Thermal regulation in the heat during exercise after caffeine and ephedrine ingestion.
ABSTRACT Ingesting a combination of caffeine and ephedrine (C+E) has been shown to raise metabolic heat production and body temperature. This side effect of C+E ingestion may be positive during a cold stress scenario, however, during heat stress it could prove to be detrimental. Thus, the purpose of this study was to clarify the effect of C+E ingestion on body temperature regulation during moderate exercise in a hot dry environment.
Ten, healthy, non heat acclimated, males exercised at 50% VO2peak in a 40 degrees C and 30% RH environment until rectal temperature reached 39.3 degrees C; heart rate (HR) remained at 95% of peak value or greater for 3 min, dizziness or nausea precluded further exercise, or 3 h had elapsed. They did this four times at weekly intervals: familiarization (Fam), control (Cont), placebo, and C+E (5 mg . kg(-1) caffeine + 1 mg . kg(-1) ephedrine) trials. The Fam and Cont treatments were done first and sequentially while the placebo and C+E treatments were balanced and double-blind. Tolerance times, mean skin temperature (Tsk), rectal temperature (Tre), Vo2, Vco2, VE, sweat rate (SR), HR, and sensation of thermal comfort were measured.
Tolerance times (mean+/-SD in minutes) were similar for the placebo (120.0+/-28.4) and C+E (121.3+/-33.9) trials and both times were significantly longer than Cont (106.6+/-24.0) trial. C+E did not affect Tsk, initial TrC, delta Tre, SR or the sensation of thermal comfort. VO2 and VF, were significantly increased by C+E. HR was elevated by C+E compared with the other trials, but only during the initial 20 min of exercise.
Although the metabolic rate was slightly increased with C+E treatment, it was sufficiently offset by increased heat loss mechanisms so that internal body temperature was not increased during moderate exercise in a hot, dry environment.
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ABSTRACT: Abstract Text: The objective of this study was to test the hypothesis that glucose-insulin homeostasis, and activation of AMP-activated protein kinase (AMPK), the protein kinase Akt, and the Akt substrate protein of 160 kDa (AS160) in equine skeletal muscle are altered by acute, exhaustive exercise and by aging. Unconditioned aged (n=6; 22.6 ± 2.25 years) and young (n=6; 5.5 ± 2.8 years) Standardbred mares were assessed for glucose-insulin homeostasis via frequently sampled intravenous glucose tolerance test (FSIGTT). All mares underwent a single bout of submaximal exercise. Plasma insulin and glucose concentrations were measured via radioimmunoassay and enzyme-electrode interface, respectively. Mid-gluteal muscle biopsies were taken pre-exercise, and at 0, 4, 24 and 48 h post-exercise. Muscle samples were analyzed via western immunoblotting for changes in activation of AMPK, Akt and AS160. Minimal model analysis of FSIGTT and repeated measures ANOVA were utilized to analyze data. Null hypothesis was rejected when P<0.05. FSIGTT results indicated that there was no difference between young and aged mares for insulin sensitivity (SI), glucose effectiveness (SG), acute insulin response to glucose (AIRg) or disposition index (AIRg x SI) (P>0.05). Area under the curve for both insulin (AUCi) and glucose (AUCg) were not different between young and aged mares (P>0.05). In response to acute exercise, young mares displayed elevated insulin concentrations at 2 (P=0.009) and 4 (P=0.007) h while aged mares displayed elevated insulin at 30 (P<0.001) and 60 (P=0.001) minutes post-exercise. Neither age nor exercise caused a significant change in AUCi (P>0.05). Glucose concentration was elevated at 2 h post-exercise in young mares (P<0.001), while in aged mares glucose remained elevated only until 60 min post-exercise (P=0.037). Exercise caused an increase in AUCg in young (P=0.007) and aged (P=0.031) mares, however there was no age effect on AUCg (P>0.05). Neither age nor exercise altered total protein concentrations or phosphorylated protein concentrations of AMPK, Akt or AS160 (P>0.05). In conclusion, age alone is not sufficient to alter insulin sensitivity in horses, but does alter glucose-insulin dynamics in response to exercise. Also, a single bout of submaximal exercise was not sufficient to alter activation of proteins believed to be involved in glucose uptake in skeletal muscle at the timepoints measured. The comparative literature suggests that these proteins are important for endocrine- and exercise-related glucose uptake and energy homeostasis. Keywords: Aging, Exercise, Muscle2014 ADSA-ASAS-CSAS Joint Annual Meeting; 07/2014
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ABSTRACT: This article presents a historical overview and an up-to-date review of hyperthermia-induced fatigue during exercise in the heat. Exercise in the heat is associated with a thermoregulatory burden which mediates cardiovascular challenges and influence the cerebral function, increase the pulmonary ventilation, and alter muscle metabolism; which all potentially may contribute to fatigue and impair the ability to sustain power output during aerobic exercise. For maximal intensity exercise, the performance impairment is clearly influenced by cardiovascular limitations to simultaneously support thermoregulation and oxygen delivery to the active skeletal muscle. In contrast, during submaximal intensity exercise at a fixed intensity, muscle blood flow and oxygen consumption remain unchanged and the potential influence from cardiovascular stressing and/or high skin temperature is not related to decreased oxygen delivery to the skeletal muscles. Regardless, performance is markedly deteriorated and exercise-induced hyperthermia is associated with central fatigue as indicated by impaired ability to sustain maximal muscle activation during sustained contractions. The central fatigue appears to be influenced by neurotransmitter activity of the dopaminergic system, but inhibitory signals from thermoreceptors arising secondary to the elevated core, muscle and skin temperatures and augmented afferent feedback from the increased ventilation and the cardiovascular stressing (perhaps baroreceptor sensing of blood pressure stability) and metabolic alterations within the skeletal muscles are likely all factors of importance for afferent feedback to mediate hyperthermia-induced fatigue during submaximal intensity exercise. Taking all the potential factors into account, we propose an integrative model that may help understanding the interplay among factors, but also acknowledging that the influence from a given factor depends on the exercise hyperthermia situation. © 2014 American Physiological Society. Compr Physiol 4:657-689, 2014.04/2014; 4(2):657-89. DOI:10.1002/cphy.c130012
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ABSTRACT: Multiple doses of the dietary supplement L-ephedrine can cause severe hyperthermia and modest dopamine depletions in the rat brain. Since D-amphetamine treatment can result in neurodegeneration, the potential of L-ephedrine to produce similar types of degeneration was investigated. Adult male rats, some implanted in the caudate/putamen (CPu) for microdialysis, were given four doses of 25 mg/kg L-ephedrine or 5 mg/kg D-amphetamine (2 h between doses) at an ambient temperature of 23 degrees C. L-ephedrine-induced degeneration in the forebrain was dependent on the degree of hyperthermia. Layer IV of the parietal cortex was the most sensitive to L-ephedrine treatment with peak body temperatures of at most 40.0 degrees C necessary to produce degeneration. Extensive neurodegeneration in the parietal cortex after L-ephedrine treatment was as pronounced as that previously described for D-amphetamine treatment and also occurred in the intralaminar, ventromedial and ventrolateral thalamic nuclei in rats with severe hyperthermia (peak body temperatures>41.0 degrees C). The neurodegeneration induced by L-ephedrine may have resulted in part from excitotoxic mechanisms involving the indirect pathways of the basal ganglia and related areas. No differences were observed between microdialysis and non-implanted rats with respect to degree of tyrosine hydroxylase (TH) loss in the CPu after either D-amphetamine or L-ephedrine treatment. However, neurodegeneration resulting from D-amphetamine and L-ephedrine was reduced in the microdialysis animals in the hemisphere ipsilateral to the probe, which raises concerns when using the technique of in vivo microdialysis to evaluate neurodegeneration. The results of this study, in conjunction with human clinical evaluation of ephedrine neurotoxicity, indicate that regionally specific damage may occur in the cortex of some humans exposed to ephedrine in the absence of stroke or hemorrhage.Toxicology Letters 12/2001; 125(1-3):151-66. DOI:10.1016/S0378-4274(01)00440-4 · 3.36 Impact Factor