Effects of high-intensity training on prostate cancer-induced cardiac atrophy.
Prostate cancer
cardiac atrophy
high-intensity exercise
Journal
American journal of translational research
ISSN: 1943-8141
Titre abrégé: Am J Transl Res
Pays: United States
ID NLM: 101493030
Informations de publication
Date de publication:
2021
2021
Historique:
received:
26
05
2020
accepted:
20
11
2020
entrez:
2
2
2021
pubmed:
3
2
2021
medline:
3
2
2021
Statut:
epublish
Résumé
Recent evidence suggests prostate cancer independent of treatment has atrophic effects on whole heart and left ventricular (LV) masses, associated with reduced endurance exercise capacity. In a pre-clinical model, we tested the hypothesis that high-intensity training could prevent cardiac atrophy with prostate cancer and alter cardiac protein degradation mechanisms. Dunning R-3327 AT-1 prostate cancer cells (1×10 There were no significant differences in tumor mass between groups (TBEX 3.4±0.7, TBS 2.8±0.6 g, P=0.3), or body mass (TBEX 317±5, TBS 333±7 g, P=0.2). Heart-to-body mass ratio was lower in TBS group compared to TBEX (2.3±0.1 vs. 2.5±0.1 mg/g, P<0.05). LV/body mass ratio was also lower in the TBS group (1.6±0.1 vs. 1.8±0.1 mg/g, P<0.05). From Pre-Post, TBEX had significant increases in SV (~20% P<0.05) whereas TBS had no significant change. There were no significant differences between groups for markers of protein degradation. This study suggests that high-intensity exercise can improve LV function and increase LV mass concurrent with prostate cancer development, versus sedentary counterparts. Given cardiac dysfunction often manifests with conventional anti-cancer treatments, a short-term high-intensity training program, prior to treatment, may improve cardiac function and fatigue resistance in cancer patients.
Sections du résumé
BACKGROUND
BACKGROUND
Recent evidence suggests prostate cancer independent of treatment has atrophic effects on whole heart and left ventricular (LV) masses, associated with reduced endurance exercise capacity. In a pre-clinical model, we tested the hypothesis that high-intensity training could prevent cardiac atrophy with prostate cancer and alter cardiac protein degradation mechanisms.
METHODS
METHODS
Dunning R-3327 AT-1 prostate cancer cells (1×10
RESULTS
RESULTS
There were no significant differences in tumor mass between groups (TBEX 3.4±0.7, TBS 2.8±0.6 g, P=0.3), or body mass (TBEX 317±5, TBS 333±7 g, P=0.2). Heart-to-body mass ratio was lower in TBS group compared to TBEX (2.3±0.1 vs. 2.5±0.1 mg/g, P<0.05). LV/body mass ratio was also lower in the TBS group (1.6±0.1 vs. 1.8±0.1 mg/g, P<0.05). From Pre-Post, TBEX had significant increases in SV (~20% P<0.05) whereas TBS had no significant change. There were no significant differences between groups for markers of protein degradation.
CONCLUSION
CONCLUSIONS
This study suggests that high-intensity exercise can improve LV function and increase LV mass concurrent with prostate cancer development, versus sedentary counterparts. Given cardiac dysfunction often manifests with conventional anti-cancer treatments, a short-term high-intensity training program, prior to treatment, may improve cardiac function and fatigue resistance in cancer patients.
Types de publication
Journal Article
Langues
eng
Pagination
197-209Subventions
Organisme : NHLBI NIH HHS
ID : R15 HL137156
Pays : United States
Informations de copyright
AJTR Copyright © 2021.
Déclaration de conflit d'intérêts
None.
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