Exercise intensity: effect on postexercise O2 uptake in trained and untrained women

1991 ◽  
Vol 70 (4) ◽  
pp. 1713-1719 ◽  
Author(s):  
K. E. Chad ◽  
B. M. Quigley

Despite many reports of long-lasting elevation of metabolism after exercise, little is known regarding the effects of exercise intensity and duration on this phenomenon. This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal O2 consumption (VO2max)] on 3-h recovery of oxygen uptake (VO2). VO2 and respiratory exchange ratios were measured by open-circuit spirometry in five trained female cyclists (age 25 +/- 1.7 yr) and five untrained females (age 27 +/- 0.8 yr). Postexercise VO2 measured at intervals for 3 h after exercise was greater (P less than 0.01) after exercise at 50% VO2max in trained (0.40 +/- 0.01 l/min) and untrained subjects (0.39 +/- 0.01 l/min) than after 70% VO2max in (0.31 +/- 0.02 l/min) and untrained subjects (0.29 +/- 0.02 l/min). The lower respiratory exchange ratio values (P less than 0.01) after 50% VO2max in trained (0.78 +/- 0.01) and untrained subjects (0.80 +/- 0.01) compared with 70% VO2max in trained (0.81 +/- 0.01) and untrained subjects (0.83 +/- 0.01) suggest that an increase in fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P less than 0.05) after 50% VO2max in trained (147 +/- 4 mg/min) and untrained subjects (133 +/- 9 mg/min) compared with 70% VO2max in trained (101 +/- 6 mg/min) and untrained subjects (85 +/- 7 mg/min).

1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 78 (3_suppl) ◽  
pp. 1335-1344 ◽  
Author(s):  
Christopher C. Dunbar ◽  
Carole Goris ◽  
Donald W. Michielli ◽  
Michael I. Kalinski

The accuracy of regularing exercise intensity by Ratings of Perceived Exertion (RPE) was examined. Subjects underwent 4 production trials, 2 on a treadmill (PIA, P1B) and 2 on a cycle ergometer (P2A, P2B). 9 untrained subjects used only their perceptions of effort to regulate exercise intensity. Target intensity was the RPE equivalent to 60% VO2mx. Exercise intensity (VO2) during P1A, P1B, and P2A did not differ from the target, but during P2B was lower than target. During P1A and P1B heart rate did not differ from the target but was lower than target during P2A and P2B. RPE seems a valid means of regulating exercise intensity during repeated bouts of treadmill exercise at 60% VO2max; however, exercise intensity during repeated bouts on the cycle ergometer may be lower than target.


1997 ◽  
Vol 82 (4) ◽  
pp. 1360-1369 ◽  
Author(s):  
Anne L. Friedlander ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Melvin J. Huie ◽  
George A. Brooks

Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (V˙o 2 peak)] and two posttraining trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra (4.63 ± 0.25), Rd (4.65 ± 0.24), Rox (3.77 ± 0.43), and Rd E (15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Rox was lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.


1981 ◽  
Vol 50 (1) ◽  
pp. 27-31 ◽  
Author(s):  
B. J. Martin ◽  
E. J. Morgan ◽  
C. W. Zwillich ◽  
J. V. Weil

Ventilation (VE) climbs steadily throughout prolonged heavy exercise. While this VE "drift" has implications for the adequacy of gas exchange in long-term exercise, its mechanism remains unknown. We examined the behavior of previously proposed mediators of VE drift during one hour of cycle ergometer exercise at constant work rate requiring 2/3 VO2 max in 10 subjects. VE increased 13% from 12 to 61 min of exercise (P less than 0.05). Although body core temperature rose as VE rose, equal elevation of core temperature by passive means failed to increase exercise VE. Rising VE during the hour of exercise occurred despite unchanged arterial pH, PCO2, and lactate and despite unchanged VCO2. Thus, all of the VE increase was calculated to be due to increased dead space ventilation (VD). Tidal volume (VT) was unchanged, while VD/VT rose from 0.16 to 0.24 from 12 to 61 min of work (P less than 0.05). These results show that increased body core temperature does not mediate VE drift, and that changes in previously proposed mediators (arterial pH, arterial lactate, and VCO2) are not necessary for a slow VE rise to occur in prolonged heavy exercise.


1998 ◽  
Vol 85 (3) ◽  
pp. 1175-1186 ◽  
Author(s):  
Anne L. Friedlander ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Melvin J. Huie ◽  
Maria Francesca Piacentini ◽  
...  

We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 12-wk cycle ergometer training program [5 days/wk, 1-h duration, 75% peak O2 consumption (V˙o 2 peak)] in healthy female subjects ( n = 17; age 23.8 ± 2.0 yr). Two pretraining trials (45 and 65% of V˙o 2 peak) and two posttraining trials [same absolute workload (65% of oldV˙o 2 peak) and same relative workload (65% of newV˙o 2 peak)] were performed on nine subjects by using a primed-continuous infusion of [1-13C]- and [6,6-2H]glucose. Eight additional subjects were studied by using [6,6-2H]glucose. Subjects were studied postabsorption for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 25.2 ± 2.4%. Pretraining, the intensity effect on glucose kinetics was evident between 45 and 65% ofV˙o 2 peak with rates of appearance (Ra: 4.52 ± 0.25 vs. 5.53 ± 0.33 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd: 4.46 ± 0.25 vs. 5.54 ± 0.33 mg ⋅ kg−1 ⋅ min−1), and oxidation (Rox: 2.45 ± 0.16 vs. 4.35 ± 0.26 mg ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than in the 45% trial. Training reduced Ra (4.7 ± 0.30 mg ⋅ kg−1 ⋅ min−1), Rd (4.69 ± 0.20 mg ⋅ kg−1 ⋅ min−1), and Rox (3.54 ± 0.50 mg ⋅ kg−1 ⋅ min−1) at the same absolute workload ( P ≤ 0.05). When subjects were tested at the same relative workload, Ra, Rd, and Rox were not significantly different after training. However, at both workloads after training, there was a significant decrease in total carbohydrate oxidation as determined by the respiratory exchange ratio. These results show the following in young women: 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose flux during exercise; but 4) training does reduce total carbohydrate oxidation.


1993 ◽  
Vol 75 (1) ◽  
pp. 70-75 ◽  
Author(s):  
A. R. Coggan ◽  
D. L. Habash ◽  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
C. L. Kien

Endurance training reduces the rate of CO2 release (i.e., VCO2) during submaximal exercise, which has been interpreted to indicate a reduction in carbohydrate oxidation. However, decreased ventilation, decreased buffering of lactate, and/or increased fixation of CO2 could also account for a lower VCO2 after training. We therefore used a primed continuous infusion of NaH13CO3 to determine the whole body rate of appearance of CO2 (RaCO2) in seven men during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2peak) before and after endurance training. RaCO2 is independent of the above-described factors affecting VCO2 but may overestimate net CO2 production due to pyruvate carboxylation and subsequent isotopic exchange in the tricarboxylic acid cycle. Training consisted of cycling at 75–100% VO2peak for 45–90 min/day, 6 days/wk, for 12 wk and increased VO2peak by 28% (P < 0.001). VCO2 during submaximal exercise was reduced from 86.8 +/- 3.7 to 76.2 +/- 4.2 mmol/min, whereas RaCO2 fell from 88.9 +/- 4.0 to 76.4 +/- 4.4 mmol/min (both P < 0.001). VCO2 and RaCO2 were highly correlated in the untrained (r = 0.98, P < 0.001) and trained (r = 0.99, P < 0.001) states, as were individual changes in VCO2 and RaCO2 with training (r = 0.88, P < 0.01). These results support the hypothesis that endurance training decreases CO2 production during exercise. The magnitude and direction of this change cannot be explained by reported training-induced alterations in amino acid oxidation, indicating that it must be the result of a decrease in carbohydrate oxidation and an increase in fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)


2005 ◽  
Vol 99 (3) ◽  
pp. 902-908 ◽  
Author(s):  
Hiroyuki Mitono ◽  
Hiroshi Endoh ◽  
Kazunobu Okazaki ◽  
Takashi Ichinose ◽  
Shizue Masuki ◽  
...  

We examined the hypothesis that elevation of the body core temperature threshold for forearm skin vasodilation (THFVC) with increased exercise intensity is partially caused by concomitantly increased plasma osmolality (Posmol). Eight young male subjects, wearing a body suit perfused with warm water to maintain the mean skin temperature at 34 ± 1°C (ranges), performed 20-min cycle-ergometer exercise at 30% peak aerobic power (V̇o2 peak) under isoosmotic conditions (C), and at 65% V̇o2 peak under isoosmotic (HEXIOS) and hypoosmotic (HEXLOS) conditions. In HEXLOS, hypoosmolality was attained by hypotonic saline infusion with DDAVP, a V2 agonist, before exercise. Posmol (mosmol/kgH2O) increased after the start of exercise in both HEX trials ( P < 0.01) but not in C. The average Posmol at 5 and 10 min in HEXIOS was higher than in C ( P < 0.01), whereas that in HEXLOS was lower than in HEXIOS ( P < 0.01). The change in THFVC was proportional to that in Posmol in every subject for three trials. The change in THFVC per unit change in Posmol (ΔTHFVC/ΔPosmol, °C·mosmol−1·kgH2O−1) was 0.064 ± 0.012 when exercise intensity increased from C to HEXIOS, similar to 0.086 ± 0.020 when Posmol decreased from HEXIOS to HEXLOS ( P > 0.1). Moreover, there were no significant differences in plasma volume, heart rate, mean arterial pressure, and plasma lactate concentration around THFVC between HEXIOS and HEXLOS ( P > 0.1). Thus the increase in THFVC due to increased exercise intensity was at least partially explained by the concomitantly increased Posmol.


2007 ◽  
Vol 39 (Supplement) ◽  
pp. S485
Author(s):  
Mark A. Schafer ◽  
Katie Koch ◽  
Jeff Rothstein ◽  
Fredric Goss ◽  
Deborah Aaron ◽  
...  

1995 ◽  
Vol 79 (5) ◽  
pp. 1562-1566 ◽  
Author(s):  
E. A. Gulve ◽  
R. J. Spina

Previous studies in animals and humans have shown that endurance exercise-training protocols of several weeks to many months in duration induce adaptive increases in skeletal muscle GLUT-4 protein concentration. It is generally assumed that the increase in GLUT-4 concentration is a long-term adaptation to training. The present study examined whether 7–10 days of cycle ergometer exercise could induce increases in skeletal muscle GLUT-4 levels. Eight healthy subjects (4 men, 4 women) aged 31 +/- 2 (SE) yr exercised 2 h daily at 65–70% of peak O2 uptake (VO2peak) for either 7 (n = 3) or 10 (n = 5) consecutive days. Muscle biopsies (vastus lateralis) were obtained before initiation of the exercise program and 36–48 h after the final bout of exercise. Glucose transporter protein was quantitated by Western blotting using antiserum specific for GLUT-4. VO2peak was increased by 10% (from 3.0 +/- 0.2 to 3.3 +/- 0.2 l/min; P < 0.01) in response to the training. Body weight did not change (74.3 +/- 4.6 before vs. 75.0 +/- 4.2 kg after) as a result of training. Muscle GLUT-4 immunoreactivity was increased 98% (from 584 +/- 50 to 1,154 +/- 40 counts per minute 125I/25 micrograms protein; P < 0.001) in response to training. Increase in VO2peak and GLUT-4 protein were similar for 7 and 10 days of training. These results suggest that, given an adequate training stimulus, adaptations in skeletal muscle GLUT-4 protein occur very rapidly. Furthermore, the increase in GLUT-4 after 7–10 days of exercise is as large as that reported in studies employing long-term training protocols.


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