The cardiomyocyte (CMC) adapts to stress by cellular hypertrophy. However, the type of stress (physiological or pathological) has important consequences for remodeling. Previous studies indicated that pathologic remodeling is accompanied by a reduced transverse tubule (TT) density. Here, we examined the effects on TT-density after exercise training (ExTr) in two models of cardiac dysfunction (heart failure and metabolic syndrome), and in failing hearts that were unloaded with angiotensin II type 1 antagonism (Losartan). Healthy, post-myocardial infarction (MI) heart failure and metabolic syndrome adult rats were exercised for 8 weeks on a daily treadmill running program that increased exercise capacity by ~50%. Isolated CMCs were stained with Di-8-ANEPPS to image the TT-system with confocal microscopy. In healthy rats, ExTr associated with increased CMC length (sedentary 101±3μm vs. ExTr 112±5μm) and unchanged relative TT-density (sedentary 0.2±0.04 vs. ExTr 0.21±0.04). In rats with heart failure 12 weeks post-MI, cell length increased (sham 101±3μm vs. MI 130±7μm), and TT-density decreased (sham 0.2±0.04 vs. MI 0.1±0.01). ExTr from weeks 4-12 after MI reduced pathologic hypertrophy (MI sedentary 130±7μm vs. MI ExTr 117±4μm). However, TT-density remained low (MI sedentary 0.1±0.01 vs. MI ExTr 0.13±0.03). In separate experiments, Losartan lowered blood pressure in heart failure rats, but did not cause any changes in TT structure. Nor did it add any additive effects when combined with ExTr. In contrast to heart failure, CMCs from metabolic syndrome rats (LCR; low capacity running) showed depressed contractile function, but had smaller cell sizes (LCR sedentary 118±2μm vs. controls (HCR (high capacity running) sedentary 124±2μm). Metabolic syndrome was associated with reduced TT-density (LCR sedentary 0.18±0.01 vs. HCR sedentary 0.21±0.02). ExTr induced a greater hypertrophy in HCR than LCR (LCR 125±3μm; 6% vs. HCR 141±4μm;14%), but did not change TT-density in any group. Thus, CMC TT-density is sustained in physiologic, but not in pathologic hypertrophy. Moreover, cardiac dysfunction in metabolic syndrome is also associated with reduced TT-density. ExTr reduces pathological hypertrophy in heart failure after MI, induces physiological growth in metabolic syndrome hearts, but has little effect on TT-density.