Proceedings of The Physiological Society

Physiology 2016 (Dublin, Ireland) (2016) Proc Physiol Soc 37, PCB213

Poster Communications

Type I skeletal myofibre density mediates the interactive effects of maternal and post-weaning high-fat diet on muscle contraction force in adult mouse offspring

V. L. Reay1, L. E. Jones1, F. R. Cagampang1, K. R. Poore1, F. P. markiewicz2, P. L. Newland2, L. R. Green1

1. Institute of Developmental Sciences, University of Southampton, Southampton, United Kingdom. 2. Centre for Biological Sciences, University of Southampton, Southampton, United Kingdom.


Obesity impairs skeletal muscle strength. However, most myofibres are formed prenatally and their density is reduced by prenatal undernutrition (1) and high-fat (HF) feeding (2). In mice, maternal HF feeding during pregnancy and lactation minimized the reduction in isometric contraction force in adult female offspring soleus muscle (m.) caused by a post-weaning HF diet (3). Here, we determined if this interactive effect was mediated by altered soleus m. structure. Female C57BL/6J mice were fed a control (C; 7% kcal fat) or HF (45% kcal fat) diet 6 wks pre-mating and throughout pregnancy and lactation (PRE). Offspring were weaned onto the C or HF diet (POST), creating 4 diet groups: C/C, C/HF, HF/C, HF/HF (n=7-8 per group). Female 30 wk offspring soleus m. peak force of isometric contraction was measured in response to several electrical stimulation frequencies. 10 μm mid-belly sections of frozen muscle were cut. Fluorescent secondary antibodies (AlexaFluor) were used against primary antibodies (DSHB, Iowa) for type I (BA-F8), type IIA (SC-71), type IIB (BF-F3) and type IIX (6H1) myofibres. Average myofibre density and cross sectional area (CSA) were determined in 5 fields of view. Data are mean±SEM and were analysed by 2-way ANOVA. Across all offspring groups, higher type I myofibre density (R2 0.185, B 64.11, p<0.05), and lower type I (R2 0.197, B -9.47, p<0.05) and IIA (R2 0.234, B-14.34, p<0.01) CSA, were associated with higher peak force contraction. Across all groups, greater myofibre density was associated with smaller CSA in type I (R2 0.353, B-0.85, p=0.001) and IIA (R2 0.256, B-0.81, p<0.01) myofibres. Type I myofibre density was increased with PRE HF alone (fibres/mm2: C/C, 209.7±15.0; HF/C, 258.7±13.1, p<0.05). Conversely, type I myofibre density was decreased (fibres/mm2: C/C, 209.7±15.0; C/HF, 153.6±18.9, p<0.05) and CSA was increased (μm2: C/C, 1640±130.9; C/HF, 2098±109.1, p<0.05) with POST HF alone. Type IIA myofibre density tended to be increased in POST HF animals (fibres/mm2: C/C+HF/C, 256.7±11.6; C/HF+HF/HF, 288.9±11.2, p=0.057), and CSA was higher with POST HF alone (μm2: C/C, 1395±85.9; C/HF, 1728±116.9, p<0.05). Across all myofibre types, density was lower in C/HF (fibres/mm2: C/C, 533.8±23.9; C/HF, 450.3±23.8, p<0.05), but not in HF/HF offspring. Our data suggest that reduced type I myofibre density contributes to lower peak force in the C/HF offspring soleus muscle (3). Increased type I myofibre density in HF/C animals suggests a mechanism by which peak force contraction is maintained better in the HF/HF group. Overall, these findings reinforce the potential importance of prenatal nutrition in determining muscle health in an obese adult.

Where applicable, experiments conform with Society ethical requirements