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Guinea pig hindlimbs were unilaterally immobilized at resting length to evaluate histochemical, biochemical, and contractile properties of immobilized muscle. Contralateral limbs remained unrestrained. Four weeks later contractile properties were measured under chloral hydrate anesthesia. Average time-to-peak tension of the immobilized soleus was 30% less, whereas that of the gastrocnemius was not significantly changed relative to contralateral muscles. Immobilized soleus muscles acquired as much as 25% fibers with high alkaline myofibrillar adenosine triphosphatase activity; these fibers do not occur in the normal muscle. Neither the immobilized soleus nor gastrocnemius fatigued more quickly than their contralateral counterparts. In the immobilized gastrocnemius myofibrillar protein (mg/g muscle) decreased to 76% and maximum tetanic tension to 70% of contralateral values. However, tetanic tension per gram wet muscle weight or 100 mg myofibrillar protein was significantly greater in the immobilized gastrocnemius. No specific factor responsible for the increased tetanic tension could be identified.

Various studies have indicated that human muscles in-vivo manifest a substantially similar, if not the identical force-velocity relationship established for isolated, maximally stimulated animal muscles. In the present study, fifteen healthy males and females, 18 to 38 years old and representing varied activity patterns from sedentary to athletic, performed maximal dynamic knee extensions on an isokinetic loading dynamometer. Maximal torque forces attained at a specific point in the range (30 degrees before full extension) and at seven loading velocities from 0 (isometric) to 288 degrees/sec were recorded. The maximum 30 degrees torques exhibited by the various subjects ranged from 29 to 245 Newton-meters. However, over the four lower test velocities (0, 48, 96 & 144 degrees/sec), all subjects exhibited less than a 15% deviation from their respective maximum 30 degrees torque values, which occurred most often at the 96 degree/sec test velocity. Maximal instantaneous power output at the 30 degree position ranged from 98 to 680 Watts. In all 15 subjects this was attained at and remained generally constant over the three highest test velocities (192 to 288 degrees/sec). A neural mechanism that restricts a muscle's maximal tension in-vivo is postulated as being responsible for the marked difference between the force-velocity relationship found for human muscles in-vivo and that exhibited by isolated animal muscles.

The maximum tetanic tension (Po) generated by a skeletal muscle is determined by its functional cross-sectional area (CSA) and its specific tension (tension/CSA). Measurements of average fiber length (normalized to a sarcomere length of 2.2 micron), muscle mass, and approximate angle of pinnation of muscle fibers within a muscle were taken from 26 different guinea pig hindlimb muscles and were used to calculate CSA. The specific tension was assumed to be 22.5 N X cm-2 and was used to determine the estimated Po of each muscle studied. In a second group of guinea pigs the in situ Po of 11 selected hindlimb muscles and muscle groups were determined. Estimated and measured Po values were found to have a strong linear relationship (r = 0.99) for muscle and muscle groups tested. The specific tension of the soleus, a homogeneously slow-twitch muscle, was shown to be approximately 15.4 N X cm-2 (P less than 0.01). Therefore, in our hands a specific tension value of 22.5 N X cm-2 appears to be a reasonable value for all mixed muscles studied in the guinea pig hindlimb and can be used to estimate their Po.

The architectural features of the major knee extensors and flexors and ankle plantar flexors and dorsiflexors were determined in three human cadavers. There was marked uniformity of fiber length throughout a given muscle and a trend toward similar fiber lengths within muscles of a synergistic group. Muscle length/fiber length ratios were remarkably similar for all three limbs. Angles of fiber pinnation were relatively small (0 degree-15 degrees) and generally consistent throughout the muscle. From these architectural data, the performance of a muscle was studied with respect to its tension production and velocity of shortening potentials. The tension is a function of the number of sarcomeres in parallel, and the velocity of shortening is a function of the number of sarcomeres in series. Muscles were grouped according to whether they showed a predilection for tension or velocity of shortening.

Iron-deficiency anemia leads directly to both reduced hemoglobin levels and work performance in humans and experimental animals. In an attempt to observe a direct link between work performance and insufficient iron at the cellular level, we produced severe iron deficiency in female weanling Sprague-Dawley rats following five weeks on a low-iron diet. Deficient rats were compared with normal animals to observe major changes in hematological parameters, body weight, and growth of certain organs and tissues. The overall growth of iron-deficient animals was approximately 50% of normal. The ratio of organ weight: body weight increased in heart, liver, spleen, kidney, brain, and soleus muscle in response to iron deficiency. Further, mitochondria from heart and red muscle retained their iron more effectively under the stress of iron deficiency than mitochondria from liver and spleen.Metabolism of iron in normal and depleted tissue was measured using tracer amounts of(59)Fe administered orally. As expected, there was greater uptake of tracer iron by iron-deficient animals. The major organ of iron accumulation was the spleen, but significant amounts of isotope were also localized in heart and brain. In all muscle tissue examined the(59)Fe preferentially entered the mitochondria. Enhanced mitochondrial uptake of iron prior to any detectable change in the hemoglobin level in experimental animals may be indicative of nonhemoglobin related biochemical changes and/or decrements in work capacity.