Abstract
Background: Abnormalities of myosin heavy chain (MHC) isoforms, enzyme activity, and capillarity contribute to the exercise intolerance that is characteristic of patients with heart failure. To what extent these changes can be reversed with exercise training and whether differences exist in the responses of men and women remains uncertain. We described and compared the effects of exercise training on exercise capacity and skeletal muscle histochemistry in men and women with chronic heart failure. Methods: Fifteen patients (10 male) undergoing standard medical therapy completed a 14- to 24-week exercise training program. Peak oxygen consumption, MHC isoforms, capillary density, and selected metabolic enzymes were assessed before and after training. Results: Peak oxygen consumption was improved 14% (P <.05); however, this increase was mostly because of the improvement observed in men versus women (+20% versus +2%, respectively, P < .01). At baseline, MHC I content was lower in men than in women (33% ± 3% vs 49.6% ± 5.5%, P < .05). MHC I improved with training in men, to 45.6% ± 4.5% (+38%, P < .05), versus women (-3%, P = .82), and the increase in men tended (P = .12) to be significant when compared with that in women. There were no significant changes in capillary density or muscle enzyme activity with training in the group as a whole or in men and women separately. Conclusion: Among patients with chronic heart failure, improvements in peak exercise capacity may be more pronounced in men than in women. This difference in response of functional capacity to training paralleled differences observed between men and women for changes in MHC I isoforms.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 912-918 |
| Number of pages | 7 |
| Journal | American Heart Journal |
| Volume | 145 |
| Issue number | 5 |
| DOIs | |
| State | Published - May 1 2003 |
Fingerprint
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Differential effects of exercise training in men and women with chronic heart failure. / Keteyian, Steven J.; Duscha, Brian D.; Brawner, Clinton A.; Green, Howie J.; Marks, Charles R.C.; Schachat, Fred H.; Annex, Brian H.; Kraus, William E.
In: American Heart Journal, Vol. 145, No. 5, 01.05.2003, p. 912-918.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential effects of exercise training in men and women with chronic heart failure
AU - Keteyian, Steven J.
AU - Duscha, Brian D.
AU - Brawner, Clinton A.
AU - Green, Howie J.
AU - Marks, Charles R.C.
AU - Schachat, Fred H.
AU - Annex, Brian H.
AU - Kraus, William E.
PY - 2003/5/1
Y1 - 2003/5/1
N2 - Background: Abnormalities of myosin heavy chain (MHC) isoforms, enzyme activity, and capillarity contribute to the exercise intolerance that is characteristic of patients with heart failure. To what extent these changes can be reversed with exercise training and whether differences exist in the responses of men and women remains uncertain. We described and compared the effects of exercise training on exercise capacity and skeletal muscle histochemistry in men and women with chronic heart failure. Methods: Fifteen patients (10 male) undergoing standard medical therapy completed a 14- to 24-week exercise training program. Peak oxygen consumption, MHC isoforms, capillary density, and selected metabolic enzymes were assessed before and after training. Results: Peak oxygen consumption was improved 14% (P <.05); however, this increase was mostly because of the improvement observed in men versus women (+20% versus +2%, respectively, P < .01). At baseline, MHC I content was lower in men than in women (33% ± 3% vs 49.6% ± 5.5%, P < .05). MHC I improved with training in men, to 45.6% ± 4.5% (+38%, P < .05), versus women (-3%, P = .82), and the increase in men tended (P = .12) to be significant when compared with that in women. There were no significant changes in capillary density or muscle enzyme activity with training in the group as a whole or in men and women separately. Conclusion: Among patients with chronic heart failure, improvements in peak exercise capacity may be more pronounced in men than in women. This difference in response of functional capacity to training paralleled differences observed between men and women for changes in MHC I isoforms.
AB - Background: Abnormalities of myosin heavy chain (MHC) isoforms, enzyme activity, and capillarity contribute to the exercise intolerance that is characteristic of patients with heart failure. To what extent these changes can be reversed with exercise training and whether differences exist in the responses of men and women remains uncertain. We described and compared the effects of exercise training on exercise capacity and skeletal muscle histochemistry in men and women with chronic heart failure. Methods: Fifteen patients (10 male) undergoing standard medical therapy completed a 14- to 24-week exercise training program. Peak oxygen consumption, MHC isoforms, capillary density, and selected metabolic enzymes were assessed before and after training. Results: Peak oxygen consumption was improved 14% (P <.05); however, this increase was mostly because of the improvement observed in men versus women (+20% versus +2%, respectively, P < .01). At baseline, MHC I content was lower in men than in women (33% ± 3% vs 49.6% ± 5.5%, P < .05). MHC I improved with training in men, to 45.6% ± 4.5% (+38%, P < .05), versus women (-3%, P = .82), and the increase in men tended (P = .12) to be significant when compared with that in women. There were no significant changes in capillary density or muscle enzyme activity with training in the group as a whole or in men and women separately. Conclusion: Among patients with chronic heart failure, improvements in peak exercise capacity may be more pronounced in men than in women. This difference in response of functional capacity to training paralleled differences observed between men and women for changes in MHC I isoforms.
UR - http://www.scopus.com/inward/record.url?scp=0038065615&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0038065615&partnerID=8YFLogxK
U2 - 10.1016/S0002-8703(03)00075-9
DO - 10.1016/S0002-8703(03)00075-9
M3 - Article
C2 - 12766753
AN - SCOPUS:0038065615
VL - 145
SP - 912
EP - 918
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 5
ER -