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In calculating the physical activity index (PAI) on the college alumnus questionnaire, it is assumed that 8 kcal are expended for every 20 steps climbed. This value is equal to an energy cost of 0.40 kcal.step-1. Since it is assumed that subjects climb and descend an equal number of stairs, the total value reflects the energy cost of stepping up (estimated at 0.30 kcal.step-1) and stepping down (estimated at 0.10 kcal.step-1). However, these values appear to be based on theoretical calculations rather than empirical observation. The purpose of this study was to quantify the energy cost of stair climbing and stair descending by measuring oxygen uptake. Twenty subjects performed continuous stair-climbing and stair-descending on an escalator at a stepping rate of 70 step.min-1. Heart rate was monitored by telemetry, and oxygen uptake was measured by the Douglas bag technique from 5 to 7 min. Results showed that the gross energy cost of stair climbing is 8.6 METs, and that of stair descending is 2.9 METs. Thus, for a 70-kg person the gross caloric costs of ascending stairs (0.15 kcal.step-1) and descending stairs (0.05 kcal.step-1) are one-half of the values previously assumed. In conclusion, the algorithm for calculating PAI on the college alumnus questionnaire should be modified to reflect a total cost of 0.20 kcal for going up and down one step. Even more precise estimates can be obtained by adjusting for body weight (going up and down one flight of stairs requires 1.63 MET.min).

The purpose of this study was to examine the effect of moderate resistance weight training (MRWT) on peak arm aerobic power as measured by arm cranking ergometry. Fourteen sedentary college age males, divided equally into two groups, served as subjects. The seven subjects in the MRWT group completed 12, 1-hr bouts of weight lifting over a 4 week period, exercising on Monday, Wednesday and Friday of each week. Exercise sessions included 3 sets of 10 repetitions of the following lifts: bench press, overhead dumbbell press, dumbbell arm curl, and behind the neck pull down. The remaining seven subjects served as a non-training control group, whose purpose was to account for possible learning effects on the arm ergometer test that could distort the statistical relevance of the aerobic power data. These subjects did not serve as a control for the weight training exercises, as the procedures used to determine muscular strength may produce a modest training effect. Peak arm aerobic power and muscular strength, as measured by the one-repetition maximum for each lift, were determined before and after the training program. The average increase in strength for all lifts combined for the trained group was 20.0%. They also experienced a 13.4% (p < .005) increase in peak arm aerobic power, whereas there was no significant change in this variable for the control group. It is concluded that peak arm aerobic power is enhanced by the changes in muscular strength produced by 4 wks of MRWT.

We examined the metabolic responses to front crawl swimming when following directly behind (drafting) another swimmer. Seven trained male swimmers participated as subjects. VO2max (l.min-1) was measured during a progressive tethered swim test and was also estimated from a 20 s sample of expired air collected immediately after an all-out, 549 m (600 yard) swim. On different days, each subject performed two 549 m trials at 95% of his maximal swim velocity, one with drafting and one without drafting, using a counter-balanced design. Underwater pace lights were used to establish the predetermined swim velocity. Drafting significantly reduced post-exercise VO2 (2.85 +/- 0.63 vs 3.12 +/- 0.66 l.min-1), blood lactate (3.4 +/- 0.6 vs 5.0 +/- 0.5 mM), and rating of perceived exertion (11.7 +/- 0.4 vs 14.9 +/- 0.5) (P less than 0.05). A repeated measures ANOVA (condition X distance) also revealed significant reductions in HR during the 549 m swim (137.7 vs 146.8 beats.min-1) (P less than 0.05). The results indicate that drafting results in a decrease in energy expenditure for the range of speeds examined.

This study has shown, for the first time, that the change in plasma adenosine 3',5' cyclic monophosphate (cAMP), from accommodation or trough levels, correlates highly in both progressive and continuous work stress experiments with epinephrine (E) at 0.990 and 0.898, and norepinephrine (NE) at 0.954 and 0.927, respectively, in men subjected to the same relative, rather than absolute, stress levels. All three analytes increased significantly (p less than 0.05) by the time each subject had reached 80% of their Vo2 max in the progressive experiments and after working at 80% of their Vo2 max continuously for 10 min. In no case did plasma cAMP rise before the catecholamines. The possible significance of these observations to net perceived relative physiological stress are discussed.

Plasma catecholamines (Ca) increase over time during prolonged exercise at a constant work rate. Possible reasons for this include hypoglycemia, dehydration, increased perceived exertion, and rising body temperature. In an effort to ascertain the contribution of elevated core temperature on the plasma Ca response to prolonged exercise four trained men were studied under two thermal conditions during 45 min of bicycle exercise (approximately 60% Vo2max) and during passive heating. On one testing day each subject was heat-stressed during exercise wearing a nylon pullover shell and cotton pants, (heat stress treatment); on the second day fans were directed on the subjects exercising in a thermoneutral environment (fan treatment). The passive heating experiment was conducted in a hot water bath (41 degrees C). The exercise heat stress treatment produced a higher plasma norepinephrine (NE) concentration (P less than 0.05) in all subjects than the fan treatment. The plasma epinephrine (E) concentration was not significantly (P greater than 0.05) different during exercise in the heat stress treatment from that found during fan treatment. A rise in rectal temperature (Tre) during passive heating resulted in quantitatively small changes in plasma E and NE. The heat load combined with the exercise task produced an increase in plasma NE concentration greater than the sum of the values measured during exercise in the thermoneutral environment and passive heating. This suggested that the combination of stressors caused an augmentation of the sympathetic nervous system's response. Finally, the added heat load caused changes in plasma NE and little change in plasma E, suggesting a differential Ca response with heat stress.

Anticipation of a potentially stressful situation can alter the activity of the sympathetic nervous system. The purpose of this study was to measure the effect of three different intensities of exercise on epinephrine (E) and norepinephrine (NE) excretion when the work test order was randomly assigned and the subjects were not informed of the test order. Six subjects exercised at work loads which averaged 49%, 65%, and 82% Vo2max. Each subject showed an increased rate of NE excretion as the work load increased. The differences among work loads were significant (P less than 0.01). The E response was less consistent. Two subjects showed the greatest rate of excretion at the lowest work load, and one subject showed no increase above his pre-exercise resting value. While NE excretion was closely related to the work load, factors other than exercise appeared to exert considerable influence on the rate of E excretion during exercise.

The purpose of this study was to investigate the relationship between hypoxia and heart rate (HR), pulmonary ventilation, plasma epinephrine (E) and norepinephrine (NE) at rest and during exercise at 40% of maximal oxygen uptake. Six subjects were exposed to inspired gas mixtures containing 21%, 19%, 17%, 15%, and 13% O2. The duration of exposure to each mixture was 10 continuous min at rest, followed by 10 continuous min during exercise. The order of the inspired gas mixtures was randomized. During the exercise test, HR was elevated with exposure to 15% and 13% O2 (p less than 0.001). Pulmonary ventilation was higher at 13% O2 than at the higher O2 percents (p less than 0.001). There were no significant changes in plasma E or NE at rest or during exercise in response to the gas treatments. These results indicate that acute exposure to hypoxic gas mixtures at rest and during light work does not result in significant increases in sympathetic nervous system activity, as judged by the plasma E and NE response.

Twelve males (six moderate drinkers and six abstainers) were studied for the influence of varying dosages of alcohol on cardiorespiratory function and work performance. The subjects underwent three separate maximal exercise tests which consisted of progressive workloads on the bicycle ergometer. Prior to each work bout the subject consumed either a placebo (0.0 ml.kg-1), small (0.44 ml.kg-1), or a moderate (0.88 ml.kg-1) dose of a 95 per cent ethanol solution. Analysis of the results indicated that the ingestion of a small or moderate amount of alcohol had no significant effect on heart rate, blood pressure, ventilation, oxygen uptake or work performance.

The use of inspired gas mixtures with an oxygen fraction in excess of 0.3 has been associated with a decrease in the gas exchange ratio (R) during prolonged work in humans. It had been hypothesized that the lower R was due to a lower plasma catecholamine concentration caused by the hyperoxia (Med. Sci. Sports 10: 167-170, 1978). We tested this hypothesis by measuring changes in plasma epinephrine and norepinephrine when the subjects were switched from breathing air to 60% O2 (and vice versa) during 40 min of cycle ergometer exercise at 67% maximal oxygen uptake (VO2max). The subject breathed one gas mixture for the first 30 min and was switched to the other in the last 10 min. The order was reversed in the second test. The switch in gas mixtures from air to 60% O2 resulted in a significant reduction in R, heart rate, minute ventilation, blood lactate concentration, and plasma epinephrine concentration (P less than 0.05). The plasma norepinephrine concentration (0.1 greater than P greater than 0.05) and the plasma free fatty acid concentration were not significantly changed. Although the direction of the epinephrine change was consistent with the change in R, the epinephrine change was quantitatively small (20 pg/ml) and of questionable physiological significance. This suggests a direct effect of PO2 on cellular metabolism as one cause of the change in R when the subjects were switched from air to 60% O2.

This study was undertaken to examine the relationship between energy expenditure and work rate on a bicycle ergometer in five sprinters and five distance runners who differed in maximal oxygen uptake (VO2max) and type of training. Each subject performed at work rates of 30, 60, 90, 120, and 150 watts (W). The relationship between energy expenditure and work rates was most accurately described by a quadratic curve for both groups: for sprinters, energy expenditure (kJ) = 11.57 + 0.1812 (W) + 0.00046 (W)2; for distance runners, energy expenditure (kJ) = 11.74 + 0.1386 (W) + 0.00060 (W)2. Delta efficiency (delta work accomplished divided by delta energy expended X 100%) decreased as work rate increased. Statistical analyses revealed no significant differences between groups in delta efficiency at the same work rate (P greater than 0.25) or at the same relative work rate (P greater than 0.75). These results suggest that differences in VO2max and/or type of training have little or no causal effect on the decrease in delta efficiency with increasing work rate. The observed decrease in delta efficiency may be due to increases in metabolism not directly related to the performance of the external work or to an increasing amount of unmeasured work as work rate increases on a bicycle ergometer.