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The purpose of this study was to investigate the influence of the size of the active muscle mass on the cardiovascular response to static contraction. Twelve male subjects performed one-arm handgrip (HG), two-leg extension (LE), and a "dead-lift" maneuver (DL) in a randomly assigned order for 3 min at 30% of maximal voluntary contraction. O2 uptake (VO2), heart rate (HR), and mean intra-arterial blood pressure (MABP) were measured at rest and, in addition to absolute tension exerted, throughout contraction. There was a direct relationship between the size of the active muscle mass and the magnitude of the increases in VO2, HR, and MABP, even though all contractions were performed at the same relative intensity. Tension, VO2, HR, and MABP increased progressively from HG to LE to DL. It was concluded that at the same percentage of maximal voluntary contraction, the magnitude of the cardiovascular response to isometric exercise is directly influenced by the size of the contracting muscle mass.

Previous investigators have reported that oxygen consumption (VO2) continues to rise after the initial 2- to 3-min transient period of exercise when work exceeds approximately 60% of VO2 max. The purpose of this investigation was to examine the possible causes of this slow rise in VO2. Eighteen subjects exercised for 20 min at 65% and at 80% of VO2 max on the bicycle ergometer. VO2, ventilation (VE), and respiratory exchange ratio were monitored by a continuous computer-based system. Blood lactate concentration and rectal temperatures were measured at 2- to 3-min intervals during the exercise. VO2 increased significantly from the 5th to 20th min of exercise in 81% of the tests at both levels of work intensity. The magnitude of the rise was not different for the two work loads. No evidence was found to support the lactacid explanation proposed for this rise. Increased temperature could account for 30% of the rise; the estimated cost of increased VE could account for 30 and 81% of the rise at the two work loads. The sum of these factors could account for 60 and 111% of the rise in VO2 at the 65 and 80% of VO2 max work loads.

Experiments were performed to determine whether endurance time, mean arterial pressure, or heart rate was related to either muscle length or external torque production in humans during isometric knee extension. Eight men and nine women performed isometric knee extension to the endurance limit at each of three muscle lengths, determined by knee angles of 40 degrees (0.698 rad, shortest), 60 degrees (1.047 rad, intermediate), and 90 degrees (1.571 rad, longest), and at intensities of 30 and 50% maximal voluntary contraction (MVC). Knee extension forms an ascending-descending length-torque curve, and lengths were chosen to result in different external torques. MVC was greatest at a knee angle of 60 degrees (P < 0.05 vs. 40 degrees, 90 degrees), with no significant difference between 90 degrees and 40 degrees. Endurance time was inversely related to muscle length, independent of torque production, at 30% MVC [40 degrees, 395 +/- 139 (SE); 60 degrees, 237 +/- 60; 90 degrees, 165 +/- 51 s; P < 0.05 vs. each other] and 50% MVC (40 degrees, 176 +/- 64; 60 degrees, 137 +/- 40; 90 degrees, 85 +/- 23 s; P < 0.05 vs. each other). Evidence is presented that endurance is a function of internal muscle force and not resultant external torque. The experimental design allowed the relationship of external torque and cardiovascular responses to be examined independent of exercise intensity. Muscle mass was also controlled in that the same muscle group was involved in all contractions. There were no differences in mean arterial pressure, heart rate, or rating of perceived exertion at any percentage of endurance time under any condition.(ABSTRACT TRUNCATED AT 250 WORDS)

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