8 +/- 0.1 l/min; P < 0.01) in the men and 22% (1.36 +/- 0.1 to 1.66 +/- 0.1 l/min; P < 0.01) in the women in response to training. In the men, stroke volume during maximal exercise was 15% higher after training, and this increase accounted for 66% of the increase in VO2max. The remainder of the increase in VO2max was accounted for by a 7% greater arteriovenous O2 content difference during maximal exercise. In contrast, training resulted in no change in stroke volume in women, in whom the entire increase in VO2max was accounted for by a greater arteriovenous O2 content difference (12.2 +/- 0.4 before vs. 14.4 +/- 0.4 ml O2/100 ml blood after; P < 0.01) during maximal exercise. There were no changes in these variables in the control subjects. The mechanisms responsible for the training-induced increase in VO2max in the older men were similar to those found in young people.(ABSTRACT TRUNCATED AT 250 WORDS)


1997 ◽  
Vol 82 (6) ◽  
pp. 1862-1868 ◽  
Author(s):  
Richard M. McAllister ◽  
Brian L. Reiter ◽  
John F. Amann ◽  
M. Harold Laughlin

McAllister, Richard M., Brian L. Reiter, John F. Amann, and M. Harold Laughlin. Skeletal muscle biochemical adaptations to exercise training in miniature swine. J. Appl. Physiol. 82(6): 1862–1868, 1997.—The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16–20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 ± 1.1 μmol ⋅ min−1 ⋅ g−1; Trn, 23.9 ± 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 ± 2; Trn, 22 ± 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.


2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.


2005 ◽  
Vol 37 (Supplement) ◽  
pp. S96
Author(s):  
Justin W. Johnson ◽  
Tongjian You ◽  
Stephen Messier ◽  
Gary Miller ◽  
Barbara Nicklas

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