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Body acceleration distribution and its relation to the mode of generation were determined in eight young males (19-26 yr) who walked and ran on a treadmill operated at four speeds and jumped on a trampoline at four heights. With increasing treadmill speed, peak acceleration at the ankle (Aa = 3.0-12.0 Gz) always exceeded that at the back and forehead (Ab = 0.9-5.0 Gz, and Ah = 0.8-3.9 Gz); these acceleration profiles included higher frequency components than those during jumping. Corresponding ranges of oxygen uptake (VO2) and heart rate (HR) were 0.8-3.0 l/min and 90-180 beats/min, respectively. With increasing jumping height, acceleration levels were more symmetrically distributed (Aa = 3.0-7.0 Gz, Ab = 3.9-6.0 Gz, and Ah = 3.0-5.6 Gz); VO2 and HR ranges were 1.1-2.5 l/min and 102-175 beats/min, respectively. VO2 was linearly related to HR for both types of exercise. The results indicate that, for similar levels of HR and VO2, the magnitude of the biomechanical stimuli is greater with jumping on a trampoline than with running, a finding that might help identify acceleration parameters needed for the design of remedial procedures to avert deconditioning in persons exposed to weightlessness.

Eight young men (group A) underwent 5 h of quiet sitting, preceded by 30 min of recumbency, 20 min of standing, and 20 s of walking, and five other young men (group B) underwent 70 min of sitting, preceded by recumbency only, to determine the effects of prolonged sitting and previous posture on hemodynamic responses (measured by impedance plethysmography). Group A showed more calf blood pooling and a decrease in thigh blood flow during sitting in comparison with the control group, but after 1 h of sitting hemodynamic responses of the two groups were similar. Sitting for 5 h (1st vs. 5th h) resulted in an increase in calf venous pooling (17%) and a decrease in calf BF (13%), a reduction in gravitational pooling in the thigh (corresponding to increased pooling in the calf), increases in diastolic and mean arterial pressures (6 and 7.3 mmHg, respectively), and minor changes in heart rate, stroke volume, and cardiac output. The results show that it is necessary to sit for 1 h before hemodynamic responses can be assessed in this position, regardless of the posture maintained previously. The main effect of prolonged sitting is pooling in the calf, which is compensated for by an increase in peripheral resistance.

Nine young men who had suffered from heatstroke on previous occasions (heat-intolerant subjects) and 10 young volunteers (control subjects) were examined to determine their physiologic responses to exercise in temperate (23 degrees C) and hot environments (40 degrees C). The tests included an orthostatic test, work loads of 40 W and 80 W, and oxygen consumption (Vo2) determination. Although all the control subjects completed the exercise under severe heat load (3 h), none of the heat-intolerant subjects succeeded in completing this test due to high rectal temperatures and high heart rates. Sweat rates were similar in both groups, with Vo2 slightly higher in the control subjects. Orthostatic responses were similar in each group. The results suggest that inefficient thermoregulation, possibly due to decreased heat conductance from core to periphery, contributes to heat intolerance in former heatstroke patients.

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Three groups of subjects (6 subj in each group) underwent the following precedures: group A was given a 20-min head-up tilt at 21 degrees C followed by 4 h of exercise at 33.9 degrees C DB, 32.2 degrees C WB, and a repetition of tilting after exercise in heat; group B underwent the same procedure at 21 degrees C; group C was tilted at 21 degrees C, rested in heat for 4 h and was retilted in heat. The above procedures were repeated for 8 days, and on the last day groups B and C underwent the same treatment as group A. Group A showed the usual decreases in heart rate and rectal temperature and an increase in sweat rate on acclimation. This corresponded to marked improvements in heat-orthostatism. While five subjects in group A fainted during post-exposure tilting on the first exposure, none fainted on the last day. Resting in heat (group C) did not cause any acclimation to work in heat. This corresponded to poor heat-orthostatism after the work-heat procedure when five subjects fainted. Mild training at 21 degrees C (group B) resulted in minor improvements to work in heat as evident by some improvements in heart rate responses after the 1st and 2nd h of exposure. This corresponded to better heat-orthostatism and fewer men fainting than in group C. The results indicated that heat-orthostatism improves on acclimation to the same extent as exercise heart rate and rectal temperature.