The mechanical power output of the pectoralis muscle of cockatiel (Nymphicus hollandicus): the in vivo muscle length trajectory and activity patterns and their implications for power modulation.

In order to meet the varying demands of flight, pectoralis muscle power output must be modulated. In birds with pectoralis muscles with a homogeneous fibre type composition, power output can be modulated at the level of the motor unit (via changes in muscle length trajectory and the pattern of activation), at the level of the muscle (via changes in the number of motor units recruited), and at the level of the whole animal (through the use of intermittent flight). Pectoralis muscle length trajectory and activity patterns were measured in vivo in the cockatiel (Nymphicus hollandicus) at a range of flight speeds (0-16 m s(-1)) using sonomicrometry and electromyography. The work loop technique was used to measure the mechanical power output of a bundle of fascicles isolated from the pectoralis muscle during simulated in vivo length change and activity patterns. The mechanical power-speed relationship was U-shaped, with a 2.97-fold variation in power output (40-120 W kg(-1)). In this species, modulation of neuromuscular activation is the primary strategy utilised to modulate pectoralis muscle power output. Maximum in vivo power output was 22% of the maximum isotonic power output (533 W kg(-1)) and was generated at a lower relative shortening velocity (0.28 V(max)) than the maximum power output during isotonic contractions (0.34 V(max)). It seems probable that the large pectoralis muscle strains result in a shift in the optimal relative shortening velocity in comparison with the optimum during isotonic contractions as a result of length-force effects.

Comparison between mechanical power requirements of flight estimated using an aerodynamic model and in vitro muscle performance in the cockatiel (Nymphicus hollandicus).

There have been few comparisons between the relationship between the mechanical power requirements of flight and flight speed obtained using different approaches. It is unclear whether differences in the power-speed relationships reported in the literature are due to the use of different techniques for determining flight power or due to inter-specific differences. Here we compare the power-speed relationships in cockatiels (Nymphicus hollandicus) determined using both an aerodynamic model and measurements of in vitro performance of bundles of pectoralis muscle fibres under simulated in vivo strain and activity patterns. Aerodynamic power was calculated using different ranges of values for the coefficients in the equations: induced power factor (k 1.0-1.4), the profile (C(D, pro) 0.01-0.03) and parasite drag (C(D, par) 0.05-0.195) coefficients. We found that the aerodynamic power-speed relationship was highly sensitive to the values assumed for these coefficients and best fit the power calculated from in vitro muscle performance when k=1.2, C(D, pro)=0.02 and C(D, par)=0.13.

The metabolic power requirements of flight and estimations of flight muscle efficiency in the cockatiel (Nymphicus hollandicus).

Little is known about how in vivo muscle efficiency, that is the ratio of mechanical and metabolic power, is affected by changes in locomotory tasks. One of the main problems with determining in vivo muscle efficiency is the large number of muscles generally used to produce mechanical power. Animal flight provides a unique model for determining muscle efficiency because only one muscle, the pectoralis muscle, produces nearly all of the mechanical power required for flight. In order to estimate in vivo flight muscle efficiency, we measured the metabolic cost of flight across a range of flight speeds (6-13 m s(-1)) using masked respirometry in the cockatiel (Nymphicus hollandicus) and compared it with measurements of mechanical power determined in the same wind tunnel. Similar to measurements of the mechanical power-speed relationship, the metabolic power-speed relationship had a U-shape, with a minimum at 10 m s(-1). Although the mechanical and metabolic power-speed relationships had similar minimum power speeds, the metabolic power requirements are not a simple multiple of the mechanical power requirements across a range of flight speeds. The pectoralis muscle efficiency (estimated from mechanical and metabolic power, basal metabolism and an assumed value for the 'postural costs' of flight) increased with flight speed and ranged from 6.9% to 11.2%. However, it is probable that previous estimates of the postural costs of flight have been too low and that the pectoralis muscle efficiency is higher.

A new monoclonal antibody DAG-6F4 against human alpha-dystroglycan reveals reduced core protein in some, but not all, dystroglycanopathy patients.

We generated a novel monoclonal antibody, DAG-6F4, against alpha-dystroglycan which immunolabels the sarcolemma in human muscle biopsies. Its seven amino-acid epitope, PNQRPEL, was identified using phage-displayed peptides and is located immediately after the highly-glycosylated mucin domain of alpha-dystroglycan. On Western blots of recombinant alpha-dystroglycan, epitope accessibility was reduced, but not entirely prevented, by glycosylation. DAG-6F4 immunolabelling was markedly reduced in muscle biopsies from Duchenne muscular dystrophy patients consistent with disruption of the dystroglycan complex. In a range of dystroglycanopathy patients with reduced/altered glycosylation, staining by DAG-6F4 was often less reduced than staining by IIH6 (antibody against the glycan epitope added by LARGE and commonly used to identify glycosylated alpha-dystroglycan). Whereas IIH6 was reduced in all patients, DAG-6F4 was hardly changed in a LARGE patient, less reduced than IIH6 in limb-girdle muscular dystrophy type 2I, but as reduced as IIH6 in some congenital muscular dystrophy patients. Although absence of the LARGE-dependent laminin-binding site appears not to affect alpha-dystroglycan stability at the sarcolemma, the results suggest that further reduction in aDG glycosylation may reduce its stability. These studies suggest that DAG-6F4 may be a useful addition to the antibody repertoire for evaluating the dystroglycan complex in neuromuscular disorders.