Use of exercise as a relaxation technique.
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Biomedical subjects
Publications and source records attributed to D H Horstman.
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The purpose of this study was to compare perceptual responses (RPE) and selected physiological measures during both short term and prolonged exercise of equal relative intensities at 4300 m to those at sea level. Specifically, we compared results obtained (n=20) for 6 min of exercise at 60, 80 and 95% VO2max and at 5 min intervals during exercise to exhaustion at 85% VO2max. At 4300 m, VO2max was reduced 19%, while VEmax and Rmax increased 17 and 8%, respectively. HRmax and RPEmax was unchanged. For any given relative exercise intensity, VO2 and absolute exercise intensity (kpm-min-1) were reduced, while VE was about 12% and R about 7% greater at 4300 m; HR was unchanged. At 4300 m, RPE at the lower intensities of submaximal exercise and early during prolonged exercise were significantly less than at sea level. These differences were reduced and finally eliminated as exercise intensity increased toward maximal or as prolonged exercise continued to exhaustion. Endurance time to exhaustion at 4300 m was not different from that at sea level. To account for the perceptual differences between exercise at 4300 m an sea level, we proposed that local factors (muscular strain) exert greater influence on the perception of effort at exercise intensities which do not greatly stress ventilation and circulation, while central factors exert greater influence on the perception of effort at exercise intensities at which tachypnea and tachycardia are of sufficient magnitude to be perceived as extremely stressful.
There is disagreement in the literature as to whether responsivity to painful stimuli possesses psychometric correlates. A series of methodological and statistical factors are specified in this paper which could account for the equivocality of the literature. A series of experiments were performed in which (a) various methodological and statistical issues were first resolved and (b) psychometric correlates of pain perception were then identified by means of a stepwise multiple regression procedure. The criterion variable consisted of the psychophysical judgment of pain during a 2-min. exposure to a 3,000 gm. force on the periosteum of the left fore-finger's second digit. The predictor variables consisted of selected psychological states and traits measured by the State-Trait Anxiety Inventory, Somatic Perception Questionnaire, Depression Adjective Checklist, Profile of Mood States, Eysenck Personality Inventory, and the Embedded Figures Test. The test-retest reliability of the pain test ranged from .64 to .84 across trials separated by a 3-wk. period. In the first experiment significant multiple regressions ranging between .57 and .72 were observed and psychological traits (field dependence, extraversion and trait anxiety) accounted for the variance in these analyses. In the next experiment significant multiple Rs ranging from .62 to .68 were observed. This served as cross-validation for the first experiment. The major difference was that psychological states (depression and vigor) as well as traits entered the multiple regression equations for certain of the analyses. It was concluded that selected psychological states and traits are significantly correlated with the perception of pain.
To identify components of reduced core temperature (Tre) with exposure to hypoxia, oxygen uptake (VO2) and skin temperatures were measured in chair-restrained squirrel monkeys during conditions of 21% O2, 11% O2, and 11% O2 + 5% CO2. Exposure to 11% O2 resulted in a 20% decrease in VO2 and a 1.8 degrees C reduction of Tre with skin temperatures closely paralleling Tre. The addition of 5% CO2 to 11% O2 effectively blocked the decrease of both VO2 and Tre. The responses of one monkey (LD) exhibiting decreased Tre (greater than 2.0 degrees C) and 20% decrease in VO2 were compared to those of another (SD) exhibiting decreased Tre (less than 0.5 degrees C) and little change of VO2 under the same experimental conditions. Increased mean arterial blood pressure (BPa) and heart rate (HR) occurred for monkey SD, while for monkey LD BPa decreased and HR increased slightly. Arterial pressure of oxygen (PaO2) and calculated arterial saturation of oxygen (SaO2) were higher, while PaCO2 was lower for monkey SD than for monkey LD. When 5% CO2 was added to 11% O2 both animals exhibited decreased PaO2, little change of Tre, VO2, PaCO2, arterial pH, and calculated SaO2, and increased BPa and HR. These data suggest that decreased Tre resulted from reduced heat production and reduced oxygen transport was primarily responsible for reduction of heat production.
Normal acid-base status of arterial blood (pHa =7.40, PaCO2=38.1 Torr) was demonstrated for conscious, restrained squirrel monkeys when environmental stimuli were minimized and monkeys are habituated to experimental procedures. These results indicate the potential for using squirrel monkeys in experiments in which normal acid-base status is a significant factor.
Maximal oxygen consumption (VO2 max) and muscle blood flow (Q max) were measured in an isolated gracilis muscle preparation before and after alteration in perfusion pressure (BP), arterial oxygen saturation (SaO2), and hemoglobin concentration (Hb). Q varied directly with BP and inversely with Hb (viscosity) but was unaffected by changes in arterial SaO2. VO2 max varied directly with oxygen delivery under all conditions. These results indicate that VO2 max is normally limited by oxygen delivery rather than any intrinsic limiting of oxygen consumption of the muscle.
Treatment by 4 d of residence at 1600 m plus the administration of 500 mg acetazolamide b.i.d. for the last 2 d at 1600 m and the first 2 d at 4300 m was compared with no treatment prior to ascent to 4300 m for prophylaxis of acute mountain sickness. The treatment successfully prevented almost all symptoms of acute mountain sickness. It had no effect on the diminished capacity for maximal or prolonged heavy physical work. The treatment produced a relative acidosis and a comparatively greater arterial oxygen tension at 4300 m.
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Recent evidence suggests that prolonged exposures of exercising men to 0.08 ppm ozone (O3) result in significant decrements in lung function, induction of respiratory symptoms, and increases in nonspecific airway reactivity. The purpose of this study was to confirm or refute these findings by exposing 38 healthy young men to 0.08 ppm O3 for 6.6 h. During exposure, subjects performed exercise for a total of 5 h, which required a minute ventilation of 40 l/min. Significant O3-induced decrements were observed for forced vital capacity (FVC, -0.25 l), forced expiratory volume in 1 s (FEV1.0, -0.35 l), and mean expiratory flow rate between 25% and 75% of FVC (FEF25-75, -0.57 l/s), and significant increases were observed in airway reactivity (35%), specific airway resistance (0.77 cm H2O/s), and respiratory symptoms. These results essentially confirm previous findings. A large range in individual responses was noted (e.g., percentage change in FEV1.0; 4% increase to 38% decrease). Responses also appeared to be nonlinear in time under these experimental conditions.
Indices of red blood cell (RBC) antioxidant capacity can undergo changes upon exposure to oxidants, either acutely or chronically. To investigate whether these changes might provide a biochemical marker for acute environmental ozone exposure, we assessed RBC glutathione (GSH) and catalase (CAT) responses in seven normal volunteers exposed to 0.16 ppm ozone for 7.5 hours compared to the same measurements following sham exposure to clean air. For each subject, an interim period of two weeks separated the two exposure studies. Investigators performing the RBC assays were unaware of the environmental conditions. No changes in either GSH or CAT were observed for any study condition when compared to pre-study values. Our conclusion is that RBC antioxidants do not accurately reflect in vivo exposure to ozone at concentrations readily attainable during periods of heavy urban pollution. Our data dispute the value of these indices as markers of acute environmental photochemical oxidant exposure.
To determine if asthmatic subjects (ASTH, n = 17) experience greater O3-induced pulmonary decrements than nonasthmatic subjects (NONA, n = 13), both groups were exposed for 7.6 h to both clean air and 0.16 ppm O3. Exposures consisted of seven 50-min periods of light exercise (VE = 14.2 and 15.3 l/min/m2 for ASTH and NONA, respectively), each followed by 10 min rest. A 35-min lunch period followed the third exercise. Following O3 exposure, decrements in forced expiratory volume in one second (FEV1) and FEV1 divided by forced vital capacity (FVC), corrected for air exposure, for ASTH (-19.4 +/- 3.1% and -6.2 +/- 2%, respectively) were significantly greater (p = 0.04 and 0.02) than for NONA (-9.8 +/- 1.9% and -1 +/- 1%, respectively). There was no difference (p = 0.33) for decrements in FVC between ASTH (-11.8 +/- 1.9%) and NONA (-8.8 +/- 2.1%). Nine of 17 ASTH experienced wheezing with O3, while only one experienced wheezing with air (p = 0.004); no NONA experienced wheezing. Six of 17 ASTH requested inhaled beta-agonist bronchodilator prior to and/or during O3 exposure and experienced some temporary alleviation of decrements. At end exposure, however, ASTH who were medicated had greater O3-induced decrements than those who were not medicated. ASTH who had the larger O3-induced decrements had lower baseline FEV1/FVC and lower baseline %predicted FEV1. These data indicate that in ASTH, unlike NONA, some portion of O3-induced pulmonary decrements experienced was related to bronchoconstriction, and that O3-responsiveness for ASTH depended upon baseline airway status.