A comparison of the oxygen drift in downhill vs. level running KIM
C. WESTERLIND,
Department
WILLIAM
C. BYRNES,
WILLIAMC. BYRNES,ANDROBERTS. of the oxygen drift in downhill vs. level running. J. Appl. Physiol. 72(2): 796~800,1992.-This investigation explored the recent theory that muscle damage causes the drift in oxygen consumption (VO& during low-intensity downhill running. Seven subjects participated in a maximal VO, (To2 max) test and three submaximal bouts [one level (Level) and two downhill runs (Down 1, Down 2) at 40% peak VO,]. Two downhill runs (30 min at -10% grade) were performed to vary the extent of muscle damage. Creatine kinase (CK) increased more after Down 1 (61%) than after Down 2 (ll%), as did soreness ratings, indicating reduced muscle damage during Down 2. Significantly greater increases in vo2 over time were noted for Down 1 (15.6%) and Down 2 (14.7%) than for Level (1.2%). Heart rate increased 8 beats/min for Level but 29 and 25 beats/min for Down 1 and Down 2, respectively. Expired ventilation increased more for Down 1 (20.5%) and Down 2 (24%) than for Level (3.5%). Rectal temperature increased --023°C for all bouts. Because the magnitude of the drift was similar in the two downhill bouts, the findings suggest that muscle damage does not cause the drift in To2 during lowintensity downhill running. WESTERLIND,
KIMC.,
MAZZEO.A comparison
eccentric;
creatine
AND
ROBERT
S. MAZZEO
of Kinesiology, University of Colorado, Boulder, Colorado 80309
kinase; muscle damage;
muscle soreness
10% increase in VO, that was associated with an increase in muscle electromyography, evidence of increased motor unit recruitment. Although their findings suggest that muscle damage was contributing to the drift in VO,, it would appear important to evaluate the VO, response to a second bout of downhill running in which muscle damage would be significantly reduced. This repeated bout effect, in regard to muscle damage, has been well documented in the animal model (28,29) and in humans (9). If the drift in Vo2 were significantly reduced during a second downhill bout, the muscle damage-oxygen drift hypothesis would be more conclusively supported. The primary purpose of the present investigation was to evaluate the hypothesis that muscle fiber damage is the cause of the increase in Vo2 during low-intensity downhill running by incorporation of a second downhill run in the experimental design. In addition, this study examined heart rate, ventilation, rectal temperature, and blood lactate, factors that have previously been associated with the drift in VO, during higher-intensity concentric exercise (7, 14, l&18,34) but had not been measured by Dick and Cavanaugh (8) in their analysis of the drift in Vo2 during downhill running.
RECENTLY it has been noted that there is an increase in
METHODS
oxygen consumption (VO,) with low-intensity downhill running (8). Muscle contractions during this form of exercise are predominantly eccentric in nature, i.e., they involve the muscle lengthening against gravity (4,8,27). This upward drift in irO, has been noted at exercise intensities of 3550% of maximal vo2 (VO, m,) (6,8), levels that would not incur an increase in energy expenditure had the exercise involved predominantly concentric muscle contractions, such as with level running. It is well known that during low-intensity level running, the body initially responds with an increase in heart rate, ventilation, VO,, and other physiological parameters, followed by the attainment of a steady state within 2 or 3 min (2). The steady state is characterized by a plateau in these responses as the exercise duration continues. Dick and Cavanaugh (8) have proposed that an upward drift in VO, during low-intensity downhill running is related to the skeletal muscle damage that occurs with this form of exercise (8). These authors suggested that, with muscle damage, certain skeletal muscle fibers are no longer able to generate sufficient force and that additional motor units must be recruited to maintain a given level of work. The damaged fibers, however, continue to utilize oxygen, as do the newly recruited fibers, thus resulting in an increase in Vo2 (8). Their results showed a
Seven subjects (4 males, 3 females) were recruited from the University of Colorado’s student population to participate in this study. Subjects had not been involved in downhill running within the prior 6 mo. All were moderately active and engaged in activities such as running, aerobic dance, skiing, and cycling. Before participation, all volunteers read and signed an informed consent document approved by the University of Colorado Human Subjects Committee. Each subject participated in four exercise sessions in the following order: 1) a graded maximal exercise test to determine peak iTg, and exercise intensity levels for subsequent exercise sessions, 2) a level run for 30 min at 40% peak Vo2, 3) an initial downhill run at -10% grade for 30 min at 40% peak Vo2, and 4) a second downhill run under conditions identical to the first downhill bout. The second downhill bout was performed to evaluate the VO, response during an eccentric exercise session in which muscle damage is reduced or does not occur. Research indicates that a single eccentric bout has a prophylactic effect on a second bout that, in regard to muscle damage, can last as long as 6 wk (4). This reduction in skeletal muscle damage has been demonstrated directly by ultrastructural analysis (28,29) and indirectly by evidence of reduced serum creatine kinase activity (16, 20)
796
0161-7567/92
$2.00
Copyright 0 1992 the American Physiological
Society
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
OXYGEN
DRIFT
IN
DOWNHILL
and muscle soreness (10) after the second eccentric bout. One week separated the maximal exercise test from the level run and the level run from the first downhill bout. Two weeks separated the two downhill runs. Downhill running was chosen because of the predominantly eccentric muscular contractions involved in this type of exercise (30). During the maximal graded-exercise test, subjects ran at a comfortable pace on a motorized treadmill. The grade of the treadmill was increased 2.5% every 2 min until volitional exhaustion. Verbal encouragement was provided to elicit a maximal effort from subjects. Two of the three following criteria constituted attainment of peak 60,: a respiratory exchange ratio d.15, attainment of age-predicted maximal heart rate, and plateau of Vo2 despite an increase in work load. 00, was determined by a computer-assisted standard open-circuit indirect-calorimetry system. Expired gases were channeled through low-resistance tubing to a 5liter mixing chamber and directed to gas analyzers previously calibrated with three micro-Scholandered gases. The percentage of expired carbon dioxide was determined by use of a medical gas analyzer (Beckman LB2). The percentage of expired oxygen was determined with an Applied Electrochemistry analyzer (S-3A). Ventilation was determined by a pneumotachometer (Hans Rudolph) and a pressure transducer (Validyne). Before testing, the system was calibrated over a range of flow rates from 0 to 120 l/min with a 3-liter syringe. All information was processed by a computer (MINC-23, Digital). Values for VO, and expired ventilation (VE) were obtained every 30 s. Heart rate (HR) was monitored continuously with a modified V5 ECG lead. For the level and first downhill bout, the on-line opencircuit system provided TO, values every 30 s. The speed of the treadmill was adjusted until 40% of peak To2 was elicited continuously for 2 min. This required 5-7 min of adjustment and was considered the subjects’ warm-up period. After this criterion of 2 min was attained, the 30-min bout commenced. During the second downhill bout, subjects ran at the same pace as their first downhill bout but were allowed a similar 5-min warm-up period before beginning the 30-min exercise period. Speed was monitored with a digital tachometer (Biddle, Plymouth Meeting, PA). During the level and downhill runs, the following parameters were assessed: OO,, VE, HR, rectal temperature (T,), and blood lactate (LA). Perceived soreness and serum creatine kinase (CK) activity were assessed before and 24 h after each of the three exercise sessions. Methodologies for determining VpZ, TE, and HR were previously described. Values for VO, and VE are represented by an average of the 30-s values obtained every other minute during the exercise sessions. T, was assessed with a rectal thermistor inserted by the subject 12 cm past the anal sphincter. Temperature readings were obtained every 2 min with a telethermometer (Yellow Springs). Room temperature was recorded, and subjects were not allowed to participate in either downhill session on a day when ambient temperatures differed by >2OC of the temperature during the level run. LA was measured with the Stromm calorimetric method (32). Venous blood samples were obtained from a 20-gauge 2.5.in. plastic catheter inserted in a forearm
VS.
LEVEL
797
RUNNING
vein. Heparin-saline solution was used to keep the system patent. After a preexercise sample, blood samples were obtained every 5 min during the 30-min bouts. Samples were deproteinized in 10% trichloroacetic acid and centrifuged, and the supernatant was stored at -7OOC until analysis. All samples, standards, and controls were assayed in duplicate. All samples from one subject were assayed together to avoid interassay variability. The coefficient of variation for the LA assay was 8.2%. From the catheter, blood samples were obtained preexercise to determine serum CK activity. Standard venipuncture techniques were used to obtain blood samples 24 h after each of the three bouts to assess again for serum CK activity. Blood samples were allowed to clot and then were centrifuged to obtain serum. Samples were stored at -7OOC until analysis. Serum CK activity was determined by use of the calorimetric method of Szasz (Sigma Chemical) (33). Rate of change of absorbance was determined with a spectrophotometer (Perkin-Elmer) at 30°C. Samples, standards, and controls were assayed in duplicate. A coefficient of variation of 4.1% was obtained. CK activity was expressed in units per liter. Subjects subjectively rated muscle soreness before and 24 h after the level and downhill bouts. Soreness for different muscle groups was rated on a verbally anchored scale of 0 (no soreness) to 10 (very/very sore) (4). Repeated-measures analyses of variance with Greenhouse-Geiser correction factors were utilized to assess for statistical differences in vo2, VE, HR, T,, LA, and perceived soreness over time and among the three exercise bouts. A one-tailed paired t test was used to look at CK changes between the two downhill bouts. P = 0.05 was preset as the level necessary to achieve statistical significance for all analyses. RESULTS
Subjects were between the ages of 19 and 24 yr (mean 21.2 yr). Peak VO, values for female and male subjects were 44.2 t 1.3 and 57.0 t 3.1 (SD) ml kg-l. min-‘, respectively, a statistically significant (P < 0.05) difference. The male subjects were significantly heavier (74.4 t 13.7 kg) and taller (179.7 t 4.9 cm) than the female subjects (55.5 t 5.3 kg and 163.4 t 5.2 cm, respectively; P < 0.05). No significant gender differences were noted between bouts or over time for any of the dependent parameters assessed. The results were therefore presented in the aggregate. Subjects demonstrated significantly less of an increase in serum CK activity after the second than after the first downhill run (P < 0.05; Fig. 1). The changes corresponded to a mean increase of 11% 24 h after the second downhill bout vs. a 61% increase noted 24 h after the first. No change in CK activity was noted after the level run. Perceived soreness scores were also significantly lower (P < 0.05) 24 h after the second downhill bout (mean 1.1) than 24 h after the first (mean 4.3; Fig. 2). Repeated-measures analysis of variance indicated a significant increase in VO, over time (P < 0.01). Furthermore a significant interaction was noted between the three exercise bouts and time (P < 0.05). This interaction indicated that VO, changed differentially over time for the three bouts, i.e., the slopes were different. Further analysis indicated that the Oo, responses of the two l
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
798
OXYGEN h 2507 A K 2003
DRIFT
IN DOWNHILL
22
n PRE q POST
5r
50-
ii v)
0
RUNNING
1
p
DOWN1 DOWN
2
-
k 150> i= y IOO5 5
VS. LEVEL
LEVEL
I DOWNHILL
1 EXERCISE
I DOWNHILL BOUT
2
FIG. 1 Serum creatine kinase (CK) activity (means k SE) before and 24 h after two 30-min downhill running sessions. CK cha nge in downhill 2 significantly less (P < 0.05) than in downhill 1. l
I
I
”
”
1
0
”
”
I
5
”
”
I
10
”
”
I
15
”
”
20
I”“1
25
30
( min )
TIME
FIG. 3. Changes in mean oxygen consumption (VO,) in 7 subjects during 30-min level, downhill 1 (Down l), and downhill 2 (Down 2) exercise bouts. Time effect (P < 0.01) and bout-by-time i nteraction (P < 0.05) were both significant.
6 1
v
‘c
(3 5: z I t4K 3
n DOWNHILL 1 q DOWNHILL2
:
150 -m-
LEVEL
-
+
DOWN1
_
-f-
DOWN2
3:
iii! E20
: :
v) 1:
24 HOURS
I,,,,
POST
2. Perceived muscle soreness (means * SE) noted by 7 subjects 24 h after 2 downhill running bouts. Soreness significantly less (P -c 0.05) after downhill 2.
0
FIG.
downhill bouts were not different from each other but were significantly different from the level run. This analysis is depicted in Fig. 3. Time 0 is the 1st min of the 30-min bout after the initial warm-up period. No difference existed in VO, values at time 0. VO, increased 15.6% for the first downhill bout (from 18.83 t 0.91 to 21.77 t 1.40 ml kg-l min-l), 14.7% for the second downhill run (from 18.15 t 0.87 to 20.81 t 1.32 ml kg-‘. min-‘), and 1.2% for the level running exercise session (from 19.36 t 0.96 to 19.65 t 1.10 ml kg-’ min-I). Significant differences in HR were noted among the three bouts (P < 0.05). HR also increased significantly over time for the 30-min bouts (P < 0.05; Fig. 4). HR increased from 115 t 4.8 to 123 t 5.0 (SE) beats/min for the level run, from 114 t 5.3 to 143 t 4.7 beats/min for the first downhill bout, and from 117 t 3.2 to 142 t 4.4 beats/min for the second downhill bout. A significant bout-by-time interaction was observed (P < 0.01). Further analysis indicated that HR increased more for the two downhill runs than for the level running session l
l
l
l
l
(P < 0.05).
Ventilatory response was similar to that of the HR in that VE increased from 33.52 t 3.21 to 34.73 t 3.53 l/min (3.5%) for the level run compared with an increase from 35.78 & 4.20 to 43.00 t 4.53 l/min (20.5%) for the first downhill run and from 33.44 t 3.83 to 41.52 t 4.55 I/min (24%) for the second downhill run (Fig. 5). These changes were significantly different between bouts as well as over time (P < 0.05). Again a significant interaction was observed (P < 0.05), suggesting a greater increase in VE for both downhill runs than for the level run. On analysis it was noted that the VE responses of the two downhill runs were not different (P > 0.05) but were significantly different from the level run (P < 0.05). HR and
,,,, 5
,,,, 10
,,,, 15
,,,, 20
,,,,, 25
30
TIME ( min ) FIG. 4. Changes in mean heart rate in 7 subjects during 30-min level, Down 1, and Down 2 exercise bouts. Bout effect, time effect, and bout-by-time interaction were all significant (P < 0.05).
VE values for the three runs were not statistically
different at time 0 (P > 0.05). T,, increased over time in parallel for all three bouts (P < 0.01; Fig. 6). This increase corresponded to a mean change of 0.8OC for the three exercise sessions. No difference in T,, response was noted among the three bouts (P > 0.05). Furthermore no statistically significant interaction was observed between the exercise bouts and time (P > 0.05). No significant changes in LA were observed among the three runs (P > 0.05) or over time for any of the three exercise sessions (P > 0.05). Average LA values of the six blood samples for each of the 30-min exercise sessions were 9.85 t 1.26,8.29 t 1.12, and 9.12 t 0.83 (SE) U/l for the level, first downhill, and second downhill runs, respectively. DISCUSSION VO, increased in similar magnitude for the two downhill bouts (15.6% for the first, 14.7% for the second) and minimally for the level bout (1.2%). The magnitude of the increase in Vo2 during the downhill runs was similar to that reported by Dick and Cavanaugh (8), who noted a 10% increase in vo2 in subjects running downhill at 44% OfVO 2 maxfor 40 min. The present findings are somewhat greater than the 5.5% increase in Vo2 calculated from the data of Byrnes and colleagues (4) between minutes 10 and 30 of 30 min of downhill running at 57% 00, mBx. As anticipated, subjects demonstrated significantly less of an increase in serum CK activity 24 h after the second downhill bout than after the first. Furthermore, subjective soreness evaluations were reduced after the
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
OXYGEN
322 0
5
IO
15 20 TIME ( min )
25
DRIFT
IN DOWNHILL
-I-
LEVEL
-e-
DOWN1
+
DOWN2
30
FIG. 5. Mean ventilatory changes in 7 subjects during 3O-min level, Down 1, and Down 2 exercise bouts. Bout effect, time effect, and boutby-time interaction were all significant (P < 0.05).
second downhill run from those made 24 h after the first. These findings would suggest that there was a reduction in muscle fiber damage after the second eccentric exercise task and are in agreement with previous research in humans and in the animal model (1,25,28-30). Findings of an increase in VO, over time during the second downhill bout suggest that muscle damage is not contributing to the drift. Had damage been responsible for the drift in VO,, one would have anticipated a metabolic creep in VO, during the first downhill bout but significantly less or none during the second. Other physiological factors that have previously been associated with the upward drift in.VO, during higher-intensity concentric exercise [>60% VO, m8X(5)] did change differentially across the three exercise bouts. Significant differences in HR existed among the three bouts. HR increased only 8 beats/min from the beginning to the end of the level exercise session but increased 29 and 25 beats/min over the first and second downhill bouts, respectively. It may be suggested that HR, or work of the myocardium, is related to the drift in VO, during downhill running. Because of the small size of the heart, it is doubtful that its increased muscular work, as evidenced by an increased HR, would cause the entire increase in Vo2. An estimate of the percentage of the drift in Vo2 contributed by the heart would be ~20%, on the basis of a myocardial oxygen cost for light exercise of 11 ml min-l 100 g-l of the left ventricle (if an average left ventricular weight of 0.33 kg is assumed) (23). Findings similar to the HR response were noted for VE. A significant increase of 3.5% (1.2 l/min) in iTE over time was observed for the level run, but significantly greater increases were noted for the first [20.5% (7.2 I/ min)] and second [24% (8.1 l/min)] downhill runs. Although the oxygen cost of ventilatory work appears to be extremely variable (31), a rough estimate of the increase in ventilatory cost can be obtained. If one calculates the oxygen cost of breathing on the basis of a range of 3-5 ml of oxygen consumed per liter of air breathed (19), ll24% of the increase in VO, noted during the two downhill runs could be explained by the increased ventilatory work. Therefore the increased.metabolic cost associated with the changes in HR and VE could explain only 3144% of the observed increase in VO,. Interestingly, the T, response did not differ among the three bouts but increased in parallel for all three. This would agree with Nielsen (26), who reported that the change in core temperature during eccentric exercise foll
l
VS. LEVEL
799
RUNNING
lows a curve similar to that observed during concentric exercise. The findings of no difference in T,, between bouts and an increase in T,, over tim .e lead t% the proposal of one of two hypotheses. Fi .rst, therm .oregulatory factors, specifically as measured by T,,, do not contribute to the increase of TO, during low-intensity downhill running. This speculation is doubtful in light of the established Q10 relationship linking increases in temperature with increases in mitochondrial respiration and the subsequent increase in 60, (3). Second, it may be suggested that the increases in T,, contribute to the drift in VO, in the two downhill bouts, as well as to the slight increase in Oo, noted during the level bout. The data of Grimby (13) indicate a 5.5% increase in Tjoz for a 1.3OC increase in T,. By utilizing this information, one would be able to account for >lOO% of the increase in vo2 for the level bout but only 24 and 22% for the first and second downhill bouts, respectively. Thus, although the increase in T, may explain part of the drift in VO, during the downhill runs and all of that observed during the level run, it does not explain the greater drift in 60, noted during the downhill bouts. It may be proposed that T,, is not the most appropriate Intramuscuindicator of changes in body temperature. lar, skin, olr other m.easures of core temperature may be necessary to detect alterati .ons in thermoregulation between downhill and level running. Klausen and Knuttgen (17) attributed the 25% drift in \joB in their subjects &ho performed eccentric cycling to an increase in muscle temperature. They sugge sted that the increase in muscle temperature resulted in a decrease in muscle viscosity. Because eccentric contractions involve force induced from the passive stretch of the muscle’s elastic component, it is possible that the change in viscosity reduces or alters this elasticity and might result in an increased motor unit recruitment, and therefore VO,, to perform a given amount of work. An increase in muscle temperature may also evoke the Q10 effect, thereby causing an increase in VO,. The speculation that muscle temperature is related to the drift in VO, is supported by the findings of Nielsen (26), who reported that skin an .d muscle temperature we re higher during eccentric th .an during concentric exercise. Likewi se, Nadel et al. (24) reported that meas ures of muscle and skin temperature were I
38.2 38.1 G
38
-a-
37.2
LEVEL
-a--
DOWN1
+
DOWN2
,, , , , , , a,, , , 1, , , , , ,, ,, , 8, ,,, 0 5 10 15 20 25 TIME ( min )
,, , 30
FIG. 6. Changes in mean rectal temperature in 7 subjects during 30-min level, Down 1, and Down 2 exercise bouts. Time effect was significant (P < 0.01).
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
800
OXYGEN
DRIFT
IN DOWNHILL
higher during eccentric exercise, and core temperature measures were lower than those reported during similarintensity concentric exercise performed at the same level of total heat production. It may also be suggested that alterations in the levels of plasma hormones, such as thyroxine, epinephrine, and/or norepinephrine, may contribute to the increase in VO,. These parameters were not assessed in the present investigation. Although this hypothesis has not been tested during low-intensity downhill running, catecholamines and thyroxine have been associated with an elevation in metabolic rate and an increase in VO, during the postexercise period (11, 12). Prior work from this laboratory has shown a strong correlation between plasma catecholamine content and LA during both maximal and submaximal exercise (21,22). This relationship has been attributed to the stimulatory effect of catecholamines on muscle glycogenolysis, thus leading to lactate production (21,22). On the basis of the present findings of no difference in LA concentration among the three exercise bouts and the steady-state lactate conditions observed during each of the bouts, one might speculate that catecholamines did not contribute to the drift in VO, noted during the two downhill running bouts. The relationship between thyroxine and oxygen drift during downhill running remains unexplored. In conclusion, the present results do not support the hypothesis that muscle damage is related to, or is causing, the drift in VO, during low-intensity downhill running. This is evidenced by the increase in VO, observed during the second downhill bout, without concomitant increases in serum CK activity or perceived muscular soreness. Second, these data suggest that ventilatory, myocardial, and thermoregulatory factors may contributein part to, but do not entirely explain, the alterations in VO, during downhill running. It is clear from the findings of this investigation that muscle damage is not related to the drift in VO, and that future research is necessary to determine the exact mechanism(s) that is contributing to the upward drift in Vo2 during constant-load low-intensity downhill running. This study was funded by a Grant-in-Aid of Research from Sigma Xi, the Scientific Research Society. Address for reprint requests: K. C. Westerlind, Dept. of Kinesiology, Campus Box 354, Boulder, CO 80309.
VS. LEVEL
8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
19. 20. 21.
22. 23. 24. 25. 26. 27.
Received 14 March 1991; accepted in final form 5 September 1991. 28. REFERENCES 1. ABRAHAM, W. M. Factors in delayed muscle soreness. Med. Sci. Sports Exercise 9: 11-20, 1977. 2. BROOKS, G. A., AND T. D. FAHEY. Exercise Physiology. Human Bioenergetics and Its Applications. New York: Wiley, 1984. 3. BROOKS, G. A., K. J. HITTLEMAN, J. A. FAULKNER, AND R. E. BEYER. Temperature, skeletal muscle mitochondrial functions, and oxygen debt. Am. J. Physiol. 220: 1053-1059,197l. 4. BYRNES, W., P. CLARKSON, J. WHITE, S. HSHIEH, P. FR~KMAN, AND R. MAUGHAN. Delayed onset muscle soreness following repeated bouts of downhill running. J. Appl. Physiol. 59: 710-715, 1985. 5. COSTILL, D. L. Metabolic responses during distance running. J. Appl. Physiol. 28: 251-255, 1970. 6. DAVIES, C., AND C. BARNES. Negative (eccentric) work. I. Effects of repeated exercise. Ergonomics 15: 3-14, 1972. 7. DEMPSEY, J. A., AND W. G. REDDAN. Hyperventilation during pro-
29. 30.
31. 32. 33. 34.
RUNNING
longed work: cause and effect (Abstract). Med. Sci. Sports Exercise 8: 62, 1976. DICK, R. W., AND P. R. CAVANAUGH. An explanation of the upward drift in oxygen uptake during prolonged sub-maximal downhill running. Med. Sci. Sports Exercise 19: 310-317, 1987. FFUDEN, J., J. SEGER, M. SJOSTROM, AND B. EKBLOM. Adaptive response in human skeletal muscle subjected to prolonged eccentric training. Int. J. Sports Med. 4: 177-183, 1983. FRIDEN, J., M. SJOSTROM, AND B. EKBLOM. Myofibrillar damage following intense eccentric exercise in man. Int. J. Sports Med. 4: 170-176,1983. GAESSER, G. A., AND G. A. BROOKS. Metabolic bases of excess postexercise oxygen consumption: a review. Med. Sci. Sports Exercise 16: 29-43,1984. GLADDEN, L. B., W. N. STAINSBY, AND B. R. MACINTOSH. Norepinephrine increases canine skeletal muscle VO, during recovery. Med. Sci. Sports Exercise 14: 471-476, 1982. GRIMBY, G. Exercise in man during pyrogen-induced fever. Acta Physiol. Stand. Suppl. 67: l-114,1962. HAGBERG, J. M., J. P. MULLIN, AND F. J. NAGLE. Oxygen consumption during constant-load exercise. J. Appl. Physiol. 45: 381-384, 1978. HENRY, F. M. Aerobic oxygen consumption and alactic debt in muscular work. J. Appl. Physiol. 3: 427-438, 1951. HUNTER, J. B., AND J. B. CRITZ. Effect of training on plasma enzyme levels in man. J. Appl. Physiol. 3: 20-23,197l. KLAUSEN, K., AND H. KNUTTGEN. Effect of training on oxygen consumption in negative muscular work. Acta Physiol. Stand. 83: 319-323,197l. KNUTTGEN, H. G., E. R. NADEL, K. B. PANDOLF, AND J. F. PATTON. Effects of training with eccentric muscle contractions on exercise performance, energy expenditure and body temperature. Int. J. Sports Med. 3: 13-17, 1982. M&RTIN, B. J., AND J. M. STAGER. Ventilatory endurance in athletes and non-athletes. Med. Sci. Sports Exercise 13: 21-26, 1981. MAXWELL, J. H., AND C. M. BLOOR. Effects of conditioning on exertional rhabdomyolysis and serum creatine kinase after severe exercise. Enzyme BaseZ26: 177-181, 1981. MAZZEO, R. S., P. R. BENDER, G. A. BROOKS, G. E. BUITERFIELD, B. M. GROVES, J. R. SUTTON, E. E. WOLFEL, AND J. T. REEVES. Arterial catecholamine responses during exercise with acute and chronic high-altitude exposure. Am. J. Physiol. 261 (Endocrinol. Metab. 24): E419-E424, 1991. MAZZEO, R. S., AND P. MARSHALL. Influence of plasma catecholamines on the lactate threshold during graded exercise. J. Appl. Physiol. 67: 1319-1322, 1989. MESSER, J., AND W. A. NEILL. The oxygen supply of the human heart. Am. J. Cardiol. 9: 384-394,1962. NADEL, E. R., U. BERGH, AND B. SALTIN. Body temperatures during negative work exercise. J. Appl. Physiol. 33: 553-558, 1972. NEWHAM, D. J., G. MCPHAIL, K. R. MILLS, AND R. H. T. EDWARDS. Ultrastructural changes after concentric and eccentric contractions of human muscle. J. Neural. Sci. 61: 109-122, 1983. NIELSEN, B. Thermoregulation in rest and exercise. Acta Physiol. Stand. Suppl. 323: l-74,1969. PIERRYNOWSKI, M. R., P. M. TUDUS, AND M. J. PL~LEY. Effects of downhill or uphill training prior to a downhill run. Eur. J. AppZ. Physiol. Occup. Physiol. 56: 668-672, 1987. SALMINEN, A., K. HONHISTO, AND V. VIHKO. Lysosomal changes related to exercise injuries and training-induced protection in mouse skeletal muscle. Acta Physiol. Stand. 120: 15-19, 1984. SCHWANE, J. A., AND R. B. ARMSTRONG. Effect of training on skeletal muscle injury in rats. J. Appl. Physiol. 55: 969-975, 1983. SCHWANE, J. A., S. R. JOHNSON, C. B. VANDENAKKER, AND R. B. ARMSTRONG. Delayed onset muscular soreness and plasma CPK and LDH activities after downhill running. Med. Sci. Sports Exercise 15: 51-56,1983. SHEPARD, R. J. The oxygen cost of breathing during vigorous exercise. Q. J. Exp. Physiol. 51: 336-350, 1966. STROMM, G. The influence of anoxia on lactate utilization in man after prolonged muscular work. Acta Physiol. Stand. 17: 440-451, 1949. SZASZ, G., W. GRUBER, AND E. BERNT. Creatine kinase in serum. I. Determination of optimum reaction conditions. Clin. Chem. 22: 650-656,1976. WHIPP, J., AND K. WASSERMAN. Oxygen uptake kinetics for various intensities of constant-load work. J. Appl. Physiol. 33: 35l356,1972.
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
C. WESTERLIND,
Department
WILLIAM
C. BYRNES,
WILLIAMC. BYRNES,ANDROBERTS. of the oxygen drift in downhill vs. level running. J. Appl. Physiol. 72(2): 796~800,1992.-This investigation explored the recent theory that muscle damage causes the drift in oxygen consumption (VO& during low-intensity downhill running. Seven subjects participated in a maximal VO, (To2 max) test and three submaximal bouts [one level (Level) and two downhill runs (Down 1, Down 2) at 40% peak VO,]. Two downhill runs (30 min at -10% grade) were performed to vary the extent of muscle damage. Creatine kinase (CK) increased more after Down 1 (61%) than after Down 2 (ll%), as did soreness ratings, indicating reduced muscle damage during Down 2. Significantly greater increases in vo2 over time were noted for Down 1 (15.6%) and Down 2 (14.7%) than for Level (1.2%). Heart rate increased 8 beats/min for Level but 29 and 25 beats/min for Down 1 and Down 2, respectively. Expired ventilation increased more for Down 1 (20.5%) and Down 2 (24%) than for Level (3.5%). Rectal temperature increased --023°C for all bouts. Because the magnitude of the drift was similar in the two downhill bouts, the findings suggest that muscle damage does not cause the drift in To2 during lowintensity downhill running. WESTERLIND,
KIMC.,
MAZZEO.A comparison
eccentric;
creatine
AND
ROBERT
S. MAZZEO
of Kinesiology, University of Colorado, Boulder, Colorado 80309
kinase; muscle damage;
muscle soreness
10% increase in VO, that was associated with an increase in muscle electromyography, evidence of increased motor unit recruitment. Although their findings suggest that muscle damage was contributing to the drift in VO,, it would appear important to evaluate the VO, response to a second bout of downhill running in which muscle damage would be significantly reduced. This repeated bout effect, in regard to muscle damage, has been well documented in the animal model (28,29) and in humans (9). If the drift in Vo2 were significantly reduced during a second downhill bout, the muscle damage-oxygen drift hypothesis would be more conclusively supported. The primary purpose of the present investigation was to evaluate the hypothesis that muscle fiber damage is the cause of the increase in Vo2 during low-intensity downhill running by incorporation of a second downhill run in the experimental design. In addition, this study examined heart rate, ventilation, rectal temperature, and blood lactate, factors that have previously been associated with the drift in VO, during higher-intensity concentric exercise (7, 14, l&18,34) but had not been measured by Dick and Cavanaugh (8) in their analysis of the drift in Vo2 during downhill running.
RECENTLY it has been noted that there is an increase in
METHODS
oxygen consumption (VO,) with low-intensity downhill running (8). Muscle contractions during this form of exercise are predominantly eccentric in nature, i.e., they involve the muscle lengthening against gravity (4,8,27). This upward drift in irO, has been noted at exercise intensities of 3550% of maximal vo2 (VO, m,) (6,8), levels that would not incur an increase in energy expenditure had the exercise involved predominantly concentric muscle contractions, such as with level running. It is well known that during low-intensity level running, the body initially responds with an increase in heart rate, ventilation, VO,, and other physiological parameters, followed by the attainment of a steady state within 2 or 3 min (2). The steady state is characterized by a plateau in these responses as the exercise duration continues. Dick and Cavanaugh (8) have proposed that an upward drift in VO, during low-intensity downhill running is related to the skeletal muscle damage that occurs with this form of exercise (8). These authors suggested that, with muscle damage, certain skeletal muscle fibers are no longer able to generate sufficient force and that additional motor units must be recruited to maintain a given level of work. The damaged fibers, however, continue to utilize oxygen, as do the newly recruited fibers, thus resulting in an increase in Vo2 (8). Their results showed a
Seven subjects (4 males, 3 females) were recruited from the University of Colorado’s student population to participate in this study. Subjects had not been involved in downhill running within the prior 6 mo. All were moderately active and engaged in activities such as running, aerobic dance, skiing, and cycling. Before participation, all volunteers read and signed an informed consent document approved by the University of Colorado Human Subjects Committee. Each subject participated in four exercise sessions in the following order: 1) a graded maximal exercise test to determine peak iTg, and exercise intensity levels for subsequent exercise sessions, 2) a level run for 30 min at 40% peak Vo2, 3) an initial downhill run at -10% grade for 30 min at 40% peak Vo2, and 4) a second downhill run under conditions identical to the first downhill bout. The second downhill bout was performed to evaluate the VO, response during an eccentric exercise session in which muscle damage is reduced or does not occur. Research indicates that a single eccentric bout has a prophylactic effect on a second bout that, in regard to muscle damage, can last as long as 6 wk (4). This reduction in skeletal muscle damage has been demonstrated directly by ultrastructural analysis (28,29) and indirectly by evidence of reduced serum creatine kinase activity (16, 20)
796
0161-7567/92
$2.00
Copyright 0 1992 the American Physiological
Society
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
OXYGEN
DRIFT
IN
DOWNHILL
and muscle soreness (10) after the second eccentric bout. One week separated the maximal exercise test from the level run and the level run from the first downhill bout. Two weeks separated the two downhill runs. Downhill running was chosen because of the predominantly eccentric muscular contractions involved in this type of exercise (30). During the maximal graded-exercise test, subjects ran at a comfortable pace on a motorized treadmill. The grade of the treadmill was increased 2.5% every 2 min until volitional exhaustion. Verbal encouragement was provided to elicit a maximal effort from subjects. Two of the three following criteria constituted attainment of peak 60,: a respiratory exchange ratio d.15, attainment of age-predicted maximal heart rate, and plateau of Vo2 despite an increase in work load. 00, was determined by a computer-assisted standard open-circuit indirect-calorimetry system. Expired gases were channeled through low-resistance tubing to a 5liter mixing chamber and directed to gas analyzers previously calibrated with three micro-Scholandered gases. The percentage of expired carbon dioxide was determined by use of a medical gas analyzer (Beckman LB2). The percentage of expired oxygen was determined with an Applied Electrochemistry analyzer (S-3A). Ventilation was determined by a pneumotachometer (Hans Rudolph) and a pressure transducer (Validyne). Before testing, the system was calibrated over a range of flow rates from 0 to 120 l/min with a 3-liter syringe. All information was processed by a computer (MINC-23, Digital). Values for VO, and expired ventilation (VE) were obtained every 30 s. Heart rate (HR) was monitored continuously with a modified V5 ECG lead. For the level and first downhill bout, the on-line opencircuit system provided TO, values every 30 s. The speed of the treadmill was adjusted until 40% of peak To2 was elicited continuously for 2 min. This required 5-7 min of adjustment and was considered the subjects’ warm-up period. After this criterion of 2 min was attained, the 30-min bout commenced. During the second downhill bout, subjects ran at the same pace as their first downhill bout but were allowed a similar 5-min warm-up period before beginning the 30-min exercise period. Speed was monitored with a digital tachometer (Biddle, Plymouth Meeting, PA). During the level and downhill runs, the following parameters were assessed: OO,, VE, HR, rectal temperature (T,), and blood lactate (LA). Perceived soreness and serum creatine kinase (CK) activity were assessed before and 24 h after each of the three exercise sessions. Methodologies for determining VpZ, TE, and HR were previously described. Values for VO, and VE are represented by an average of the 30-s values obtained every other minute during the exercise sessions. T, was assessed with a rectal thermistor inserted by the subject 12 cm past the anal sphincter. Temperature readings were obtained every 2 min with a telethermometer (Yellow Springs). Room temperature was recorded, and subjects were not allowed to participate in either downhill session on a day when ambient temperatures differed by >2OC of the temperature during the level run. LA was measured with the Stromm calorimetric method (32). Venous blood samples were obtained from a 20-gauge 2.5.in. plastic catheter inserted in a forearm
VS.
LEVEL
797
RUNNING
vein. Heparin-saline solution was used to keep the system patent. After a preexercise sample, blood samples were obtained every 5 min during the 30-min bouts. Samples were deproteinized in 10% trichloroacetic acid and centrifuged, and the supernatant was stored at -7OOC until analysis. All samples, standards, and controls were assayed in duplicate. All samples from one subject were assayed together to avoid interassay variability. The coefficient of variation for the LA assay was 8.2%. From the catheter, blood samples were obtained preexercise to determine serum CK activity. Standard venipuncture techniques were used to obtain blood samples 24 h after each of the three bouts to assess again for serum CK activity. Blood samples were allowed to clot and then were centrifuged to obtain serum. Samples were stored at -7OOC until analysis. Serum CK activity was determined by use of the calorimetric method of Szasz (Sigma Chemical) (33). Rate of change of absorbance was determined with a spectrophotometer (Perkin-Elmer) at 30°C. Samples, standards, and controls were assayed in duplicate. A coefficient of variation of 4.1% was obtained. CK activity was expressed in units per liter. Subjects subjectively rated muscle soreness before and 24 h after the level and downhill bouts. Soreness for different muscle groups was rated on a verbally anchored scale of 0 (no soreness) to 10 (very/very sore) (4). Repeated-measures analyses of variance with Greenhouse-Geiser correction factors were utilized to assess for statistical differences in vo2, VE, HR, T,, LA, and perceived soreness over time and among the three exercise bouts. A one-tailed paired t test was used to look at CK changes between the two downhill bouts. P = 0.05 was preset as the level necessary to achieve statistical significance for all analyses. RESULTS
Subjects were between the ages of 19 and 24 yr (mean 21.2 yr). Peak VO, values for female and male subjects were 44.2 t 1.3 and 57.0 t 3.1 (SD) ml kg-l. min-‘, respectively, a statistically significant (P < 0.05) difference. The male subjects were significantly heavier (74.4 t 13.7 kg) and taller (179.7 t 4.9 cm) than the female subjects (55.5 t 5.3 kg and 163.4 t 5.2 cm, respectively; P < 0.05). No significant gender differences were noted between bouts or over time for any of the dependent parameters assessed. The results were therefore presented in the aggregate. Subjects demonstrated significantly less of an increase in serum CK activity after the second than after the first downhill run (P < 0.05; Fig. 1). The changes corresponded to a mean increase of 11% 24 h after the second downhill bout vs. a 61% increase noted 24 h after the first. No change in CK activity was noted after the level run. Perceived soreness scores were also significantly lower (P < 0.05) 24 h after the second downhill bout (mean 1.1) than 24 h after the first (mean 4.3; Fig. 2). Repeated-measures analysis of variance indicated a significant increase in VO, over time (P < 0.01). Furthermore a significant interaction was noted between the three exercise bouts and time (P < 0.05). This interaction indicated that VO, changed differentially over time for the three bouts, i.e., the slopes were different. Further analysis indicated that the Oo, responses of the two l
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
798
OXYGEN h 2507 A K 2003
DRIFT
IN DOWNHILL
22
n PRE q POST
5r
50-
ii v)
0
RUNNING
1
p
DOWN1 DOWN
2
-
k 150> i= y IOO5 5
VS. LEVEL
LEVEL
I DOWNHILL
1 EXERCISE
I DOWNHILL BOUT
2
FIG. 1 Serum creatine kinase (CK) activity (means k SE) before and 24 h after two 30-min downhill running sessions. CK cha nge in downhill 2 significantly less (P < 0.05) than in downhill 1. l
I
I
”
”
1
0
”
”
I
5
”
”
I
10
”
”
I
15
”
”
20
I”“1
25
30
( min )
TIME
FIG. 3. Changes in mean oxygen consumption (VO,) in 7 subjects during 30-min level, downhill 1 (Down l), and downhill 2 (Down 2) exercise bouts. Time effect (P < 0.01) and bout-by-time i nteraction (P < 0.05) were both significant.
6 1
v
‘c
(3 5: z I t4K 3
n DOWNHILL 1 q DOWNHILL2
:
150 -m-
LEVEL
-
+
DOWN1
_
-f-
DOWN2
3:
iii! E20
: :
v) 1:
24 HOURS
I,,,,
POST
2. Perceived muscle soreness (means * SE) noted by 7 subjects 24 h after 2 downhill running bouts. Soreness significantly less (P -c 0.05) after downhill 2.
0
FIG.
downhill bouts were not different from each other but were significantly different from the level run. This analysis is depicted in Fig. 3. Time 0 is the 1st min of the 30-min bout after the initial warm-up period. No difference existed in VO, values at time 0. VO, increased 15.6% for the first downhill bout (from 18.83 t 0.91 to 21.77 t 1.40 ml kg-l min-l), 14.7% for the second downhill run (from 18.15 t 0.87 to 20.81 t 1.32 ml kg-‘. min-‘), and 1.2% for the level running exercise session (from 19.36 t 0.96 to 19.65 t 1.10 ml kg-’ min-I). Significant differences in HR were noted among the three bouts (P < 0.05). HR also increased significantly over time for the 30-min bouts (P < 0.05; Fig. 4). HR increased from 115 t 4.8 to 123 t 5.0 (SE) beats/min for the level run, from 114 t 5.3 to 143 t 4.7 beats/min for the first downhill bout, and from 117 t 3.2 to 142 t 4.4 beats/min for the second downhill bout. A significant bout-by-time interaction was observed (P < 0.01). Further analysis indicated that HR increased more for the two downhill runs than for the level running session l
l
l
l
l
(P < 0.05).
Ventilatory response was similar to that of the HR in that VE increased from 33.52 t 3.21 to 34.73 t 3.53 l/min (3.5%) for the level run compared with an increase from 35.78 & 4.20 to 43.00 t 4.53 l/min (20.5%) for the first downhill run and from 33.44 t 3.83 to 41.52 t 4.55 I/min (24%) for the second downhill run (Fig. 5). These changes were significantly different between bouts as well as over time (P < 0.05). Again a significant interaction was observed (P < 0.05), suggesting a greater increase in VE for both downhill runs than for the level run. On analysis it was noted that the VE responses of the two downhill runs were not different (P > 0.05) but were significantly different from the level run (P < 0.05). HR and
,,,, 5
,,,, 10
,,,, 15
,,,, 20
,,,,, 25
30
TIME ( min ) FIG. 4. Changes in mean heart rate in 7 subjects during 30-min level, Down 1, and Down 2 exercise bouts. Bout effect, time effect, and bout-by-time interaction were all significant (P < 0.05).
VE values for the three runs were not statistically
different at time 0 (P > 0.05). T,, increased over time in parallel for all three bouts (P < 0.01; Fig. 6). This increase corresponded to a mean change of 0.8OC for the three exercise sessions. No difference in T,, response was noted among the three bouts (P > 0.05). Furthermore no statistically significant interaction was observed between the exercise bouts and time (P > 0.05). No significant changes in LA were observed among the three runs (P > 0.05) or over time for any of the three exercise sessions (P > 0.05). Average LA values of the six blood samples for each of the 30-min exercise sessions were 9.85 t 1.26,8.29 t 1.12, and 9.12 t 0.83 (SE) U/l for the level, first downhill, and second downhill runs, respectively. DISCUSSION VO, increased in similar magnitude for the two downhill bouts (15.6% for the first, 14.7% for the second) and minimally for the level bout (1.2%). The magnitude of the increase in Vo2 during the downhill runs was similar to that reported by Dick and Cavanaugh (8), who noted a 10% increase in vo2 in subjects running downhill at 44% OfVO 2 maxfor 40 min. The present findings are somewhat greater than the 5.5% increase in Vo2 calculated from the data of Byrnes and colleagues (4) between minutes 10 and 30 of 30 min of downhill running at 57% 00, mBx. As anticipated, subjects demonstrated significantly less of an increase in serum CK activity 24 h after the second downhill bout than after the first. Furthermore, subjective soreness evaluations were reduced after the
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
OXYGEN
322 0
5
IO
15 20 TIME ( min )
25
DRIFT
IN DOWNHILL
-I-
LEVEL
-e-
DOWN1
+
DOWN2
30
FIG. 5. Mean ventilatory changes in 7 subjects during 3O-min level, Down 1, and Down 2 exercise bouts. Bout effect, time effect, and boutby-time interaction were all significant (P < 0.05).
second downhill run from those made 24 h after the first. These findings would suggest that there was a reduction in muscle fiber damage after the second eccentric exercise task and are in agreement with previous research in humans and in the animal model (1,25,28-30). Findings of an increase in VO, over time during the second downhill bout suggest that muscle damage is not contributing to the drift. Had damage been responsible for the drift in VO,, one would have anticipated a metabolic creep in VO, during the first downhill bout but significantly less or none during the second. Other physiological factors that have previously been associated with the upward drift in.VO, during higher-intensity concentric exercise [>60% VO, m8X(5)] did change differentially across the three exercise bouts. Significant differences in HR existed among the three bouts. HR increased only 8 beats/min from the beginning to the end of the level exercise session but increased 29 and 25 beats/min over the first and second downhill bouts, respectively. It may be suggested that HR, or work of the myocardium, is related to the drift in VO, during downhill running. Because of the small size of the heart, it is doubtful that its increased muscular work, as evidenced by an increased HR, would cause the entire increase in Vo2. An estimate of the percentage of the drift in Vo2 contributed by the heart would be ~20%, on the basis of a myocardial oxygen cost for light exercise of 11 ml min-l 100 g-l of the left ventricle (if an average left ventricular weight of 0.33 kg is assumed) (23). Findings similar to the HR response were noted for VE. A significant increase of 3.5% (1.2 l/min) in iTE over time was observed for the level run, but significantly greater increases were noted for the first [20.5% (7.2 I/ min)] and second [24% (8.1 l/min)] downhill runs. Although the oxygen cost of ventilatory work appears to be extremely variable (31), a rough estimate of the increase in ventilatory cost can be obtained. If one calculates the oxygen cost of breathing on the basis of a range of 3-5 ml of oxygen consumed per liter of air breathed (19), ll24% of the increase in VO, noted during the two downhill runs could be explained by the increased ventilatory work. Therefore the increased.metabolic cost associated with the changes in HR and VE could explain only 3144% of the observed increase in VO,. Interestingly, the T, response did not differ among the three bouts but increased in parallel for all three. This would agree with Nielsen (26), who reported that the change in core temperature during eccentric exercise foll
l
VS. LEVEL
799
RUNNING
lows a curve similar to that observed during concentric exercise. The findings of no difference in T,, between bouts and an increase in T,, over tim .e lead t% the proposal of one of two hypotheses. Fi .rst, therm .oregulatory factors, specifically as measured by T,,, do not contribute to the increase of TO, during low-intensity downhill running. This speculation is doubtful in light of the established Q10 relationship linking increases in temperature with increases in mitochondrial respiration and the subsequent increase in 60, (3). Second, it may be suggested that the increases in T,, contribute to the drift in VO, in the two downhill bouts, as well as to the slight increase in Oo, noted during the level bout. The data of Grimby (13) indicate a 5.5% increase in Tjoz for a 1.3OC increase in T,. By utilizing this information, one would be able to account for >lOO% of the increase in vo2 for the level bout but only 24 and 22% for the first and second downhill bouts, respectively. Thus, although the increase in T, may explain part of the drift in VO, during the downhill runs and all of that observed during the level run, it does not explain the greater drift in 60, noted during the downhill bouts. It may be proposed that T,, is not the most appropriate Intramuscuindicator of changes in body temperature. lar, skin, olr other m.easures of core temperature may be necessary to detect alterati .ons in thermoregulation between downhill and level running. Klausen and Knuttgen (17) attributed the 25% drift in \joB in their subjects &ho performed eccentric cycling to an increase in muscle temperature. They sugge sted that the increase in muscle temperature resulted in a decrease in muscle viscosity. Because eccentric contractions involve force induced from the passive stretch of the muscle’s elastic component, it is possible that the change in viscosity reduces or alters this elasticity and might result in an increased motor unit recruitment, and therefore VO,, to perform a given amount of work. An increase in muscle temperature may also evoke the Q10 effect, thereby causing an increase in VO,. The speculation that muscle temperature is related to the drift in VO, is supported by the findings of Nielsen (26), who reported that skin an .d muscle temperature we re higher during eccentric th .an during concentric exercise. Likewi se, Nadel et al. (24) reported that meas ures of muscle and skin temperature were I
38.2 38.1 G
38
-a-
37.2
LEVEL
-a--
DOWN1
+
DOWN2
,, , , , , , a,, , , 1, , , , , ,, ,, , 8, ,,, 0 5 10 15 20 25 TIME ( min )
,, , 30
FIG. 6. Changes in mean rectal temperature in 7 subjects during 30-min level, Down 1, and Down 2 exercise bouts. Time effect was significant (P < 0.01).
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
800
OXYGEN
DRIFT
IN DOWNHILL
higher during eccentric exercise, and core temperature measures were lower than those reported during similarintensity concentric exercise performed at the same level of total heat production. It may also be suggested that alterations in the levels of plasma hormones, such as thyroxine, epinephrine, and/or norepinephrine, may contribute to the increase in VO,. These parameters were not assessed in the present investigation. Although this hypothesis has not been tested during low-intensity downhill running, catecholamines and thyroxine have been associated with an elevation in metabolic rate and an increase in VO, during the postexercise period (11, 12). Prior work from this laboratory has shown a strong correlation between plasma catecholamine content and LA during both maximal and submaximal exercise (21,22). This relationship has been attributed to the stimulatory effect of catecholamines on muscle glycogenolysis, thus leading to lactate production (21,22). On the basis of the present findings of no difference in LA concentration among the three exercise bouts and the steady-state lactate conditions observed during each of the bouts, one might speculate that catecholamines did not contribute to the drift in VO, noted during the two downhill running bouts. The relationship between thyroxine and oxygen drift during downhill running remains unexplored. In conclusion, the present results do not support the hypothesis that muscle damage is related to, or is causing, the drift in VO, during low-intensity downhill running. This is evidenced by the increase in VO, observed during the second downhill bout, without concomitant increases in serum CK activity or perceived muscular soreness. Second, these data suggest that ventilatory, myocardial, and thermoregulatory factors may contributein part to, but do not entirely explain, the alterations in VO, during downhill running. It is clear from the findings of this investigation that muscle damage is not related to the drift in VO, and that future research is necessary to determine the exact mechanism(s) that is contributing to the upward drift in Vo2 during constant-load low-intensity downhill running. This study was funded by a Grant-in-Aid of Research from Sigma Xi, the Scientific Research Society. Address for reprint requests: K. C. Westerlind, Dept. of Kinesiology, Campus Box 354, Boulder, CO 80309.
VS. LEVEL
8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
19. 20. 21.
22. 23. 24. 25. 26. 27.
Received 14 March 1991; accepted in final form 5 September 1991. 28. REFERENCES 1. ABRAHAM, W. M. Factors in delayed muscle soreness. Med. Sci. Sports Exercise 9: 11-20, 1977. 2. BROOKS, G. A., AND T. D. FAHEY. Exercise Physiology. Human Bioenergetics and Its Applications. New York: Wiley, 1984. 3. BROOKS, G. A., K. J. HITTLEMAN, J. A. FAULKNER, AND R. E. BEYER. Temperature, skeletal muscle mitochondrial functions, and oxygen debt. Am. J. Physiol. 220: 1053-1059,197l. 4. BYRNES, W., P. CLARKSON, J. WHITE, S. HSHIEH, P. FR~KMAN, AND R. MAUGHAN. Delayed onset muscle soreness following repeated bouts of downhill running. J. Appl. Physiol. 59: 710-715, 1985. 5. COSTILL, D. L. Metabolic responses during distance running. J. Appl. Physiol. 28: 251-255, 1970. 6. DAVIES, C., AND C. BARNES. Negative (eccentric) work. I. Effects of repeated exercise. Ergonomics 15: 3-14, 1972. 7. DEMPSEY, J. A., AND W. G. REDDAN. Hyperventilation during pro-
29. 30.
31. 32. 33. 34.
RUNNING
longed work: cause and effect (Abstract). Med. Sci. Sports Exercise 8: 62, 1976. DICK, R. W., AND P. R. CAVANAUGH. An explanation of the upward drift in oxygen uptake during prolonged sub-maximal downhill running. Med. Sci. Sports Exercise 19: 310-317, 1987. FFUDEN, J., J. SEGER, M. SJOSTROM, AND B. EKBLOM. Adaptive response in human skeletal muscle subjected to prolonged eccentric training. Int. J. Sports Med. 4: 177-183, 1983. FRIDEN, J., M. SJOSTROM, AND B. EKBLOM. Myofibrillar damage following intense eccentric exercise in man. Int. J. Sports Med. 4: 170-176,1983. GAESSER, G. A., AND G. A. BROOKS. Metabolic bases of excess postexercise oxygen consumption: a review. Med. Sci. Sports Exercise 16: 29-43,1984. GLADDEN, L. B., W. N. STAINSBY, AND B. R. MACINTOSH. Norepinephrine increases canine skeletal muscle VO, during recovery. Med. Sci. Sports Exercise 14: 471-476, 1982. GRIMBY, G. Exercise in man during pyrogen-induced fever. Acta Physiol. Stand. Suppl. 67: l-114,1962. HAGBERG, J. M., J. P. MULLIN, AND F. J. NAGLE. Oxygen consumption during constant-load exercise. J. Appl. Physiol. 45: 381-384, 1978. HENRY, F. M. Aerobic oxygen consumption and alactic debt in muscular work. J. Appl. Physiol. 3: 427-438, 1951. HUNTER, J. B., AND J. B. CRITZ. Effect of training on plasma enzyme levels in man. J. Appl. Physiol. 3: 20-23,197l. KLAUSEN, K., AND H. KNUTTGEN. Effect of training on oxygen consumption in negative muscular work. Acta Physiol. Stand. 83: 319-323,197l. KNUTTGEN, H. G., E. R. NADEL, K. B. PANDOLF, AND J. F. PATTON. Effects of training with eccentric muscle contractions on exercise performance, energy expenditure and body temperature. Int. J. Sports Med. 3: 13-17, 1982. M&RTIN, B. J., AND J. M. STAGER. Ventilatory endurance in athletes and non-athletes. Med. Sci. Sports Exercise 13: 21-26, 1981. MAXWELL, J. H., AND C. M. BLOOR. Effects of conditioning on exertional rhabdomyolysis and serum creatine kinase after severe exercise. Enzyme BaseZ26: 177-181, 1981. MAZZEO, R. S., P. R. BENDER, G. A. BROOKS, G. E. BUITERFIELD, B. M. GROVES, J. R. SUTTON, E. E. WOLFEL, AND J. T. REEVES. Arterial catecholamine responses during exercise with acute and chronic high-altitude exposure. Am. J. Physiol. 261 (Endocrinol. Metab. 24): E419-E424, 1991. MAZZEO, R. S., AND P. MARSHALL. Influence of plasma catecholamines on the lactate threshold during graded exercise. J. Appl. Physiol. 67: 1319-1322, 1989. MESSER, J., AND W. A. NEILL. The oxygen supply of the human heart. Am. J. Cardiol. 9: 384-394,1962. NADEL, E. R., U. BERGH, AND B. SALTIN. Body temperatures during negative work exercise. J. Appl. Physiol. 33: 553-558, 1972. NEWHAM, D. J., G. MCPHAIL, K. R. MILLS, AND R. H. T. EDWARDS. Ultrastructural changes after concentric and eccentric contractions of human muscle. J. Neural. Sci. 61: 109-122, 1983. NIELSEN, B. Thermoregulation in rest and exercise. Acta Physiol. Stand. Suppl. 323: l-74,1969. PIERRYNOWSKI, M. R., P. M. TUDUS, AND M. J. PL~LEY. Effects of downhill or uphill training prior to a downhill run. Eur. J. AppZ. Physiol. Occup. Physiol. 56: 668-672, 1987. SALMINEN, A., K. HONHISTO, AND V. VIHKO. Lysosomal changes related to exercise injuries and training-induced protection in mouse skeletal muscle. Acta Physiol. Stand. 120: 15-19, 1984. SCHWANE, J. A., AND R. B. ARMSTRONG. Effect of training on skeletal muscle injury in rats. J. Appl. Physiol. 55: 969-975, 1983. SCHWANE, J. A., S. R. JOHNSON, C. B. VANDENAKKER, AND R. B. ARMSTRONG. Delayed onset muscular soreness and plasma CPK and LDH activities after downhill running. Med. Sci. Sports Exercise 15: 51-56,1983. SHEPARD, R. J. The oxygen cost of breathing during vigorous exercise. Q. J. Exp. Physiol. 51: 336-350, 1966. STROMM, G. The influence of anoxia on lactate utilization in man after prolonged muscular work. Acta Physiol. Stand. 17: 440-451, 1949. SZASZ, G., W. GRUBER, AND E. BERNT. Creatine kinase in serum. I. Determination of optimum reaction conditions. Clin. Chem. 22: 650-656,1976. WHIPP, J., AND K. WASSERMAN. Oxygen uptake kinetics for various intensities of constant-load work. J. Appl. Physiol. 33: 35l356,1972.
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on January 16, 2019.
