The purpose of this study was to determine whether the reflex hemodynamic responses to static contraction of predominately glycolytic muscle are greater than the changes elicited by primarily oxidative muscle. Low-frequency electrical stimulation (continuous 21 days) of the tibial nerve of one hindlimb of adult rabbits converted the metabolic characteristics of the predominately glycolytic gastrocnemius to a muscle that was primarily oxidative. After 21 days of stimulation, the rabbits were decerebrated, and static contraction of the glycolytic muscle (unstimulated gastrocnemius) initially decreased heart rate (HR; -16 +/- 3 beats/min) and mean arterial pressure (MAP; -17 +/- 3 mmHg). Thereafter, MAP increased 13 +/- 3 mmHg above baseline. Static contraction of the oxidative muscle (stimulated gastrocnemius) produced similar decreases in HR and MAP (-12 +/- 4 beats/min and -12 +/- 3 mmHg, respectively). However, the subsequent increase in MAP (8 +/- 3 mmHg; above baseline) was less than that evoked by contraction of the glycolytic muscle. The responses evoked by stretch of each muscle and high-intensity electrical stimulation were the same, indicating that the afferents from the muscle were not destroyed by the chronic-stimulation technique. These results support the hypothesis that metabolic by-products play a role in the pressor response to static contraction of skeletal muscle. In addition, these data confirm that contraction of predominately oxidative muscle can evoke a reflex pressor response, albeit smaller than the change elicited from primarily glycolytic muscle.
This study investigated the effect of age on peripheral factors involved in the systemic response to maximal exercise. Skeletal muscle was analyzed and regional blood flow distribution was determined at rest and during maximal exercise in senescent (old) and in younger mature (young) beagles. Maximal exercise capacity was significantly reduced (P less than 0.05) in old and was associated with a reduction in cardiac output (CO), as well as a tendency for arteriovenous O2 difference to be reduced, with a concomitant reduction in maximal O2 consumption. In each regional circulation evaluated, resting blood flow was similar in young and old. During exercise, blood flow was similar in young and old to the diaphragm, heart, tongue, and six of seven locomotory muscles. Concomitant blood flow reductions in splanchnic regions tended to be more pronounced in old than in young. Skeletal muscle analyses of triceps, semitendinosus, and gastrocnemius muscles disclosed similar percent fiber type distribution in young and old but a reduction in type II fiber area in old. In addition, both muscle capillary density and capillary-to-fiber ratio were reduced in old. These results demonstrate that age-related changes in blood flow distribution during maximal exercise enable skeletal muscle blood flow to be maintained in old, despite reductions in maximal CO and in muscle capillary density. However, this pattern of blood flow distribution only partially compensates for the combined effects of age-related changes in metabolic potential of the periphery, O2 content of arterial blood, and cardiac function during maximal exercise in old.
The relative contribution of increases in fiber area and number was evaluated in the chicken anterior latissimus dorsi (ALD) muscle in which enlargement was induced by hanging a weight on one wing. ALD muscles from wings to which weights had been attached for periods ranging from 6 to 65 days weighed an average of 105% (range 22-225%) more than control muscles. Total muscle fiber number, determined by direct counts after nitric acid digestion and fiber dissection, and the frequency of branched fibers were unchanged by muscular enlargement. Fiber cross-sectional area was greater (P less than 0.01) in the enlarged muscles. A close relationship existed (r = 0.78) between actual muscle weight and weight calculated as the product of fiber volume, total fiber number, and muscle density for the control and enlarged muscles. Histochemical staining revealed a conversion of type IIa to type I fibers in the stretched muscles. These results support the concept that skeletal muscle enlargement in response to chronic overload is produced by hypertrophy of preexisting fibers and not be a formation of new fibers.
A method is described for identifying fiber types of skeletal muscle from several mammalian species on the basis of the sequential inactivation of myofibrillar actomyosin ATPase during acid preincubation. When this method is used in combination with the standard alkaline preincubation at least 5 types of fibers can be identified. Of these, 2 are type I fibers with those of the slow twitch soleus muscle being different from those that exist in mixed muscles. The 3 subtypes of type II fibers exist independent of their metabolic properties. The need for careful standardization of histochemical methods for the visualization of myofibrillar actomyosin ATPase and the implication of the existence of different fiber types in apparently homogeneous muscle for the preparation of antibodies used for immunocytochemical methods of fiber identification are discussed.
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