Exercise training reverses cardiac aging phenotypes associated with heart failure with preserved ejection fraction in male mice.

Borderline significance toward enhanced production or cellular responses to NO was detected in our pathway analysis, which could suggest that NO biology may still be a promising therapeutic target for age‐related HFpEF.

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Interestingly, pathways associated with drug targets previously tested in clinical HFpEF trials, that is, adrenergic, renin–angiotensin–aldosterone (RAAS) and nitric oxide‐cGMP‐phosphodiesterase signaling pathways, were generally not significantly altered by ExT, although positive regulation of nitric oxide synthase biosynthesis reached our significance threshold (NES 1.67; FDR 0.24) and cellular responses to nitric oxide (NO) had a positive trend (NES 1.64, FDR 0.26) (Table 2 ).

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Of these 216 pathways, the most highly significant changes predominantly occurred in cell cycle or cell division pathways (Figure 5c ), suggesting that reversing impairments in this hallmark of aging (Lopez‐Otin, Blasco, Partridge, Serrano, & Kroemer, 2013 ) may be an important contributor by which ExT improves the performance of the aged heart.

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