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1 Laboratory of Exercise
Physiology, Although insulin and exercise cause dramatic
changes in physiological parameters, the impact of exercise on neural
and hemodynamic responses to insulin administration has not been
described. In a study of the effects of a single bout of exercise on
blood pressure (BP), muscle sympathetic nerve activity (MSNA), and
forearm blood flow (FBF) responses to insulin infusion during the
postexercise period, 11 healthy men underwent, in a random order, two
hyperinsulinemic euglycemic clamps performed after 45 min of
1) bicycle exercise (50% peak
O2 uptake, Exercise session) and
2) seated rest (Control session).
Data were analyzed during baseline and steady-state periods. Although
insulin levels and insulin sensitivity were similar, baseline plasma
glucose levels were significantly lower in the Exercise than in the
Control session. Mean BP was significantly lower (3%) and FBF was
higher (27%) in the Exercise session. Exercise increased
insulin-induced MSNA enhancement (84%) without changing FBF and BP
responses to hyperinsulinemia. In conclusion, a single bout of exercise
that does not alter insulin sensitivity exacerbates insulin-induced
increase in MSNA without changing FBF and BP responses to hyperinsulinemia.
exercise; insulin sensitivity; blood pressure
THE PREVALENCE of diabetes mellitus and hypertension
has increased in Western societies. The fact that these disorders
usually develop together suggests a common pathogenic factor, which has been proposed to be the insulin resistance and its consequent hyperinsulinemia (8). Because exercise reduces insulin resistance and
hyperinsulinemia (4, 6, 11, 21, 29) and alters cardiovascular
parameters (5, 7, 12, 13, 15-17, 23), it has been recommended as a
nonpharmacological treatment for hypertensive and diabetic patients.
Anderson et al. (2) demonstrated, in healthy subjects, that insulin
increased muscle sympathetic nerve activity (MSNA) and decreased
forearm vascular resistance (FVR) without changing arterial blood
pressure (BP). In contrast, other investigators (22, 25) observed that
acute insulin infusion increased mean BP levels. Insulin-induced
enhancement of sympathetic nerve activity seems to be dose dependent
(2, 22, 25) and greater in insulin-resistant subjects (20). Similarly,
insulin-induced vasodilation is also dose dependent (2, 19, 28) and
directly related to insulin sensitivity (3, 19, 20).
Physical exercise causes metabolic, neural, and cardiovascular effects.
Wasserman et al. (29) found that a single bout of exercise increased
insulin sensitivity and reduced plasma insulin levels during the
postexercise period. Halliwill et al. (15) observed that, after an
acute bout of exercise, muscle blood flow was higher, and MSNA and BP
were lower than in a nonexercise control session.
Because exercise induces changes in MSNA, muscle blood flow, insulin
sensitivity, and BP, it could be expected that physiological responses
to hyperinsulinemia may be modified after a single bout of exercise.
To test this hypothesis, we studied the aftereffects of a single bout
of exercise on MSNA, forearm blood flow (FBF), and arterial BP
responses to a euglycemic and hyperinsulinemic clamp in
healthy men.
Subjects
ABSTRACT
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
INTRODUCTION
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
METHODS
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
Table 1.
Physical and functional characteristics of the volunteers
Peak oxygen uptake
(
O2 peak) was
measured directly by a metabolic cart (CAD/NET 2001, Medical Graphics)
during a graded maximal exercise test performed on a cycle ergometer,
with 30-W increments every 3 min until the subjects were unable to continue.
Measurements
BP and heart rate (HR). BP and HR were measured by an oscillometric automatic sphygmomanometer (Dixtal, 2710) that was calibrated regularly by comparison with a mercury column.
Muscle blood flow. FBF (ml/min per 100 ml of tissue) was measured by venous occlusion plethysmography (26). An air-filled latex plethysmography cuff was applied to the forearm and connected to a differential pressure transducer (Gould, Validyne). The arm was elevated above the right atrium. During measurements, circulation to the hand was interrupted by a wrist cuff inflated to 180-200 mmHg, while a venous occlusion cuff around the upper arm was inflated to 60 mmHg for 7 s of every 15 s. The calibration procedure was performed at the beginning and end of each experimental procedure by adding known volumes of air to the plethysmographic cuff, which was still placed on the subject's forearm. FVR (in U) was calculated by the mean BP and FBF ratio. No systemic hemodynamic measurements were performed in the present study.
MSNA. Multiunit, postganglionic MSNA was recorded by microneurography, as described previously (1). Briefly, a tungsten microelectrode (200-µm wide, tapering to an uninsulated tip of 1-5 µm) was inserted into a muscle fascicle of the peroneal nerve, posterior to the fibular head, and an uninsulated reference electrode was positioned 1-3 cm away. The recorded signal was fed to a preamplifier (gain: 1,000), an amplifier (variable gain: 40-60), a bandpass filter (700-2,000 Hz), and a resistance capacity integrating network (time constant: 0.1 s) to obtain a mean voltage neurogram. MSNA was distinguished from other sources of nerve activity by the following criteria: 1) electrical stimulation elicited muscle contraction but not paresthesias; 2) tapping or stretching innervated muscle elicited afferent mechanoreceptor discharges, whereas stroking the skin did not; and 3) neurogram revealed spontaneous, intermittent, pulse-synchronous bursts that increased during held expiration and Valsalva maneuvers. MSNA was quantified in terms of burst frequency (bursts/min).
Euglycemic and hyperinsulinemic clamp.
Regular human insulin (Novolin R, Novo-Norvisk), diluted in saline with
1 ml of subject's blood, was infused by digital pump (model
55-2222, Harvard Apparatus). To achieve a plasma insulin concentration of 100 µU/ml, an initial 10-min priming infusion of
insulin was started according to the procedure described by DeFronzo et
al. (9) and was followed by a 110-min continuous infusion (50.7 µU · m
2 · min1;
total infusion time: 120 min). Blood glucose concentration was maintained at baseline level by adjusting the infusion rate of 50%
dextrose solution (9). Blood glucose was measured every 5 min with
an automated device (Glucometer II, Milles do Brasil), and glucose
infusion was initiated 4 min after insulin infusion.
Experimental Protocol
Subjects were submitted to two experimental sessions (Control and Exercise) carried out in the morning after an overnight fast. The order of the sessions was randomized between a 45-min period of seated rest (Control) and a 45-min period of seated upright cycling at 50%O2 peak (Exercise).
We have previously observed that this protocol of cycling exercise
produces a sustained (at least 90-min) postexercise hypotension (12).
Due to technical needs (insertion of catheters and nerve localization
procedures), measurements of HR, BP, MSNA, and FBF were started ~90
min after exercise (Exercise session) or seated rest (Control session), and they were recorded before (baseline) and during insulin clamping.
MSNA was continuously recorded during the experimental sessions. FBF
was measured for 3 min at baseline and every 15 min during insulin
infusion. BP and HR were recorded every minute during the FBF
measurements. During exercise, O2
uptake (O2) was directly measured to check the exercise intensity.
Data studied were collected during insulin infusion within the steady-state period of plasma glucose, which was determined to be the 20-min period when plasma glucose was constant and similar to baseline (coefficient of variation <10%) and when plasma insulin levels were close to 100 µU/ml. Steady-state period data were not taken before 20 min of insulin infusion, and they occurred within similar time intervals in both sessions (Control and Exercise).
The amount of glucose metabolized (M) was calculated on the basis of glucose-infusion rate and plasma glucose concentration at the beginning and the end of the steady-state period (9). Glucose clearance rate (MCR) and insulin-sensitivity index (M/I) were calculated, respectively, as M and plasma glucose level ratio and M and plasma insulin ratio.
Saline Protocol
To determine whether time and vehicle could alter physiological responses after rest or exercise, three subjects returned for saline experiments in which the same protocol was performed but, instead of insulin or glucose, only saline was infused for 120 min.Biochemical Analysis
Plasma glucose levels were analyzed by a colorimetric enzymatic method (GOD/POD; Merck, Darmstadt, Germany). Plasma insulin levels were measured in duplicate by radioimmunoassay (CIS-Bio International kit; ICN Biomedicals, Costa Mesa, CA).Statistical Analysis
M, MCR, and M/I in both experimental sessions were compared by the Wilcoxon test.The effects of exercise on plasma glucose, plasma insulin, BP, HR, MSNA, FBF, and FVR responses to insulin infusion were analyzed by a two-way ANOVA for repeated measures [BMDP Statistical Software (1985) University of California, Los Angeles, CA]. Session (Control vs. Exercise) and period (baseline vs. steady state) were set as the main factors. Post hoc comparisons were performed by Scheffé's test. P < 0.05 was accepted as statistically significant. Data are presented as means ± SE.
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RESULTS |
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INTRODUCTION
METHODS
RESULTS
DISCUSSION
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Exercise and Control Sessions
Five subjects initiated the protocol with the Exercise session and six with the Control session. The mean interval period between experimental sessions was 69 ± 11 days. Measurements were taken at similar times in both Control and Exercise sessions. Baseline measurements were performed at 97 ± 7 min after rest and 90 ± 8 min after exercise, whereas insulin infusion was started at 111 ± 8 min after rest and 104 ± 7 min after exercise.The exercise bout was conducted at 91 ± 4 W. During exercise,
O2 was measured in eight
subjects, and the mean value found was 18.0 ± 1.1 ml
O2 · kg1 · min1,
which corresponded to 54 ± 2% of
O2 peak.
Metabolic Responses
Plasma glucose levels were kept close to baseline during the steady-state period in both sessions (Control: 87 ± 2 vs. 86 ± 3 mg/dl; Exercise: 82 ± 2 vs. 83 ± 2 mg/dl, baseline vs. steady state, respectively). Glucose concentration was significantly lower in the Exercise than in the Control session. The coefficients of variation of plasma glucose during the steady-state period were 4.7 ± 0.4% in the Control session and 5.2 ± 1.3% in the Exercise session.Insulin levels were similar between the two experimental sessions. Baseline plasma insulin concentration averaged 11.0 ± 2.1 µU/ml in the Control session and 9.7 ± 1.8 µU/ml in Exercise session. During euglycemic-hyperinsulinemic clamp, the insulin concentration increased to a similar level in both experimental sessions (102.5 ± 7.3 vs. 95.3 ± 4.7 µU/ml, Control vs. Exercise, respectively).
M values (8.16 ± 1.39 vs. 8.01 ± 1.11 mg · kg1 · min1,
Control vs. Exercise, respectively) and MCR values (0.100 ± 0.022 vs. 0.097 ± 0.013 ml · kg1 · min1,
Control vs. Exercise, respectively) did not change significantly with
exercise. Similarly, the M/I index (0.085 ± 0.017 vs. 0.079 ± 0.012 mg · kg1 · min1/µU · ml1,
Control vs. Exercise, respectively) was not different between Control
and Exercise sessions.
HR and BP Responses
HR and systolic, mean, and diastolic BP responses to insulin infusion in both experimental sessions are shown in Fig. 1. Systolic BP was similar in Control and Exercise sessions, and it increased significantly with insulin infusion (127 ± 2 vs. 131 ± 2 mmHg, baseline vs. steady state, respectively; P < 0.05). Mean BP was significantly lower in the Exercise than in the Control session (89 ± 2 vs. 92 ± 2 mmHg, respectively; P < 0.05). Mean BP did not change significantly with insulin infusion. Exercise and insulin infusion had no significant effects on diastolic BP or HR levels.
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MSNA Responses
Baseline and steady-state levels of MSNA in both Exercise and Control sessions are shown in Figs. 2 and 3. Baseline MSNA was significantly lower in the Exercise than in the Control session (19.5 ± 2.4 vs. 22.4 ± 2.5 bursts/min; P < 0.05). MSNA was significantly increased by insulin infusion in both sessions, and this enhancement was significantly greater in the Exercise than in the Control session (absolute change = 14.5 ± 1.8 vs. 7.9 ± 1.9 bursts/min, respectively; P < 0.05). Thus, during the steady-state period, MSNA was significantly greater in the Exercise than in the Control session (34.0 ± 3.3 vs. 30.3 ± 3.1 bursts/min, respectively; P < 0.05).
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FBF Responses
Baseline and steady-state levels of FBF and FVR in both Exercise and Control sessions are shown in Figs. 2 and 3. FBF was significantly higher (2.10 ± 0.14 vs. 1.65 ± 0.11 ml · min1 · 100 ml1,
P < 0.05) and FVR was significantly
lower (47 ± 3 vs. 63 ± 5 U, P < 0.05) in the Exercise than in the Control session. FBF and FVR
responses to insulin infusion were not significantly different between
the Control and the Exercise sessions. Insulin infusion did not
significantly change FBF and FVR; however, FVR tended to be lower in
the steady-state condition than at baseline
(P = 0.0782).
Saline Session
Time and vehicle did not modify physiological responses significantly. Changes from 10 to 120 min during saline administration were
2.2
and +1.4 bursts/min for MSNA, 3.6 and 5.0 mmHg for mean BP, 2.0 and 1.3 beats/min for HR, +0.63 and 0.45 ml/(min · 100 ml) for FBF, and 8.1 and +14.8 U for FVR in Control and Exercise sessions, respectively.
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DISCUSSION |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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The main findings of the present investigation are that, in healthy
men, a 45-min period of bicycle exercise at 50% of
O2 peak 1) decreases MSNA, increases FBF,
and decreases mean BP during postexercise period;
2) does not change M; and
3) exacerbates insulin-induced
enhancement in MSNA without changing FBF, FVR, and BP responses to
acute postexercise hyperinsulinemia.
Aftereffects of Exercise on Neural and Hemodynamic Responses
In agreement with other studies (7, 15), in the present investigation, exercise simultaneously reduced MSNA and mean BP during the postexercise period. This suggests an alteration in the baroreflex control. In fact, Halliwill et al. (15) reported that, after exercise, the baroreflex set point of sympathetic nerve activity control was shifted to lower levels without changing the reflex gain. Moreover, the alteration on the reflex control was better explained by a modification on central pathway rather than on baroreceptors (15). Exercise-induced increase in endogenous opioid secretion (27) and cardiopulmonary sensitivity (5) might be involved in such inhibition of the central pathway of sympathetic nerve activity control after acute exercise.The increase in muscle blood flow after exercise has also been
extensively reported (7, 13, 15-17). Reduction in sympathetic nerve activity (7, 15), decrease in 
-adrenergic responsiveness (15,
17), need of heat dissipation (13), release of local metabolites (18),
and increased production of nitric oxide (23) and opioids (16) have
been suggested as the most important mechanisms to explain this
vasodilatory response to exercise.
Effects of Insulin on Neural and Hemodynamic Responses
As previously reported (2, 20, 22, 25), insulin infusion significantly increased MSNA, possibly mediated by a direct effect of insulin on the central nervous system. Lembo et al. (20) observed that systemic, but not local, insulin infusion increased norepinephrine release in skeletal muscle. Pereda et al. (24) found that insulin infusion in dogs' carotid artery, at doses that have no systemic effects, produced cardiovascular responses compatible with sympathetic activation.In the present study, insulin infusion did not significantly change muscle blood flow. This response may be explained by the increase in sympathetic nerve activity, which might have counteracted the vasodilatory effect of insulin (2, 3, 19, 20, 28).
The increase of systolic BP, concomitant with the tendency of decrease in FVR during insulin infusion, suggests that the pressor effect of insulin may be caused by an increase in cardiac output. This increase might happen because of the stroke volume, once HR did not change with hyperinsulinemia.
Aftereffects of Exercise on Physiological Reponses to Insulin
The new finding of the present investigation is that a single bout of exercise, which did not change insulin sensitivity, induces an exacerbation of the MSNA response to postexercise insulin infusion.Although the mechanisms underlying this response were not investigated in the present study, we speculate that exercise-induced alterations to central pathways of the sympathetic nerve activity control might be involved, because insulin stimulates MSNA by central actions (24). Moreover, this response might be modulated by opioids released during exercise, because Hara and Floras (16) observed that the control of sympathetic activity outflow after exercise was altered by naloxone. Future studies may address this issue.
Despite the greater increase of MSNA during insulin infusion after
exercise, FBF and FVR responses to hyperinsulinemia did not change.
This suggests that exercise counteracts the increase in MSNA by a
reduction of -adrenergic responsiveness (15, 17) or even an increase
in insulin vasodilatory effects.
It is also interesting to point out that, in four subjects, M increased
significantly with exercise (7.28 ± 2.98 vs. 11.23 ± 4.23 mg · kg1 · min1,
Control vs. Exercise session, respectively;
P < 0.05). Also, in this subset of
subjects, exacerbated response of MSNA to hyperinsulinemia after
exercise was not observed (9.5 ± 8.3 vs. 13.6 ± 5.2 bursts/min, Control vs. Exercise session, respectively;
P = 0.115). Despite the small number
of subjects, these results suggest a possible association between the
increased MSNA response to insulin infusion after exercise and insulin
resistance. We believe this is the first time in the literature that
this behavior has been described. Therefore, it should be more deeply
investigated by future studies.
Aftereffects of Exercise on Insulin Sensitivity
Some authors (4, 6, 11, 21, 29), but not others (14, 30), have observed that acute exercise increases insulin sensitivity. The results from the present study agree with those of investigators who found no change in insulin sensitivity after exercise. The combination of methodological approach, population studied, exercise protocol, and time between exercise and measurements may explain the disparate results among studies. First, most studies (21, 29) employed a dose-response curve, whereas we used a single dose of insulin. Second, exercise-induced increase in insulin sensitivity is greater in insulin-resistant subjects (11). In the present study, subjects presented a large range of insulin sensitivity indexes [M/I values varied from 0.026 to 0.186 mg · kg1 · min1/(µU · ml1)].
Third, the aspects of an exercise protocol, such as exercise intensity
(4), muscle mass involved (6), and time between exercise and
measurements (14), are known to influence M; however, the ideal
protocol for postexercise enhancement of M is not known.
Study Limitations
Although vehicle and time control sessions were not performed in all subjects, saline studies carried out in three subjects suggested that time and vehicle cannot explain the response to insulin infusion that was observed in both Control and Exercise sessions. Similar results have already been obtained by other authors (2) in control trials for a longer period of time.Plasma glucose and insulin concentrations can be influenced by changes
in plasma volume that are caused by exercise. However, these changes
seem not to be the case in the present investigation, because
hematocrit and hemoglobin, as measured in our laboratory in eight
subjects before and after a bout of exercise similar to the one
employed in this study (cycle ergometer, 45 min, 50% O2 peak), did not
change significantly (hematocrit, 46.1 ± 2.1 vs. 45.6 ± 2.7, P = 0.302; hemoglobin, 15.5 ± 0.7 vs. 15.3 ± 0.9 mg/dl, P = 0.318).
Although MSNA was measured on the lower limb and muscle blood flow was measured on the upper limb, it is unlikely that the difference in measurement sites has limited our interpretation. Delius et al. (10) demonstrated that MSNA recorded in different sites was, in fact, similar.
Conclusion
In conclusion, in healthy subjects, a single bout of prolonged exercise, which does not alter insulin sensitivity, exacerbates insulin-induced increase in MSNA without changing FBF, FVR, and BP responses to hyperinsulinemia after exercise.| |
ACKNOWLEDGEMENTS |
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We thank the staff of the Hypertension Unit from the Medical School, University of São Paulo, for technical contributions, Dr. D. Giannella and M. A. H. Fortes for insulin determinations, and Mariana Curi for statistical analysis. We gratefully acknowledge the volunteers involved in this study.
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FOOTNOTES |
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This study was supported by Fundação de Amparo a Pesquisa do Estado de São Paulo 92/3979-0 and Fundação E. J. Zerbini.
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: C. E. Negrão, Av. Prof. Mello Moraes, 65, Butantã, São Paulo, SP, 05508-900 Brazil (E-mail: cenegrao{at}usp.br).
Received 11 May 1998; accepted in final form 26 April 1999.
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REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Anderson, E.A.,
and
A. L. Mark.
Microneurographic measurement of sympathetic nerve activity in humans.
In: Handbook of Research Methods in Cardiovascular Behavioral Medicine, edited by N. Schneiderman,
S. M. Weiss,
and P. G. Kaufmann. New York: Plenum, 1989, chapt. 7, p. 107-115.
2.
Anderson, E. A.,
R. P. Hoffman,
T. W. Balon,
C. A. Sinkey,
and
A. L. Mark.
Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.
J. Clin. Invest.
87:
2246-2252,
1991.
3.
Baron, A. D.,
G. Brechtel-Hook,
A. Johnson,
and
D. Hardin.
Skeletal muscle blood flow: a possible link between insulin resistance and blood pressure.
Hypertension
21:
129-135,
1993
4.
Ben-Ezra, V.,
C. Jankowski,
K. Kendrick,
and
D. Nichols.
Effect of intensity and energy expenditure on postexercise insulin responses in women.
J. Appl. Physiol.
79:
2029-2034,
1995
5.
Bennett, T.,
R. G. Wilcox,
and
I. A. Macdonald.
Post-exercise reduction of blood pressure in hypertensive men is not due to acute impairment of baroreflex function.
Clin. Sci. (Colch.)
67:
97-103,
1984[Medline].
6.
Brambrink, J. K.,
J. D. Fluckey,
M. S. Hickey,
and
B. W. Craig.
Influence of muscle mass and work on post-exercise glucose and insulin responses in young untrained subjects.
Acta Physiol. Scand.
161:
371-377,
1997[Medline].
7.
Cléroux, J.,
N. Kouamé,
A. Nadeau,
D. Coulombe,
and
Y. Lacourcière.
Aftereffects of exercise on regional and systemic hemodynamics in hypertension.
Hypertension
19:
183-191,
1992
8.
DeFronzo, R. A.,
and
E. Ferrannini.
Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease.
Diabetes Care
14:
173-194,
1991[Abstract].
9.
DeFronzo, R. A.,
J. D. Tobin,
and
R. Andres.
Glucose clamp technique: a method for quantifying insulin secretion and resistance.
Am. J. Physiol.
237 (Endocrinol. Metab. Gastrointest. Physiol. 6):
E214-E223,
1979
10.
Delius, W.,
K. E. Hagbarth,
A. Hongell,
and
B. C. G. Wallin.
General characteristics of sympathetic activity in human muscle nerves.
Acta Physiol. Scand.
84:
65-81,
1972[Medline].
11.
Devlin, J. T.,
and
E. S. Horton.
Effects of prior high-intensity exercise on glucose metabolism in normal and insulin-resistant men.
Diabetes
34:
973-979,
1985[Abstract].
12.
Forjaz, C. L. M.,
D. F. Santaella,
L. O. Rezende,
A. C. P. Barretto,
and
C. E. Negrão.
A duração do exercício determina a magnitude e a duração da hipotensão pós-exercício.
Arq. Bras. Cardiol.
70:
99-104,
1998[Medline].
13.
Franklin, P. J.,
D. J. Green,
and
N. T. Cable.
The influence of thermoregulatory mechanisms on post-exercise hypotension in humans.
J. Physiol. (Lond.)
470:
231-241,
1993
14.
Goodyear, L. J.,
M. F. Hirshman,
P. A. King,
E. D. Horton,
C. M. Thompson,
and
E. S. Horton.
Skeletal muscle plasma membrane glucose transport and glucose transporters after exercise.
J. Appl. Physiol.
68:
193-198,
1990
15.
Halliwill, J. R.,
J. A. Taylor,
and
D. L. Eckberg.
Impaired sympathetic vascular regulation in humans after acute dynamic exercise.
J. Physiol. (Lond.)
495:
279-288,
1996[Medline].
16.
Hara, K.,
and
J. S. Floras.
Effects of naloxone on hemodynamics and sympathetic activity after exercise.
J. Appl. Physiol.
73:
2028-2035,
1992
17.
Howard, M. G.,
and
S. E. DiCarlo.
Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit.
J. Appl. Physiol.
73:
2662-2667,
1992
18.
Johnson, P. C.,
P. D. Wagner,
and
D. F. Wilson.
Regulation of oxidative metabolism and blood flow in skeletal muscle: summary report of the First ACMS Basic Science Specialty Conference, Indianapolis, IN, September 28-30, 1995.
Med. Sci. Sports Exerc.
28:
305-314,
1996[Medline].
19.
Laakso, M.,
S. V. Edelman,
G. Brechtel,
and
A. D. Baron.
Decreased effects of insulin to stimulate skeletal muscle blood flow in obese man: a novel mechanism for insulin resistance.
J. Clin. Invest.
85:
1844-1852,
1990.
20.
Lembo, G.,
R. Napoli,
B. Capaldo,
V. Rendina,
G. Iaccarino,
M. Volpe,
B. Trimarco,
and
L. Saccà.
Abnormal sympathetic overactivity evoked by insulin in skeletal muscle of patients with essential hypertension.
J. Clin. Invest.
90:
24-29,
1992.
21.
Mikines, K. J.,
B. Sonne,
P. A. Farrell,
B. Tronier,
and
H. Galbo.
Effect of physical exercise on sensitivity and responsiveness to insulin in humans.
Am. J. Physiol.
254 (Endocrinol. Metab. 17):
E248-E259,
1988
22.
Minaker, K. L.,
J. W. Rowe,
J. B. Young,
D. Sparrow,
J. A. Pallotta,
and
L. Landsberg.
Effect of age on insulin stimulation of sympathetic nervous system activity in man.
Metabolism
31:
1181-1184,
1982[Medline].
23.
Patil, R. D.,
S. E. DiCarlo,
and
H. L. Collins.
Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine.
Am. J. Physiol.
265 (Heart Circ. Physiol. 34):
H1184-H1188,
1993
24.
Pereda, S. A.,
J. W. Eckstein,
and
F. M. Abboud.
Cardiovascular responses to insulin in the absence of hypoglycemia.
Am. J. Physiol.
202:
249-252,
1962.
25.
Rowe, J. W.,
J. B. Young,
K. L. Minaker,
A. L. Stevens,
J. Pallotta,
and
L. Landsberg.
Effect of insulin and glucose infusions on sympathetic nervous system activity in normal man.
Diabetes
30:
219-225,
1981[Medline].
26.
Siggaard-Andersen, J.
Venous occlusion plethysmography on the calf: evaluation of diagnosis and results in vascular surgery.
Dan. Med. Bull.
17:
1-42,
1970.
27.
Thorén, P.,
J. S. Floras,
P. Hoffmann,
and
D. R. Seals.
Endorphins and exercise: physiological mechanisms and clinical implications.
Med. Sci. Sports Exerc.
22:
417-428,
1990[Medline].
28.
Veen, S.,
and
P. C. Chang.
Prostaglandins and nitric oxide mediate insulin-induced vasodilation in the human forearm.
Cardiovasc. Res.
34:
223-229,
1997
29.
Wasserman, D. H.,
R. J. Geer,
D. E. Rice,
D. Bracy,
P. J. Flakoll,
L. L. Brown,
J. O. Hill,
and
N. N. Abumrad.
Interaction of exercise and insulin action in humans.
Am. J. Physiol.
260 (Endocrinol. Metab. 23):
E37-E45,
1991
30.
Young, C. J.,
J. Enslin,
and
B. Kuca.
Exercise intensity and glucose tolerance in trained and nontrained subjects.
J. Appl. Physiol.
67:
39-43,
1989
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 C. Rheaume, P. H. Waib, Y. Lacourciere, A. Nadeau, and J. Cleroux Effects of Mild Exercise on Insulin Sensitivity in Hypertensive Subjects Hypertension, May 1, 2002; 39(5): 989 - 995. [Abstract] [Full Text] [PDF]
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 C. E. Negrao, I. C. Trombetta, L. T. Batalha, M. M. Ribeiro, M. U. P. B. Rondon, T. Tinucci, C. L. M. Forjaz, A. C. P. Barretto, A. Halpern, and S. M. F. Villares Muscle metaboreflex control is diminished in normotensive obese women Am J Physiol Heart Circ Physiol, August 1, 2001; 281(2): H469 - H475. [Abstract] [Full Text] [PDF]
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