Changes of architecture of adult rat gastrocnemius medialis muscle (GM) due to growth were studied in relation to length-force characteristics. Myofilament lengths were unchanged, indicating constant sarcomere length-force characteristics. Number of sarcomeres within fibers was unchanged as a consequence of growth, allowing persistence of differences between proximal and distal fibers in all age groups. Distal fiber length at muscle optimum length was shorter for the 14- than for the 10- and 16-week age groups despite a lack of difference of number of sarcomeres. This is indicative of a shift of optimum length. Some evidence for the occurrence of distribution of fiber optimum lengths with respect to muscle optimum length was found in other age groups as well, albeit of a smaller magnitude. Muscle and aponeurosis length increased substantially with growth. Functional effects of increased aponeurosis lengths were increased contributions to muscle length changes by the aponeurosis, allowing smaller fiber contributions in older animals. Fiber angle increased approximately 5 degrees with growth. Despite the differences of architecture indicated above, muscle length range between optimum length and active slack length was constant. This was probably caused by widening of this length range in the youngest age group by variations of architecture within the muscle. It is concluded that adaptation of aspects of muscle architecture is an important mechanism for adult muscle growth in rat GM. Of these aspects regulation of muscle length seems a dominant factor.

The effects of growth and limb immobilization on muscle mass, total physiological cross-section (PC), the number of sarcomeres in series and the length of sarcomere components were investigated in the soleus muscle (SOL) and compared to previously obtained data on gastrocnemius (GM) muscles of rats between age 10 and 16 weeks. For SOL this period of growth was reflected in an increased muscle mass and PC. No such increases were found for GM. In contrast, immobilization caused severe atrophy of fibres of both muscles. Compared to the value at the start of the immobilization, it was found that the fast twitch muscle (GM) atrophied more than the typically slow twitch one (SOL). The number of sarcomeres in series within fibres increased after growth and decreased after immobilization of SOL. For fibres of GM no such changes were observed. Muscle architecture is proposed as an important factor for the explanation of the results concerning the number of sarcomeres in series and those arranged in parallel. Due to the difference in muscle architecture, GM being more pennate than SOL, during growth, it is thought that increases in bone length affect the length of fibres of SOL more than those of GM. During immobilization, atrophy of fibres of GM was sufficient for the muscle length adaptation to meet the muscle length change induced by immobilization but in SOL, atrophy had to be accompanied by decreases in the number of sarcomeres in series to achieve adequate muscle length adaptation.

The geometry of rat gastrocnemius medialis muscle (GM) was studied at different muscle lengths. In addition, the number of sarcomeres in series within fibres was estimated. For muscles of immobilized legs (i.e. GM was held at in vivo smallest length) as well as those of the contralateral legs, comparison was made with controls of similar age. Immobilization periods of 4 and 6 weeks were used. For immobilized GM muscles, the number of sarcomeres in series was lower only within distal fibres after 4 weeks of immobilization. Aponeuroses were 25% shorter after both immobilization periods and no differences were found for fibre and aponeurosis angle. For GM of contralateral legs no difference with respect to controls was found regarding the number of sarcomeres in series. Aponeuroses were approximately 15% shorter and the fibre and the aponeurosis angle were also smaller. Based on these geometrical differences, it was expected that both experimental muscles should exert force over a smaller range of muscle length than controls. However, for immobilized muscles a similar range of length was found for which a possible explanation could be the more compliant aponeurosis. For contralateral muscle a 2-mm larger length range as well as a change of distribution of optimal fibre length with respect to optimal muscle length was found. For immobilized muscles indications of a distribution of optimal fibre lengths were also found but these did not differ from those of the controls. The results for contralateral muscles would indicate that the distribution may be changed under the influence of an altered use of the limb and that this may be an important factor determining the length range of active force generation.

Increased cardiac perfusion results in increased oxygen consumption (VO2) and increased contractility (Gregg phenomenon) in the isolated heart. We investigated whether these two aspects of the Gregg phenomenon are related to coronary flow or arterial pressure. Coronary flow and, thus, arterial pressure were changed in the reference state and during vasoconstriction (3 nM vasopressin) in the Langendorff-perfused rat heart contracting isovolumically (ventricular balloon) at 27 degrees C (n = 5). All hearts showed an increase in developed isovolumic left ventricular pressure (measure of contractility) and in VO2 with increased perfusion. Developed left ventricular pressure depended primarily on arterial pressure, so its relationship with coronary flow was shifted by vasoconstriction. Conversely, VO2 primarily depended on coronary flow, so its relationship with arterial pressure was shifted with vasoconstriction. By use of vasoconstriction (decreased vascular radii), the effects of arterial pressure and wall shear stress (proportional to arterial pressure x radius) should be separable, but the results did not reach significance. Thus contractility is related to arterial pressure or shear stress, whereas VO2 is related to coronary flow. We conclude that the two aspects of the Gregg phenomenon are based on different mechanisms.

The perfusion-induced increase in cardiac contractility (Gregg phenomenon) is especially found in heart preparations that lack adequate coronary autoregulation and thus protection of changes in capillary pressure. We determined in the isolated perfused papillary muscle of the rat whether cardiac muscle contractility is related to capillary perfusion. Oxygen availability of this muscle is independent of internal perfusion, and perfusion may be varied or even stopped without loss of function. Muscles contracted isometrically at 27°C ( n = 7). During the control state stepwise increases in perfusion pressure resulted in all muscles in a significant increase in active tension. Muscle diameter always increased with increased perfusion pressure, but muscle segment length was unaffected. Capillary perfusion was then obstructed by plastic microspheres (15 μm). Flow, at a perfusion pressure of 66.6 ± 26.2 cmH2O, reduced from 17.6 ± 5.4 μl/min in the control state to 3.2 ± 1.3 μl/min after microspheres. Active tension developed by the muscle in the unperfused condition before microspheres and after microspheres did not differ significantly (−12.8 ± 29.4% change). After microspheres similar perfusion pressure steps as in control never resulted in an increase in active tension. Even at the two highest perfusion pressures (89.1 ± 28.4 and 106.5 ± 31.7 cmH2O) that were applied a significant decrease in active tension was found. We conclude that the Gregg phenomenon is related to capillary perfusion.