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1 Department of Kinesiology, The College of William & Mary, Williamsburg, Virginia 23187 - 8795; and 2 the Human Performance Laboratory, Ball State University, Muncie, Indiana 47306
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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On different days, 10 men
performed 30-min sessions of cycling at 50-55% of their peak
oxygen uptake (
O2); one at 40 rpm and
another at 80 rpm. Rectal temperature, heart rate (HR), mean arterial
pressure (MAP), plasma lactate, glucose, insulin, and cortisol were
measured before exercise, during the 15th and 30th min of exercise, and
at 5 and 10 min postexercise. Rating of perceived exertion (RPE) was
assessed 15 and 30 min into exercise. Electromyography established
cadence-specific different intensities of quadriceps activation during
cycling. At minute 30 of exercise and 5 min postexercise, HR
was significantly (P < 0.05) greater at 40 rpm than at
80 rpm. MAP remained elevated longer after the 40-rpm than after the
80-rpm bout. Similarly, exercise-induced increases in plasma lactate
persisted longer after the 40-rpm bout. Cortisol levels were elevated
only at 40 rpm. RPE was higher during the slower cadence. These data
indicated that the more pronounced muscle activation pattern associated
with pedaling at 40 rpm resulted in greater physiological and
psychophysiological stress than that observed at 80 rpm even though
O2 was the same.
cortisol; electromyography; rating of perceived exertion; cadence; contraction
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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NUMEROUS STUDIES HAVE BEEN conducted to determine the impact of different pedaling rates on physiological responses to cycle ergometry. In general, the purpose of these investigations has been either to assess the metabolic efficiency of cycling at different cadences (5, 8, 10, 11, 20), or to identify which physiological variable is most instrumental in the selection of preferred pedaling rates (9, 15, 16). Interestingly, it has been demonstrated that neuromuscular efficiency, rather than metabolic economy, is maximized at the high pedaling cadences (80-90 rpm) favored both by trained cyclists (25) and untrained individuals (24).
To date, the investigation of the effects of different pedaling rates
has typically employed constant mechanical power output, i.e., watts,
eliciting exercise intensities of 70-85% of peak oxygen uptake
(O2) with exercise durations of <10
min. Perhaps due to the use of such high exercise intensities and short
exercise durations, little is currently known about the consequences of various pedaling cadences on the rate of recovery after prolonged cycle
ergometry. Coast et al. (4) examined recovery patterns subsequent to cycling exercise at a constant mechanical workload at
disparate pedaling rates but only for 5 min after the cessation of
exercise. The present study is unique in that its purpose was to
determine the physiological effects of different pedaling rates during
prolonged cycling of constant exercise intensity (50-55% of
peak O2) rather than mechanical
power output and to examine the rate of recovery for up to 15 min
postexercise. Our hypothesis was that although
O2 rates did not vary, pedaling at
different rates would evoke specific patterns of quadriceps muscle
activation that, in turn, would be associated with specific
physiological responses to cycling exercise.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Ten healthy men (20.6 ± 0.4 yr, 174.9 ± 1.3 cm, 72.9 ± 3.6 kg; means ± SE) participated in the research project. None were formally trained, but all were recreationally active. After receiving a verbal description of the study, experimental procedures to be used, and potential risks involved, the subjects provided written informed consent. A physician reviewed each subject's medical records before approving his inclusion in the investigation. All experimental procedures were approved by the Committee for the Protection of Human Subjects at The College of William & Mary.
Experimental design.
Subjects initially performed a graded exercise test to volitional
exhaustion on an electrically braked cycle ergometer (Excalibur Unit,
Lode, Groningen, The Netherlands). The test protocol included a 3-min
warm-up at 80 W followed by 2-min work intervals beginning at 140 W and
increasing by 30 W at each successive stage. During testing, metabolic
data were collected with an open circuit, online system (model 2900, SensorMedics, Anaheim, CA) to establish peak O2. During this test session, subjects
were allowed to self-select pedaling rate because cycling cadence does
not affect the determination of peak O2
(22). Each subject's preferred seat height was recorded
during maximal testing so that it could be replicated in subsequent
submaximal test sessions. Toe clips were not used in the maximal or
submaximal exercise tests. This was done to maximize reliance on the
quadriceps, whose muscle activation patterns would be measured with
electromyography (EMG) during the submaximal exercise bouts featuring
different pedaling rates.
O2,
subjects returned to the laboratory to complete two submaximal exercise
tests, one with a pedaling rate of 40 rpm and one at 80 rpm, at the
same time of day (±1 h) in a balanced, randomized design. Submaximal
tests were separated by at least 48 h but no more than 1 wk.
Before each of these exercise tests, subjects were instructed to fast for 6-10 h and refrain from heavy exertion for 24 h.
On arrival at the laboratory, subjects first inserted a rectal
temperature probe ~150 mm beyond the external anal sphincter (19). Then, a 20-gauge Teflon catheter fitted with a male
adapter was placed in an antecubital vein and kept patent with
heparin-treated isotonic saline solution. After this, the vastus
medialis (VM) and vastus lateralis (VL) of the right thigh were
prepared for EMG recordings. A one-square-inch area of skin over the VM
and VL was shaved, abraded with fine sandpaper, and cleansed with an
alcohol wipe. Along the longitudinal contour of the muscle, 2-mm-diameter surface electrodes filled with electrolyte gel were secured on the skin with adhesive collars at an interelectrode distance
of 2 cm and were traced with ink. These tracings enabled electrode
placement at the same sites during the second submaximal test.
The subject then mounted the cycle ergometer, was prepared for expired
gas analysis by the metabolic cart, and remained still for 5 min, after
which preexercise data including heart rate (HR), blood pressure, and
rectal temperature were recorded. Also, a 3-ml blood sample was
obtained at this time. The subject then performed a light (40 W)
warm-up for 3 min at the predetermined cadence of either 40 or 80 rpm.
Visual and auditory (metronome) cues were provided to assist the
subject in pedaling at the proper frequency. After the warm-up, the
experimenter increased the workload so that the subject's exercise
intensity, i.e., O2, would be brought to
50-55% of his peak O2. The desired
exercise intensity was established within 5 min and was maintained for
the rest of the exercise session by altering the workload (watts) as
needed. At the completion of the 30-min exercise bout, the subject
remained still on the cycle ergometer for a 15-min passive recovery
period. The same parameters recorded preexercise were also collected
during the 15th and 30th min of exercise as well as 5 and 15 min into recovery. Rating of perceived exertion (RPE) was assessed at the 15th
and 30th min of exercise. At 5 and 25 min of exercise, EMG recordings
for a minimum of five complete revolutions of the crank shaft were collected.
Quantitation. HRs were determined with a portable telemetry unit (Cardiochamp, Sensor Dynamics, Sacramento, CA) that was secured around the subject's chest. Blood pressure was measured with a sphygmomanometer (Welch Allyn Tycos, Tycos Instruments, Arden, NC) and a stethoscope (Littmann Select, 3M Health Care, St. Paul, MN). Mean arterial pressure (MAP) was calculated as the diastolic pressure plus 33% of the difference between the systolic and diastolic pressures. This value reflects the average pressure driving blood into the tissue over the entire cardiac cycle (26). Rectal temperature was monitored with a thermistor (model 400, VWR Scientific, Bridgeport, NJ). RPE was assessed using Borg's original 15-point scale (3).
Blood samples were collected into heparin-treated tubes (Vacutainer, Becton Dickinson, Franklin Lakes, NJ). Aliquots of whole blood were immediately used for hemoglobin and hematocrit analyses. Hematocrit was assayed in triplicate using microcapillary tubes after centrifugation at 4,000 g for 5 min, and hemoglobin values were determined via the cyanmethemoglobin method. Exercise-induced plasma volume shifts were ascertained from hematocrit and hemoglobin values according to Dill and Costill (7). The remaining whole blood was centrifuged at 3,000 g for 10 min. The resultant plasma was stored at
75°C until blood-borne variables were analyzed.
Plasma lactate and glucose concentrations were determined in duplicate
with an automated blood chemistry analyzer (Vitros DT 60 II, Johnson
and Johnson Clinical Diagnostics, Rochester, NY). Cortisol and insulin
concentrations were assayed in duplicate using solid-phase
125I radioimmunoassays (Diagnostic Systems Laboratories,
Webster, TX) with sensitivities of 10 and 9 pmol/l, respectively. For
each hormone, all plasma samples were quantified in a single run to avoid interassay variance; intra-assay variance was <10%.
During recordings, EMG signals were amplified by a factor of 1,000 and
passed through a bandwidth filter set at 30 and 500 Hz along with a
60-Hz notch filter. Signals were digitized at a sampling frequency of
1,000 Hz and recorded by an online computer system. To collect
accurate, reproducible EMG data during pedaling, the cycle ergometer
was modified to include a magnetic switch that emitted a pulse when the
pedal reached top dead center defining one complete pedal revolution.
The EMG signal was then full-wave rectified and integrated (iEMG).
Statistical analysis. Standard descriptive procedures were employed in analyzing subject characteristics. Main effects of exercise on each physiological variable of interest under each rate of pedaling were determined with repeated measures of analysis. In the event of a significant F ratio, Fisher's protected least-significant differences post hoc analysis was used to identify pairwise differences. Dependent t-tests were conducted to make direct comparisons of variables at each time point of data collection under the two cadence conditions. An alpha level of 0.05 was used to determine statistical significance.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Metabolic variables.
Peak O2 data (51.0 ± 2.6 ml · kg
1 · min1; mean ± SE) indicate that although the subjects were untrained, they
were reasonably fit. During the submaximal exercise sessions, subjects
maintained the desired exercise intensity under both cadence
conditions. At 15 min of exercise, O2
was 55% and 54% of peak O2 at 40 and
80 rpm, respectively. During the 30th min of exercise, subjects were
performing at 50% of peak O2 at both
cadences. Thus subjects were exercising at the same relative
intensities during the submaximal exercise sessions at 40 and 80 rpm.
Similarly, no cadence effects were evident during passive recovery from
exercise. By 5 min postexercise, O2 had
returned to preexercise levels.
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Rectal temperature.
Prolonged, moderate-intensity exercise significantly increased rectal
temperature, and this response persisted throughout the 15-min passive
recovery period. While exercising, rate of pedaling did not affect
temperature response. However, a significant drop in temperature from 5 to 15 min postexercise was observed subsequent to the 40- but not the
80-rpm session. Although statistically significant, this difference was
not considered physiologically meaningful. It amounted to a disparity
of 0.03°C under the two cadence conditions. Rectal temperature data
can be found in Fig. 1.
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Cardiovascular variables. Significant elevations in MAP were displayed while cycling at both 40 and 80 rpm, yet these exercise-induced responses were similar for both cadences. Under both conditions, blood pressure remained steady throughout the duration of exercise; no gradual increase while exercising was observed. However, it is noteworthy that there was a trend (P = 0.08) for MAP to be higher during the final minute of cycling at 40 rpm compared with the same time point during the 80-rpm session.
Repeated-measures ANOVA revealed differential main effects of cadence on blood pressure after exercise, however. Recovery of MAP was determined to be significantly slower after cycling at 40 than at 80 rpm. For example, 5 min after the session at 40 rpm, blood pressure remained significantly higher compared with preexercise, whereas MAP returned to normal within 5 min of cessation of exercise at 80 rpm. Under both cadence conditions, blood pressure at 15 min postexercise was no different than before exercise. Blood pressure responses to, and recovery from, exercise are displayed in Fig. 2.
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Plasma glucose.
When measured over time, cycling cadence differentially impacted
glucose response. While cycling at 40 rpm, no significant variation in
plasma glucose concentrations was noted during or after exercise. In
contrast, the cadence of 80 rpm resulted in significant alterations in
glucose levels. Specifically, plasma glucose concentrations during
exercise were lower than those at 5 and 15 min of recovery. Among the
time points measured, plasma glucose concentration was greatest at 15 min postexercise. These results can be found in Fig.
4.
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Plasma lactate.
In contrast to glucose, cycling both at 40 and 80 rpm elicited
significant changes in plasma lactate concentrations. Under each
cadence condition, plasma lactate levels were elevated at 15 and 30 min
of exercise as well as 5 min postexercise. Relative to preexercise,
plasma lactate remained elevated 15 min into recovery from cycling at
40 but not 80 rpm. In addition, after 30 min of exercise at 80 but not
40 rpm, there was a significant decrement in lactate within 5 min.
These findings indicate that, with respect to plasma lactate, recovery
is quicker after pedaling at a faster rate even though exercise-induced
responses were similar between the two cadence conditions. Plasma
lactate data are presented in Fig. 5.
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Plasma insulin.
Neither the 40- nor the 80-rpm pedaling cadence elicited significant
modifications in insulin levels during exercise. Yet, in both cases,
insulin levels were higher throughout recovery than they were at 15 and
30 min of exercise. At 15 min of recovery subsequent to the 80- but not
the 40-rpm exercise bout, insulin was significantly greater than it was
before exercise (Fig. 6).
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Plasma cortisol.
Repeated-measures ANOVA analyses revealed that only during the exercise
bout at 40 rpm was significant variation in cortisol detected. Compared
with preexercise values, cortisol was elevated by the 30th min of
cycling at 40 rpm and remained so throughout the 15-min recovery
period. Direct between-condition differences in cortisol response to
cycling were also identified. That is, plasma cortisol during the
slower cadence was significantly higher at the last minute of exercise
and at 5 and 15 min postexercise than it was during the 80-rpm session
at those same time points (Fig. 7). These
differences could not be attributed to cadence-specific shifts in
plasma volume because those responses were similar (P > 0.05) between the 40- and 80-rpm sessions, including recovery periods. In fact, no significant plasma volume shifts were found at any
time point during either of the exercise trials.
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Perceived exertion.
In general, the subjects rated their level of exertion between
"fairly light" and "somewhat hard" during the
moderate-intensity exercise sessions. It was revealed that pedaling
rate significantly influenced RPE. At 15 min of exercise, similar RPE
scores were reported for each pedaling rate. However, by the 30th min
of exercise, subjects sensed their efforts to be more strenuous when
pedaling at 40 compared with 80 rpm. Differences in perceived exertion are illustrated in Table 2.
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EMG recordings.
As expected, iEMG data revealed different patterns of quadriceps muscle
activation under the two pedaling rates. When quantified as iEMG
activity per second during the force-production phase of pedaling,
muscle recruitment was significantly greater while cycling at 40 than
at 80 rpm, indicating more intense muscle contraction at the slower
cadence. This was true of both the VM and VL muscles and at both the
5th and 25th min of exercise. It was also determined from iEMG data
that muscle recruitment patterns did not vary from the 5th to the 25th
min of cycling during either pedaling rate. Data related to iEMG
activity can be found in Table 3.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The objective of this investigation was to determine whether
physiological responses to cycling exercise would vary with different pedaling rates even if relative exercise intensity, i.e., %peak O2, was similar under the
contrasting cadence conditions. We hypothesized that different pedaling
cadences would entail unique patterns of quadriceps recruitment and
that muscle involvement or intensity of muscle contraction would be
associated with cadence-specific physiological responses despite
similar rates of O2. Our iEMG data
confirmed our initial premise. During the pedaling motion, more severe
muscle activation (iEMG/s) was observed at a cadence of 40 than at 80 rpm. This could be due to a greater recruitment of higher threshold
motor units at the slower cadence and/or a faster firing rate of the
same motor units activated at 80 rpm. Regardless of the difference in
recruitment strategies, none of the metabolic variables measured,
including O2, varied between the two
exercise sessions.
Unlike metabolic variables, the two different cadences brought about distinct cardiovascular responses. Although both HR and MAP displayed similar elevations at the 15th min of exercise at 40 and 80 rpm, HR was significantly greater at the slower cadence during the last minute of exercise. The effects of different muscle involvement on cardiovascular responses persisted into the postexercise passive recovery. Specifically, 5 min after cycling at 40 rpm, HR was significantly higher than it was at the same time interval subsequent to cycling at 80 rpm. Also, exercise-induced increases in MAP extended 5 min into postexercise under the 40-rpm condition, while returning to preexercise values after cycling at 80 rpm. Previous research has shown that cardiovascular responses to exercise are related to exercise-induced increases in circulating catecholamines, particularly norepinephrine (6, 13). It is possible that the greater intensity of muscle activation associated with pedaling at 40 rpm evoked greater catecholamine responses than that associated with cycling at 80 rpm. Unfortunately, we can only speculate on this potential mechanism because plasma catecholamine levels were not determined in the present investigation. It is certain, however, that differences in HR response to the two cycling conditions were not due to differences in cardiovascular drift; plasma volume shifts during and after exercise were unaffected by pedaling rate (data not shown).
Our findings also demonstrate that perceived exertion during exercise can vary even when the mode and intensity of the exercise stimulus are fixed. A significant increase in the RPE score was detected from the 15th to the 30th min of exercise when cycling at 40 rpm; no such increment was reported while cycling at 80 rpm. In addition, during the last minute of cycling, the RPE indicated by subjects was greater when pedaling at 40 than at 80 rpm. These distinct RPE scores may be explained by the cadence-specific differences in cardiovascular responses addressed above; recall that HR was greater during the 30th minute of the 40-rpm bout relative to the 80-rpm session.
It has been postulated that both central, e.g., HR, and local factors, including muscle force, regulate the perception of exertion during exercise (17). However, Pandolf and Noble (18) compared RPE when subjects cycled at 40 and 80 rpm while mechanical power output was held constant and concluded that local factors primarily accounted for differences in perceived exertion. Yet, in our study, although muscle activation patterns were specific to cadence throughout the 30-min exercise tests, differences in RPE were identified during the 30th but not the 15th min of exercise. Likewise, HR was similar at minute 15 but dissimilar during the last minute of exercise, whereas local muscle recruitment did not vary within either of the trials. These data suggest that, at least with prolonged exercise, HR is the variable most tightly coupled with the sensation of exercise difficulty.
The plasma lactate findings of our study confirm that, although moderate, the intensity of exercise was sufficient to result in levels of ~4.0 mM, the concentration generally used to mark the onset of blood lactate accumulation (21). It appears that relative exercise intensity, rather than intensity of muscle contraction, regulates plasma lactate response during cycling. Pedaling rates of 40 and 80 rpm resulted in similar and significant increases in circulating lactate levels during exercise. However, recovery rates of lactate to normal concentrations after exercise were specific to muscle activation patterns employed during cycling. For example, a significant decrement in lactate from the last minute of exercise to 5 min postexercise occurred during the 80- but not the 40-rpm bout. In addition, plasma lactate remained elevated longer after the slower cadence, i.e., 15 vs. 5 min.
Interestingly, cycling exercise at 40 rpm induced no significant alterations in blood glucose during or after exercise, whereas cycling at the faster rate brought about significant responses. After the 80-rpm session, blood glucose concentrations at 5 and 15 min of recovery exceeded those observed while cycling. These results may be coupled with those of postexercise lactate described above. That is, after 80-rpm exercise, a significant decrement in lactate was noted that was not apparent after cycling at 40 rpm. Previously, it has been established that lactate can serve as a substrate for the process of hepatic gluconeogenesis that occurs after exercise (1, 2). Thus the rapid reduction of lactate we detected after 80-rpm cycling exercise may account for the similarly rapid increase in plasma glucose levels that occurred after that exercise session.
During the 80-rpm exercise session, plasma insulin responses mirrored
those of plasma glucose. Like glucose, insulin was elevated at both
recovery time points compared with both time points assessed during
exercise. This was not unexpected given the regulatory influence of
blood glucose on insulin release from the 
-cells of the pancreas
(12). At 40 rpm, insulin was elevated in a pattern similar
to that seen at 80 rpm (higher postexercise than during exercise), yet
unlike the effects of 80-rpm cycling, the slower pedaling rate did not
evoke changes in blood glucose either during or after exercise. In
general, during exercise at either pedaling rate, insulin responses
mirrored those of glucose. However, whereas parallel response patterns
of these variables persisted during recovery from cycling at 80 rpm,
such coupling was not evident after the 40-rpm trial.
Unlike insulin, different pedaling cadences resulted in markedly
different responses of circulating cortisol concentrations. The greater
muscle activation associated with the slower cadence elicited
significant increments in cortisol both during and for up to 15 min
after cycling exercise. In contrast, pedaling at 80 rpm failed to
increase plasma cortisol levels. Previously, it has been reported that
cortisol responses to prolonged endurance exercise are determined by
intensity, i.e., cortisol increases reflect those of
O2 (14, 23). In the present
investigation, however, exercise intensity was held constant between
the two exercise trials. Our data suggest then that intensity alone, at least not as assessed by O2, does not
determine exercise-induced alterations in blood-borne cortisol concentration.
The fact that plasma cortisol is higher during and after the 40-rpm
session than the 80-rpm bout is consistent with cadence-specific cardiovascular responses, plasma lactate responses, and perception of
physical exertion. Recall that HR and blood pressure displayed more
pronounced responses to 40- than to 80-rpm cycling during and/or after
exercise. Also, exercise-induced increments of plasma lactate
demonstrated delayed recovery after the 40-rpm trial. Subjects also
reported that they experienced a greater degree of exertion while
pedaling at 40 rpm. Together, these data suggest that greater stress
attended the muscle recruitment pattern of the slower pedaling
frequency. Stress is a primary stimulus for cortisol secretion,
and elevations in blood-borne cortisol indicate the degree of stress
experienced (12). Along with our cardiovascular, lactate,
and RPE findings, the cortisol increases observed during and after the
40-rpm bout suggest that the muscle recruitment pattern observed with
the slower cadence was associated with greater physiological stress,
despite the fact that O2 did not differ between the two cadence conditions.
The findings presented here suggest that relative exercise intensity
(rate of O2) alone does not determine
physiological responses to the stimulus of exercise. Specific patterns
of muscle activation or contraction intensity also influence
cardiovascular, plasma metabolite, and endocrine responses both during
and after exercise. And probably due to these unique physiological
responses, perceived exertion during exercise is also modulated by
muscle contraction intensity, even when metabolic demands are held constant.
Perspectives
The rate ofO2 is commonly regarded
as the best indicator of the intensity and physiological demand of
exercise. Indeed, a strong linear relationship between HR and
O2 exists during prolonged physical
activity. Given this relationship, many exercise adherents monitor HR
to assess the intensity of the stress associated with exercise. The
data presented here suggest that, in addition to metabolic factors,
specific recruitment patterns of the working muscles influence the
physiological responses (including HR) to the challenge of exercise. In
effect, input from various organ systems acts in concert to regulate,
or at least modulate, the physiological and psychophysiological stress
associated with extended physical activity. On a more practical level,
these findings should be considered in efforts to accurately monitor
exercise intensity as well as in the prescription of exercise and
fitness programs.
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ACKNOWLEDGEMENTS |
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We express appreciation to the dedicated subjects and to Dr. Clifford Henderson for reviewing the medical records of potential subjects.
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FOOTNOTES |
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This investigation was supported by grants from the Borgenicht Program for Aging Studies and Exercise Science and the Faculty Research Committee of The College of William & Mary.
Address for reprint requests and other correspondence: M. R. Deschenes, Dept. of Kinesiology, The College of William & Mary, Williamsburg, VA 23187-8795 (E-mail: mrdesc{at}wm.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 24 May 2000; accepted in final form 15 August 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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0.05)
difference from preexercise value of same (40 rpm) trial.
* Significant (P 
