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  • 001), with no differential response between groups (i.e. no group �� training effect; P= 0.51). Pairwise contrasts showed that both HF patients find more (P < 0.01) and controls (P < 0.02) experienced reductions in myofibril area fraction. Parenthetically, this reduction in myofilament area fraction was unlikely to be related to an increase in non-contractile, subcellular structures since mitochondrial fractional area, the next most prevalent organellar component of fibre area (Hoppeler et al. 1973), was not altered with training (authors�� unpublished observations). No training (P= 0.13) or group �� training (P= 0.93) effects were noted for thick to thin filament ratio. Neither thick learn more filament (P= 0.31) nor thin filament numbers per unit area (P= 0.19) were altered by training and no group �� training effects were noted (data not shown). There was a strong trend (P= 0.07) towards an effect of training to increase A-band length, with no group �� training effect (P= 0.57). Collectively, although there is some evidence for increases in myofilament size with training (e.g. trend in A-band length), the predominant effect of training was to reduce myofilament content as a fraction of fibre cross-sectional area. Of note, the difference in the average sarcomere lengths between pre- and post-training preparations for each volunteer did not correlate with changes in their myofibrillar area fraction (P= 0.27), thick-to-thin filament ratio (P= 0.18) or A-band length (P= 0.68), indicating that differences in the sarcomere length of the preparation did not explain the observed structural changes. For functional characterizations, our first step was to evaluate the force-producing capacity of single muscle fibres per unit cross-sectional area (i.e. tension; MHC I fibres in Fig. 2 and MHC IIA fibres in Fig. 3). Single DAPT muscle fibre Ca2+-activated tension was not affected by training in either MHC I (P= 0.65) or IIA (P= 0.97) fibres and no group �� training interaction effects were noted for either fibre type (P= 0.96 and 0.97, respectively). We also evaluated dynamic stiffness data under rigor and maximal Ca2+-activated conditions to estimate the number of available cross-bridges and their fraction that are recruited during Ca2+ activation, respectively. In MHC I fibres (Fig. 2), neither dynamic stiffness under maximal Ca2+-activated (P= 0.20) or rigor (P= 0.22) conditions, nor their ratio (P= 0.68), was affected by training and no group �� training effects were found (range of P values: 0.18�C0.96). Similarly, for MHC IIA fibres (Fig. 3), no training effect was noted for dynamic stiffness under maximal Ca2+-activated (P= 0.61) or rigor conditions (P= 0.26), or for their ratio (P= 0.72), and no group �� training effects were noted (range of P values: 0.19�C0.97).

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