Cardiac remodeling and physical training post myocardial infarction

Table 1 Summary of physical training protocols and outcomes in selected human studies

Ref.	Type of exercise	Exercise intensity	Exercise duration	Exercise frequency	Training period	Assessment	Outcome
Braith et al[32] 1999	Treadmill walk	40%-70% of peak oxygen uptake (VO2)	Started with 10-20 min as tolerated and increased to 30-45 min by the 10th wk	3 times/wk	4 mo	Plasma RAAS	Reduced Resting AngII, Aldosterone, vasopressin, and atrial natriuretic peptide
Myers et al[143] 2001	Outdoor walking at an elevation of 3500 ft, in addition to cycling	60%-70% of peak VO2	Two 1-h sessions of walking, 45 min of cycling	5 times/wk	2 mo	Post-exercise oxygen uptake kinetics	High-intensity training did not result in a faster recovery of oxygen debt
La Rovere et al[144] 20021	Graded exercise (cycling, calisthenics)	Adjusted to 75% of the heart rate at peak VO2	30 min	5 times/wk	1 mo	BRS, LVEF	BRS improved by 26%, while LVEF remained unchanged
Marchionni et al[145] 20032	Cycling	70%-85% of max heart rate	1 h	3 times/wk	6 mo	Total work capacity, health-related quality of life	Improved total work capacity and health-related quality of life
Zheng et al[146] 20081	Bicycle ergometer	75% of peak heart rate	30 min	3 time/wk	6 mo	HR recovery, time to reach anaerobic threshold, left ventricular end-diastolic	Exercise training prevented ventricular remodeling to a certain extent
Giallauria et al[46] 2013	Bicycle ergometer	60%-70% of peak VO2	30 min	3 times/wk	6 mo	diameter, left ventricular ejection fraction dipyridamole rest gated myocardial perfusion single photon emission computed tomography	Improved peak oxygen consumption, myocardial perfusion and LV function

¹Exercise was part of a comprehensive secondary prevention program;

²Combination study consisting of Home and Hospital/group participants. RAAS: Renin-angiotensin-aldosterone system; LVEF: Left ventricular ejection fraction; BRS: Baroreflex sensitivity.

Table 2 Summary of physical training protocols and outcomes in selected animal studies

Ref.	Type of exercise	Exercise intensity	Exercise duration	Exercise frequency	Training period	Assessment	Outcome
Hashimoto et al[76] 2004	Treadmill running	10 m/min	60 min	5 d/wk	6 wk	Myosin heavy chain isoforms, cardiac wall measurements	Exercise training resulted in a significant increase of α-MHC expression in both anterior and posterior wall, ensuring a beneficial role in the remodeling of the heart
Xu et al[35] 2008	Treadmill running	16 m/min @ 5% grade	50 min	5 d/wk	8 wk	TIMP-1, AT1, ACE, collagen volume fraction, MMP	Early exercise training after MI reduces TIMP-1 expression, improves the balance between MMPs and TIMPs, and mitigates the expressions of ACE and AT1 receptor, thus attenuating myocardial fibrosis and preserving cardiac function
De Waard et al[59] 2007	Voluntary treadmill exercise training	N/A	N/A	5 d/wk	8 wk	LV fractional shortening, Ca2+ sensitivity, PLB, SERCA	Voluntary exercise improved LV and cardiomyocyte shortening, attenuates global LV dysfunction
Wan et al[34] 2007	Treadmill running	16 m/min @ 5% grade	50 min	5 d/wk	8 wk	Echo and RAAS	Exercise training improved cardiac function and attenuated RAAS. Early and late exercise training had similar beneficial results
Xu et al[106] 2010	Treadmill running	16 m/min @ 5% grade	50 min	5 d/wk	8 wk	SOD, GPx, MnSOD	Exercise training combined with AngII receptor blockade reduced oxidative stress
Yengo et al[147] 2012	Treadmill running	15% grade, speed increased from 13 to 24 m/min	Progressively increased to 60 min	6 d/wk	10 wk	Collagen concentration, non-reducible collagen cross-linking in the RV	Exercise training normalized the observed increase in cross-linking, and favorably modifies heart extracellular matrix

RAAS: Renin-angiotensin-aldosterone system; MHC: Myosin heavy chain; TIMP-1: Tissue inhibitor matrix metalloproteinase; AT1: AngII receptor type 1; ACE: Angiotensin converting enzyme; MMP: Matrix metalloproteinase; SOD: Superoxide dismutase; GPX: Glutathione peroxidase.