| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Original Studies |
Departments of Medicine, Molecular Physiology, and Biophysics, Vanderbilt University School of Medicine, and Nashville Veterans Administration/Juvenile Diabetes Foundation Diabetes Research Center, Nashville, Tennessee 37232
Address all correspondence and requests for reprints to: Stephen N. Davis, M.D., Division of Diabetes and Endocrinology, 712 MRB II, Vanderbilt University School of Medicine, Nashville, Tennessee 37232. E-mail: steve.davis{at}mcmail.vanderbilt.edu
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
50% VO2 max). Respiratory quotient and oxygen
consumption relative to body weight were identical in men and women.
Glycemia was equated (5.3 ± 0.2 mmol/L) during exercise via an
exogenous glucose infusion. Gender had significant effects on
counterregulatory responses during exercise. Arterialized epinephrine
(1.05 ± 0.2 vs. 0.45 ± 0.04 nmol/L),
norepinephrine (9.2 ± 1.1 vs. 5.8 ± 1.1
nmol/L), and pancreatic polypeptide (52 ± 6 vs.
37 ± 6 pmol/L) were significantly (P < 0.01)
increased in men compared to women, respectively. Plasma glucagon,
cortisol, and GH levels responded similarly in men and women. Insulin
values were higher at baseline in men and fell by a greater amount to
reach similar levels during exercise compared to those in women.
Endogenous glucose production, measured with
[3-3H]glucose was similar in men and women. Carbohydrate
oxidation was significantly increased in men relative to women
(21.2 ± 2 vs. 15.6 ± 2 mg/kg fat free
mass·min; P < 0.05). Despite reduced sympathetic
nervous system (SNS) drive, lipolytic responses were increased in
women. Arterialized blood glycerol (215 ± 30 vs.
140 ± 20 µmol/L), ß-hydroxybutyrate (54 ± 9
vs. 25 ± 10 µmol/L), and plasma nonesterified
fatty acids (720 ± 56 vs. 469 ± 103
µmol/L) were significantly (P < 0.01) increased
in women. In keeping with increased SNS activity, systolic blood
pressure and mean arterial pressure were significantly increased
(P < 0.01) in men. In summary, this study demonstrates that a significant sexual dimorphism exists in neuroendocrine, metabolic, and cardiovascular counterregulatory responses to prolonged moderate exercise in man. We conclude that during exercise, men have increased autonomic nervous system (epinephrine, norepinephrine, pancreatic polypeptide), cardiovascular (systolic, mean arterial pressure) and certain metabolic (carbohydrate oxidation) counterregulatory responses, but that women have increased lipolytic (glycerol, nonesterified fatty acids) and ketogenic (ß-hydroxybutyrate) responses. Women may compensate for diminished SNS activity during exercise by increased lipolytic responses.
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Thus, it remains controversial whether counterregulatory responses differ in men and women during exercise. Most of the above conflicting data arise due to studies incorporating varying experimental designs and investigating differing parameters during diverse work loads. A cohesive, integrative study simultaneously examining all of the key counterregulatory mechanisms during exercise in healthy men and women has not been performed and potentially could clarify most of the controversy surrounding this topic. Therefore, the aim of this present study was to determine whether a sexual dimorphism exists in physiological responses during exercise by performing a comprehensive, integrative assessment of neuroendocrine, metabolic, and cardiovascular counterregulatory responses. Plasma glucose was equated between groups, and subjects were matched for age, fitness level, fat mass, and nutrient intake.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
). Percent body fat, was, however,
significantly increased (P < 0.05) in women compared
to men. None was taking medication or had a family history of diabetes.
Each subject had a normal blood count, plasma electrolytes, and liver
and renal function. Female subjects were studied during the
midfollicular phase of their menstrual cycle. The experiments included
in this report are part of a larger study investigating the effects of
antecedent hypoglycemia on subsequent responses during exercise
(19).
|
At least 2 weeks before the initial study, subjects performed an incremental work test on a stationary cycle ergometer to determine maximal aerobic capacity (VO2 max) and anaerobic threshold (AT). Air flow and O2 and CO2 concentrations in inspired and expired air were measured by a computerized, open circuit, indirect calorimetry cart (Cardio2, Medical Graphics, Yorba Linda, CA) with a mouthpiece and nose clip system. The anaerobic threshold (AT) was determined by the V-slope method (20). The anaerobic threshold determined by gas exchange corresponds to the onset of an increased lactate/pyruvate ratio in blood and indicates the level of exercise above which anaerobic mechanisms supplement aerobic energy production (21). At workloads below the AT, exercise can be continued for a prolonged period, whereas above the AT, fatigue will occur considerably faster (22). The experimental work rate was established by calculating 80% AT. This corresponded to 47 ± 4% of the subject’s VO2 max. This workload was chosen because it is close enough to the AT to produce a physically challenging stress (i.e. large experimental signal), but is sustainable for a prolonged period of time. Subjects studied ranged from sedentary to actively participating in competitive sports. Body composition was measured by skinfold caliper technique (23) and bioelectrical impedence. Subjects were asked to avoid any exercise and consume their usual weight-maintaining diet for 3 days before an experiment. Each subject was admitted to the Vanderbilt clinical research center. On the day before the exercise test, subjects underwent identical morning and afternoon 2-h hyperinsulinemic-euglycemic clamps so that insulin sensitivity could be assessed (24). After completion of the second glucose clamp, subjects consumed identical meals and bedtime snacks (total, 1500 Cal), and remained in the Clinical Research Center.
Exercise protocol
All subjects were studied after an overnight fast. The work test consisted of 90 min of continuous submaximal exercise (at 60 rpm) on an upright cycle ergometer (Medical Graphics) at 80% of the individual’s anaerobic threshold. Two iv cannulas were inserted under 1% lidocaine local anesthesia. One cannula was placed in a retrograde fashion into a vein on the back of the hand. This hand was placed in a heated box (55–60 C) so that arterialized blood could be obtained (25). The other cannula was placed in the contralateral arm so that 20% glucose, 3-tritiated glucose, and saline could be infused. Plasma glucose levels were measured every 5 min, and a variable infusion of 20% dextrose was adjusted as needed to maintain plasma glucose at euglycemic levels. Larger blood samples were taken every 15 min to measure metabolic and neuroendocrine responses during exercise. To measure glucose kinetics, a primed (18-µCi) constant infusion (0.18 µCi/min) of [3-3H]glucose was commenced 120 min before the start of exercise. Infusion rates of [3-3H]glucose were doubled during the first 20 min of exercise to minimize changes in glucose specific activity (26). Rates of glucose appearance (Ra), endogenous glucose production (EGP), and glucose utilization (Rd) were calculated according to the methods of Wall et al. (27). EGP was calculated by determining the total rate of Ra (this comprises both endogenous glucose production and exogenous glucose infused to maintain the desired glucose level) and subtracting from it the amount of glucose infused. It is now recognized that this approach is not fully quantitative, as underestimates of total Ra and Rd can be obtained. This underestimate can be largely overcome by the use of highly purified tracer and taking measurements under steady state conditions (i.e. constant specific activity) as was done in the present experiments.
Indirect calorimetry
Air flow and O2 and CO2 concentrations in expired gases were measured by a computerized open circuit system (Medical Graphics Corp.). Rates of fat and carbohydrate oxidation and energy expenditure before and during exercise were calculated from rates of measured VO2 and VCO2 as described by Frayn (28), after correction of protein oxidation. Measured urinary nitrogen excretion during the overnight fast was used to estimate protein oxidation at rest. However, as urinary nitrogen excretion during exercise does not accurately reflect protein oxidation (29), the nitrogen excretion rate during exercise was assumed to be 7.7 µg/kg·min based on the data reported by Wolfe et al. during similar exercise studies in healthy humans (29).
Analytical methods
The collection and processing of blood samples have been described previously (30). Plasma glucose concentrations were measured in triplicate using the glucose oxidase method with a glucose analyzer (Beckman Coulter, Inc., Fullerton, CA). Glucagon was measured according to the method of Morgan and Lazarow with an interassay coefficient of variation (CV) of 15% (31). Insulin was measured as described previously (31) with an interassay CV of 11%. Catecholamines were determined by high pressure liquid chromatography (32) with interassay CVs of 17% for epinephrine and 14% for norepinephrine. We made two modifications to the procedure for catecholamine determination: 1) we used a five-point rather than a one-point standard calibration curve; and 2) we spiked the initial and final samples of plasma with known amounts of epinephrine and norepinephrine so accurate identification of the relevant respective catecholamine peaks could be made. Cortisol was assayed by using the Clinical Assays Gamma Coat RIA kit, with an interassay CV of 6%. GH was determined by RIA (33), with a CV of 8.6%. Pancreatic polypeptide was measured by RIA using the method of Hagopian et al. (34), with an interassay CV of 8%. Lactate, glycerol, alanine, and ß-hydroxybutyrate were measured on deproteinized whole blood using the method of Lloyd et al. (35). Nonesterified fatty acids (NEFA) were measured using the WAKO kit adopted for use on a centrifugal analyzer (36). Blood samples for glucose flux were taken every 10 min throughout the control period and every 15 min during the experimental period. Blood for determinations of hormones and intermediary metabolites was drawn twice during the control period and every 15 minduring the experimental period. Cardiovascular parameters (pulse, systolic, diastolic, and mean arterial pressure) were measured noninvasively by a Dinamap (Critikon, Tampa, FL) every 10 min and confirmed manually by a standing sphygmomanometer. Oxygen saturation and heart rate were measured continuously by a pulse oximeter.
Materials
High pressure liquid chromatography-purified [3-3H]glucose (New England Nuclear, Boston, MA) was used as the glucose tracer (11.5 mCi/mmol/L). Human regular insulin was purchased from Eli Lilly & Co. (Indianapolis, IN). The insulin infusion solution was prepared with normal saline and contained 3% (vol/vol) of the subject’s own plasma.
Statistical analysis
Data are expressed as the mean ± SE unless otherwise stated and analyzed using a standard, parametric ANOVA with a repeated measures design. This was coupled with Duncan’s post-hoc test to delineate at what time statistical significance was reached.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Glucose levels were similar in both groups at the start of
exercise. Insulin fell by a significantly (P < 0.01)
greater proportion in males (decrease of 53 ± 7%) compared to
females (decrease of 34 ± 4%). Absolute levels of insulin were,
however, similar during the final 30 min of exercise (Fig. 1). Glucose levels were maintained similar to
baseline values during exercise (5.4 ± 0.2 mmol/L) and did not
differ in males and females (Fig. 1).
|
In response to exercise, plasma levels of epinephrine,
norepinephrine, cortisol, GH, and pancreatic polypeptide increased from
baseline (P < 0.01). Despite equivalent plasma glucose
values, epinephrine levels (Fig. 2) increased by a significantly
greater amount (P < 0.01) in males compared to
females. By the final 30 min of exercise, epinephrine had increased
from a basal value of 0.18 ± 0.03 to 1.05 ± 0.2 nmol/L in
men, but only from 0.14 ± 0.02 to 0.45 ± 0.04 nmol/L in
women. Plasma norepinephrine levels had also increased by a greater
amount (P < 0.01) by the final 30 min of exercise in
men (1.4 ± 0.2 to 9.2 ± 1.1 nmol/L) compared to women
(1.3 ± 0.2 to 5.8 ± 1.1 nmol/L). Similarly, plasma
pancreatic polypeptide levels (Fig. 2) were
further increased (P < 0.05) in men (14.3 ± 2 to
51.8 ± 6 pmol/L) relative to women (13.6 ± 2 to 37.5
± 6 pmol/L). Plasma glucagon, cortisol, and GH increased similarly
during exercise in men and women (Table 2).
|
|
Glucose specific activity (disintegrations per min/mmol) was in a
steady state during the control period and final 30 min of each
exercise protocol (Table 3). Basal rates of
EGP were equivalent at the start of exercise (11.0 ± 0.6
µmol/kg·min) and increased similarly in men and women (Table 3).
During the final 30 min of exercise, EGP had increased to 20.4 ±
1.1 and 19.3 ± 1.7 µmol/kg·min in men and women,
respectively. Similar rates of glucose infusion were required to
maintain euglycemia in men and women (1.1 ± 0.6 µmol/kg·min).
Rates of glucose disappearance were also equivalent during the final 30
min of exercise in men (21.5 ± 1.7 µmol/kg·min) and women
(20.4 ± 1.7 µmol/kg·min).
|
Blood lactate and alanine responses were equivalent during
exercise in men and women (Table 4).
Lipolytic and ketogenic responses, however, were significantly
increased in women. Blood glycerol levels in women increased from a
basal value of 60 ± 10 to 215 ± 30 µmol/L by the final 30
min of exercise. This increase was significantly greater
(P < 0.01) than the elevations in glycerol observed in
men (40 ± 10 to 140 ± 20 µmol/L). Plasma NEFA levels were
also significantly higher (P < 0.01) in women
(464 ± 63 to 720 ± 56 µmol/L) than in men (266 ± 35
to 469 ± 103 µmol/L). ß-Hydroxybutyrate levels increased
significantly (30 ± 5 to 54 ± 9 µmol/L; P
< 0.01) in women, but did not change from baseline in men (20 ±
3 to 25 ± 10 µmol/L).
|
Men and women exercised at an identical relative work intensity (48 ± 2% VO2 max). Respiratory quotient was also equivalent during exercise in both groups (0.92 ± 0.01). Men worked at a higher absolute intensity and consumed more O2 (milliliters per min) during exercise. However, when oxygen consumption was corrected for body weight, there was no difference between men (22.1 ± 2 mL/kg·min) and women (22.8 ± 2 mL/kg·min). Basal values for carbohydrate oxidation were similar at the start of exercise (2.0 ± 0.2 mg/kg·fat-free mass), but increased to significantly greater levels (P < 0.05) in men (21.2 ± 2 mg/kg fat-free mass·min) relative to women (15.6 ± 2 mg/kg fat-free mass·min). Lipid oxidation increased to similar values during exercise in men (0.5 ± 0.1 to 2.6 ± 0.4 mg/kg fat-free mass·min) and women (0.6 ± 0.1 to 2.2 ± 0.3 mg/kg fat-free mass·min).
Cardiovascular parameters
Heart rate increased similarly (P < 0.01) from baseline to the final 30 min of exercise in men (62 ± 5 to 150 ± 6 beats/min) and women (70 ± 6 to 156 ± 8 beats/min). Systolic blood pressure, however, increased by a significantly greater amount (P < 0.01) in men (110 ± 2 to 173 ± 3 mm Hg) than in women (105 ± 2 to 145 ± 2 mm Hg). Diastolic blood pressure increased similarly during exercise in both groups (men, 66 ± 2 to 76 ± 3; women, 66 ± 2 to 78 ± 3 mm Hg). Therefore, mean arterial pressure increased to significantly greater levels (P < 0.01) during exercise in men (109 ± 3 mm Hg) than in women (100 ± 3 mm Hg).
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
The role played by gender in physiological responses to stress is incompletely understood. Recently, large sexual dimorphisms have been determined in commonly occurring physiological conditions such as hypoglycemia, fasting, and cognitive testing (1, 2, 3, 4, 5). In general, these physical stresses are characterized by increased neuroendocrine (particularly catecholamine) and metabolic responses in men. During hypoglycemia, a wide spectrum of neuroendocrine counterregulatory responses is significantly increased in men, with the result that the key homeostatic mechanism of EGP is dramatically reduced in women (2, 5). Similarly, during moderate fasting, reduced counterregulatory responses in women result in significantly lower plasma glucose levels relative to those in men (1). Thus, although there is a consensus regarding the physiology of gender-related differences during hypoglycemia and fasting, there is considerable controversy regarding whether a significant sexual dimorphism exists in counterregulatory responses during exercise. Recent studies investigating this topic have provided conflicting information. Individual studies have reported either an increase or no difference in lipolytic capacity (7, 9, 10, 11, 12) in women relative to men during exercise. Similarly, data are available supporting either increased epinephrine or norepinephrine or no difference in these catecholamine levels during exercise in men relative to women (6, 7, 8, 9). Interestingly the critical neuroendocrine hormone glucagon and homeostatic mechanism of EGP have not been investigated. Furthermore, comparative information regarding other neuroendocrine hormones, such as insulin, pancreatic polypeptide, cortisol, and GH, is either unreported or extremely limited.
The exercise test performed in this present study was carried out at a work intensity of 80% at each individual’s anaerobic threshold (48% VO2 max) for 90 min. Performing the exercise test in this fashion controls for relative differences in physical fitness between subjects. Thus, if an identical work load had been applied to all subjects, this may have resulted in a relatively minor stress in a physically trained individual but a much larger stress in an untrained subject. The resultant neuroendocrine and ANS responses would have been independently influenced by the relative degree of stress and would therefore have confounded any meaningful interpretation of gender-related differences. The duration of physical activity was chosen to be commensurate with work expended during soccer or tennis matches, competitive bike rides, or a prolonged training run and is thus indicative of a broad range of exercise enjoyed by men and women. Furthermore, most physiological counterregulatory mechanisms increase with exercise duration. Therefore, a test protocol of 90 min allows for the generation of a large experimental signal, so that any gender-related differences can be clearly determined.
In the present study plasma glycemia levels were identical in men and
women, thereby allowing a direct interpretation of counterregulatory
responses. Despite identical relative exercise intensit, per kg oxygen
consumption, insulin sensitivity, and plasma glycemia, the plasma
epinephrine and norepinephrine responses were significantly increased
(
2-fold) in men relative to women. In the absence of any available
data indicating that catecholamine clearance is altered by gender
(either increased in women or decreased in men), it would appear that
the elevated levels of epinephrine and norepinephrine in men indicate
increased SNS activity during exercise. This is supported by data from
Ettinger et al., who demonstrated increased SNS drive in men
during static exercise using direct recordings of muscle sympathetic
nerve activity (13). Pancreatic polypeptide responses were also
significantly increased in men compared to women. Pancreatic
polypeptide is a marker of vagal efferent input to the pancreas and
thus can serve as an indicator of parasympathetic nervous system
activity during stress. It would therefore appear that the
constellation of elevated epinephrine, norepinephrine, and pancreatic
polypeptide responses indicates an increased ANS response to exercise
in males relative to females. This finding is similar to the increased
ANS counterregulatory responses that occur during hypoglycemia in men
relative to women (2). Insulin levels fell by a proportionally greater
amount in men during exercise. Suppression of insulin during exercise
is thought to be primarily mediated by 
-adrenergic activity (37).
Therefore, the finding of greater suppression of insulin during
exercise is consistent with the premise of increased SNS drive in men.
Plasma glucagon, cortisol, and GH responses were similar in men and
women. Thus, it would appear that exercise is characterized by a
specific increase in ANS drive (adrenal gland, sympathetic nerve
endings, pancreas) in men relative to women.
Metabolic responses during exercise can be broadly split into three main mechanisms: EGP, fuel oxidation, and lipolytic responses. EGP was similar during exercise in men and women. After an overnight fast, the source of EGP during exercise arises almost totally from the liver (37). Neuroendocrine control of hepatic glucose production during moderate intensity exercise is thought to be regulated principally via increases in glucagon and decreases in insulin levels (37). In the present study, glucagon levels were identical in men and women. Insulin levels were higher at baseline in men, but decreased by a significantly greater amount relative to those in women during the exercise. By 30 min of exercise insulin levels were similar in men and women. Thus, it would appear that during moderate intensity exercise in men, the primary regulators of EGP are glucagon and insulin. Certainly in this study, the dramatic elevation of SNS drive in men did not translate into increased EGP.
Indirect calorimetry measurements during exercise demonstrated that carbohydrate oxidation was significantly increased in men relative to women. This is supported by data from Tarnopolsky et al. (11) and is thought to result from greater mobilization of glycogen stores in men. It should be noted that each subject received an identical diet and underwent identical experimental procedures during the 36 h before exercise; therefore, glycogen levels would have been equivalent at baseline in men and women.
Paradoxically, despite similar fat masses in our male and female
subjects, elevated SNS drive in men did not translate into greater
lipolytic responses. In fact, glycerol, NEFA, and ß-hydroxybutyrate
responses were greater in women. The finding of increased lipolytic
responses during exercise in women has been observed in some, but not
all, previous studies (7, 9, 10, 11, 12). The mechanisms responsible for this
finding have not been fully elucidated, but could include increased
percent body fat per se or elevated regional lipolysis
(i.e. abdominal) and greater ß-adrenergic effects during
exercise in women (12, 38). Exercise in men results in both - and
ß-adrenoreceptor activation, whereas in women only the latter are
activated (12, 38). -Adrenergic receptors inhibit lipolysis (12, 38). Therefore, in men, SNS activation results in a net effect of
lipolytic and antilipolytic activities. The combination of simultaneous
activation of - and [beta-adrenoreceptors in men during exercise
may thus lead to reduced lipolytic responses relative to those in
women. However, the role that increased percent body fat per
se may play in enhancing lipolytic responses in women should not
be overlooked and requires further study. The increased lipolytic
responses in women may explain why glucose kinetics (both production
and utilization) were similar in males and females despite
significantly reduced SNS drive in the latter. Increased NEFA levels
would have reduced glucose uptake in women by creating an alternative
substrate for skeletal muscle oxidation. Similarly, increased glycerol
flux to the liver would represent substantial gluconeogenic substrate,
and elevated NEFA levels would have provided metabolic fuel for
gluconeogenesis. It therefore appears that the increased lipolytic
responses in women may have significant counterregulatory effects
during exercise.
The increased systolic and mean arterial blood pressures observed in men are consistent with a greater SNS drive. Ventricular contractility in humans is mediated via ß1- and ß2-adrenoreceptors. Thus, it would appear that increased SNS drive to ß-adrenoreceptors during exercise in men can result in increased systolic blood pressure. Interestingly, increased parasympathetic activity in males may have offset the chronotropic effects of elevated SNS drive and therefore produced equivalent increases in heart rate in men and women.
In summary, prolonged moderate exercise in men and women performed under conditions of equivalent glycemia is characterized by a sexual dimorphism in autonomic nervous system, metabolic, and cardiovascular responses. Plasma epinephrine, norepinephrine, pancreatic polypeptide, percent suppression of insulin, carbohydrate oxidation, and increases in systolic blood pressure were greater in men relative to women. Lipolytic responses were, however, greater in women relative to men. Plasma glucagon responses and rates of EGP were similar in men and women.
We conclude that prolonged moderate exercise produces greater autonomic nervous system counterregulatory responses in men relative to women. Greater lipolytic responses in women may compensate for their inherently reduced SNS drive occurring during exercise.
|
Acknowledgments |
|---|
|
Footnotes |
|---|
Received September 7, 1999.
Revised October 7, 1999.
Accepted October 12, 1999.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
 |
|
 |
|
  T. J. Horton, S. Dow, M. Armstrong, and W. T. Donahoo Greater systemic lipolysis in women compared with men during moderate-dose infusion of epinephrine and/or norepinephrine J Appl Physiol, July 1, 2009; 107(1): 200 - 210. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Sandoval, B. Gong, and S. N. Davis Antecedent short-term central nervous system administration of estrogen and progesterone alters counterregulatory responses to hypoglycemia in conscious male rats Am J Physiol Endocrinol Metab, December 1, 2007; 293(6): E1511 - E1516. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. J. Guelfi, N. Ratnam, G. A. Smythe, T. W. Jones, and P. A. Fournier Effect of intermittent high-intensity compared with continuous moderate exercise on glucose production and utilization in individuals with type 1 diabetes Am J Physiol Endocrinol Metab, March 1, 2007; 292(3): E865 - E870. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Scott, B. T. A. Esch, M. J. Haykowsky, S. Isserow, M. S. Koehle, B. G. Hughes, D. Zbogar, S. S. D. Bredin, D. C. McKenzie, and D. E. R. Warburton Sex differences in left ventricular function and beta-receptor responsiveness following prolonged strenuous exercise J Appl Physiol, February 1, 2007; 102(2): 681 - 687. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Momen, B. Handly, A. Kunselman, U. A. Leuenberger, and L. I. Sinoway Influence of sex and active muscle mass on renal vascular responses during static exercise Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H121 - H126. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. J. Horton, G. K. Grunwald, J. Lavely, and W. T. Donahoo Glucose kinetics differ between women and men, during and after exercise J Appl Physiol, June 1, 2006; 100(6): 1883 - 1894. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Galassetti, D. Tate, R. A. Neill, A. Richardson, S.-Y. Leu, and S. N. Davis Effect of differing antecedent hypoglycemia on counterregulatory responses to exercise in type 1 diabetes Am J Physiol Endocrinol Metab, June 1, 2006; 290(6): E1109 - E1117. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. W. Timmons, M. A. Tarnopolsky, and O. Bar-Or Sex-based effects on the distribution of NK cell subsets in response to exercise and carbohydrate intake in adolescents J Appl Physiol, May 1, 2006; 100(5): 1513 - 1519. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. R. Galassetti, K. Iwanaga, A. M. Pontello, F. P. Zaldivar, R. L. Flores, and J. K. Larson Effect of prior hyperglycemia on IL-6 responses to exercise in children with type 1 diabetes Am J Physiol Endocrinol Metab, May 1, 2006; 290(5): E833 - E839. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Volinic, J. H. Lee, K. Eto, V. Kaur, and M. K. Thomas Overexpression of the Coactivator Bridge-1 Results in Insulin Deficiency and Diabetes Mol. Endocrinol., January 1, 2006; 20(1): 167 - 182. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. W. Timmons, M. J. Hamadeh, M. C. Devries, and M. A. Tarnopolsky Influence of gender, menstrual phase, and oral contraceptive use on immunological changes in response to prolonged cycling J Appl Physiol, September 1, 2005; 99(3): 979 - 985. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y Karakoc, H Duzova, A Polat, M H Emre, and I Arabaci Effects of training period on haemorheological variables in regularly trained footballers Br. J. Sports Med., February 1, 2005; 39(2): e4 - e4. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Galassetti, D. Tate, R. A. Neill, S. Morrey, D. H. Wasserman, and S. N. Davis Effect of sex on counterregulatory responses to exercise after antecedent hypoglycemia in type 1 diabetes Am J Physiol Endocrinol Metab, July 1, 2004; 287(1): E16 - E24. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Richterova, V. Stich, C. Moro, J. Polak, E. Klimcakova, M. Majercik, I. Harant, N. Viguerie, F. Crampes, D. Langin, et al. Effect of Endurance Training on Adrenergic Control of Lipolysis in Adipose Tissue of Obese Women J. Clin. Endocrinol. Metab., March 1, 2004; 89(3): 1325 - 1331. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. White, M. A. Ferguson, S. C. McCoy, and H. Kim Intramyocellular Lipid Changes in Men and Women during Aerobic Exercise: A 1H-Magnetic Resonance Spectroscopy Study J. Clin. Endocrinol. Metab., December 1, 2003; 88(12): 5638 - 5643. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Sandoval, A. C. Ertl, M. A. Richardson, D. B. Tate, and S. N. Davis Estrogen Blunts Neuroendocrine and Metabolic Responses to Hypoglycemia Diabetes, July 1, 2003; 52(7): 1749 - 1755. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Galassetti, D. Tate, R. A. Neill, S. Morrey, and S. N. Davis Effect of Gender on Counterregulatory Responses to Euglycemic Exercise in Type 1 Diabetes J. Clin. Endocrinol. Metab., November 1, 2002; 87(11): 5144 - 5150. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Nemet, S. Hong, P. J. Mills, M. G. Ziegler, M. Hill, and D. M. Cooper Systemic vs. local cytokine and leukocyte responses to unilateral wrist flexion exercise J Appl Physiol, August 1, 2002; 93(2): 546 - 554. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. C. Ruby, A. R. Coggan, and T. W. Zderic Gender differences in glucose kinetics and substrate oxidation during exercise near the lactate threshold J Appl Physiol, March 1, 2002; 92(3): 1125 - 1132. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M Dart, X.-J. Du, and B. A Kingwell Gender, sex hormones and autonomic nervous control of the cardiovascular system Cardiovasc Res, February 15, 2002; 53(3): 678 - 687. [Full Text] [PDF]
|
|
|
|
|
|
D. A. Sandoval and K. S. Matt Gender differences in the endocrine and metabolic responses to hypoxic exercise J Appl Physiol, February 1, 2002; 92(2): 504 - 512. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. S. Stachenfeld, A. E. Splenser, W. L. Calzone, M. P. Taylor, and D. L. Keefe Genome and Hormones: Gender Differences in Physiology: Selected Contribution: Sex differences in osmotic regulation of AVP and renal sodium handling J Appl Physiol, October 1, 2001; 91(4): 1893 - 1901. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. P. Stein and C. E. Wade The catecholamine response to spaceflight: role of diet and gender Am J Physiol Endocrinol Metab, September 1, 2001; 281(3): E500 - E506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Galassetti, S. Mann, D. Tate, R. A. Neill, D. H. Wasserman, and S. N. Davis Effect of morning exercise on counterregulatory responses to subsequent, afternoon exercise J Appl Physiol, July 1, 2001; 91(1): 91 - 99. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. K. Adler Editorial: Exercise and Fatigue--Is Neuroendocrinology an Important Factor? J. Clin. Endocrinol. Metab., June 1, 2000; 85(6): 2167 - 2169. [Full Text]
|
|
|
|
|
|
S. Blanc, S. Normand, C. Pachiaudi, J.-O. Fortrat, M. Laville, and C. Gharib Fuel Homeostasis during Physical Inactivity Induced by Bed Rest J. Clin. Endocrinol. Metab., June 1, 2000; 85(6): 2223 - 2233. [Abstract] [Full Text]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
