Short communication: Maternal heat stress during the dry period alters postnatal whole-body insulin response of calves

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P < .001) and 5 mm Hg (F6,24 = 5.4, P < .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F1,12 = 44.7, P < .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

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Leucine metabolism in lactating and dry goats: effect of insulin and substrate availability

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1993.265.3.e402 ◽

1993 ◽

Vol 265 (3) ◽

pp. E402-E413 ◽

Cited By ~ 3

Author(s):

S. Tesseraud ◽

J. Grizard ◽

E. Debras ◽

I. Papet ◽

Y. Bonnet ◽

...

Keyword(s):

Protein Synthesis ◽

Amino Acid ◽

Protein Degradation ◽

Whole Body ◽

Initial Slope ◽

Sensitivity Index ◽

Early Lactation ◽

Dry Period ◽

Body Protein ◽

Lactating Goats

Early lactating goats show insulin resistance with respect to extramammary glucose utilization. However, much less is known about the two major factors, insulin and plasma amino acid concentration, that regulate protein metabolism in lactating goats. To examine this question, the in vivo effect of acute insulin was studied in goats during early lactation (12-31 days postpartum), midlactation (98-143 days postpartum), and the dry period (approximately 1 yr postpartum). Insulin was infused (at 0.36 or 1.79 nmol/min) under euglycemic and eukaliemic clamps. In addition, appropriate amino acid infusion was used to blunt insulin-induced hypoaminoacidemia or to create hyperaminoacidemia and maintain this condition under insulin treatment. Leucine kinetics were assessed using a primed continuous infusion of L-[1-14C]-leucine, which started 2.5 h before insulin. In all animals the insulin treatments failed to stimulate the nonoxidative leucine disposal (an estimate of whole body protein synthesis) under both euaminoacidemic and hyperaminoacidemic conditions. Thus, in goat as well as humans, infusion of insulin fails to stimulate protein synthesis even when combined with a substantially increased provision of amino acids. In contrast, insulin treatments caused a dose-dependent inhibition of the endogenous leucine appearance (an estimate of whole body protein degradation). Under euaminoacidemia the initial slope from the plot of the endogenous leucine appearance as a function of plasma insulin (an insulin sensitivity index) was steeper during early lactation than when compared with the dry period. A similar trend occurred during midlactation but not to any significant degree. These differences were abolished under hyperaminoacidemia. It was concluded that the ability of physiological insulin to inhibit protein degradation was improved during lactation, demonstrating a clear-cut dissociation between the effects of insulin on protein and glucose metabolism. This adaptation no doubt may provide a mechanism to save body protein.

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Effects of treadmill exercise to exhaustion on the insulin response to hyperglycemia in untrained men

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.1.246 ◽

1991 ◽

Vol 70 (1) ◽

pp. 246-250 ◽

Cited By ~ 15

Author(s):

J. P. Kirwan ◽

R. E. Bourey ◽

W. M. Kohrt ◽

M. A. Staten ◽

J. O. Holloszy

Keyword(s):

Insulin Secretion ◽

Early Phase ◽

Pancreatic Beta Cell ◽

Late Phase ◽

Insulin Response ◽

Creatine Kinase Activity ◽

Whole Body ◽

Glucose Disposal ◽

C Peptide ◽

Hyperglycemic Clamp

The effects of a single bout of exercise to exhaustion on pancreatic insulin secretion were determined in seven untrained men by use of a 3-h hyperglycemic clamp with plasma glucose maintained at 180 mg/100 ml. Clamps were performed either 12 h after an intermittent treadmill run at approximately 77% maximum O2 consumption or without prior exercise. Arterialized blood samples for glucose, insulin, and C-peptide determination were obtained from a heated hand vein. The peak insulin response during the early phase (0–10 min) of the postexercise clamp was higher (81 +/- 8 vs. 59 +/- 9 microU/ml; P less than 0.05) than in the nonexercise clamp. Incremental areas under the insulin (376 +/- 33 vs. 245 +/- 51 microU.ml-1.min) and C-peptide (17 +/- 2 vs. 12 +/- 1 ng.ml-1.min) curves were also greater (P less than 0.05) during the early phase of the postexercise clamp. No differences were observed in either insulin concentrations or whole body glucose disposal during the late phase (15–180 min). Area under the C-peptide curve was greater during the late phase of the postexercise clamp (650 +/- 53 vs. 536 +/- 76 ng.ml-1.min, P less than 0.05). The exercise bout induced muscle soreness and caused an elevation in plasma creatine kinase activity (142 +/- 32 vs. 305 +/- 31 IU/l; P less than 0.05) before the postexercise clamp. We conclude that in untrained men a bout of running to exhaustion increased pancreatic beta-cell insulin secretion during the early phase of the hyperglycemic clamp. Increased insulin secretion during the late phase of the clamp appeared to be compensated by increased insulin clearance.

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Dry Period Heat Stress Relief Effects on Prepartum Progesterone, Calf Birth Weight, and Milk Production

Journal of Dairy Science ◽

10.3168/jds.s0022-0302(88)79621-6 ◽

1988 ◽

Vol 71 (3) ◽

pp. 809-818 ◽

Cited By ~ 64

Author(s):

D. Wolfenson ◽

I. Flamenbaum ◽

A. Berman

Keyword(s):

Heat Stress ◽

Birth Weight ◽

Milk Production ◽

Stress Relief ◽

Dry Period

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Heat stress alters hemodynamic responses during the Valsalva maneuver

Journal of Applied Physiology ◽

10.1152/japplphysiol.91642.2008 ◽

2010 ◽

Vol 108 (6) ◽

pp. 1591-1594 ◽

Cited By ~ 5

Author(s):

Scott L. Davis ◽

Craig G. Crandall

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Heat Stress ◽

Phase Ii ◽

Valsalva Maneuver ◽

Late Phase ◽

Thermal Conditions ◽

Whole Body ◽

Hemodynamic Responses ◽

Arterial Blood

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ∼0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (ΔMAP) relative to pre-Valsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = −20 ± 8 mmHg; IIb = −13 ± 7 mmHg) compared with normothermia (IIa = −1 ± 15 mmHg; IIb = 3 ± 13 mmHg). ΔMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase IIb during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia ( P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.

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