“At the time, I wasn’t a post-natal personal trainer, so I didn’t know the dos and don’t of exercising after childbirth,” said Anna.
“I’ve always been very fit, so I threw myself into it. I almost felt I had something to prove.
“For many women, the pressure to bounce back, lose that baby weight and be back in your size eight jeans comes from magazines and celebrities, but in my case, it came from within.
“Fitness has always been a passion of mine. I enjoy it – it reduces stress and it’s my way of being there for myself.”
Cautious, Anna consulted her GP for advice, but said she did not get many answers at first.
She added: “Everyone thought it was just my body recovering, so I felt like I had to get on with things.”
When Lauren was five months old, Anna started leading fitness classes.
The exercise itself was no problem but, working out most days, her urinary incontinence worsened to the point where she struggled to teach.
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ROS can signal fibrosis, and chronic hypertrophy is a key cause for LV dysfunction. We, therefore, examined if control of PARP1-dependent mitochondrial impairment and oxidative stress arrested cardiac remodeling and LV dysfunction in Chagas disease. Echocardiography imaging showed the LV mass and inter-ventricular septum thickness (IVS) were increased by 29–58%, while LV posterior wall (LVPW) was thinned by 31–47% in chagasic (vs. control) WT mice (Fig 6A–6E, all, p<0.05, S2 Table). Histological evaluation of tissue sections by Masson's Trichrome staining showed the myocardial collagen content was significantly increased in chagasic myocardium (score: 4.0 ± 0.4 vs. 0.3 ± 0.04, WT.Tc vs. WT, Fig 6F–6H, p<0.001). An increase in cardiac fibrosis in WT.Tc (vs. control) mice was also evidenced by 6-fold, 8-fold, and 1.5-fold increase in mRNA levels for COL1A1, COL3A1, and COL5A2, respectively (Fig 6I–6K, all, p<0.05). The chronically infected PARP1+/- and PARP1-/- mice exhibited the ability to maintain IVS and LVPW thickness at normal levels, >50% decline in collagen deposition, and 50–90% decline in the mRNA levels of collagen isoforms when compared to that noted in WT.Tc mice (Fig 6A–6K, all, p<0.05).