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High Intensity Exercise Improves Cardiorespiratory Capacity in a Mouse Model of Hypertrophic Cardiomyopathy
Author(s) -
Herrera Jonathan,
Szczesniak Danielle,
Szczesniak Kate,
Goddard RoseCarmel,
Yob Jaime,
Day Sharlene
Publication year - 2022
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2022.36.s1.l8091
Subject(s) - medicine , cardiorespiratory fitness , hypertrophic cardiomyopathy , interval training , cardiology , treadmill , intensity (physics) , high intensity interval training , rehabilitation , heart failure , physical therapy , physics , quantum mechanics
Cardiorespiratory capacity (pVO 2 ) is an important prognostic indicator in patients with HCM. Individuals with HCM that have a lower pVO 2 possess a greater risk for heart failure (HF) and mortality. High intensity exercise (HIE) can increase pVO 2 to a greater degree compared to other training modalities, including when used for cardiac rehabilitation for in cardiac disease states (e.g., HF and Cardiovascular disease). The effects of HIE on HCM, however, are largely unknown. Our study sought to evaluate the effects of High Intensity Interval Training (HIIT) on pVO 2 , as well as cardiac structural and functional parameters, in a preclinical mouse model of HCM. Methods Female and male C57BL/6J non‐transgenic nTG (n=27) and TG (n=32) mice were subjected to HIIT protocol that mirrored methods used clinically in cardiac rehabilitation. A single treadmill training session included 4‐4 minute high intensity intervals (~80% preVO2 max speed) interspersed by 5‐3 minute recovery intervals (~50% preVO2 max speed) for 31 total minutes. Exercise training sessions were repeated 3 times per week for 6 weeks. Pre and post pVO 2 and murine echocardiography were measured and analyzed by a blinded technician. Results Following 6 weeks of the HIIT, nTG female (+13.5 mL/kg/min ± 3.6, p<0.01), nTG male (+13.5 mL/kg/min ± 3.6, p<0.01) and TG female (+7.06 ± 3.3 mL/kg/min, p<0.05) mice demonstrated an average increase in pVO 2. A change in pVO 2 observed in TG male mice did not reach statistical significance (+4.34 ± p=0.12). Sedentary female (‐15.9 mL/kg/min ± 3.3, p<0.001) and male (‐13.1 mL/kg/min ± 3.9, p<0.01) TG control mice experienced a significant decrease in pVO 2 following the same period, while no change was observed in nTG sedentary controls. Independent of sex, nTG and TG HIIT mice had a significantly greater change in pVO 2 compared to sedentary counterparts. HIIT training did not result in changes to the following echocardiography measures in either nTG or TG mice: LV mass, LA volume, cardiac output, or stroke volume. Conclusion Our results indicate that a translationally derived HIIT protocol improved cardiorespiratory capacity in a preclinical HCM mouse model, absent of adverse events or worsening of organ level disease pathology.