Rehydration with glycerol: endocrine, cardiovascular, and thermoregulatory responses during exercise in the heat.

The impact of rehydration with glycerol on cardiovascular and thermoregulatory responses during exercise in the heat was studied in eight highly trained male cyclists. Each subject completed three dehydration-rehydration experimental trials that differed only in the rehydration treatment, each separated by 7 days. Before each experimental day, subjects dehydrated to -4% of their body weight by exercise and water restriction. The experimental treatments were as follows: no fluid (NF), glycerol bolus (1 g/kg body wt) followed by water (G), and water alone (W). Rehydration (3% body weight) was given over an 80-min period. After rehydration, subjects cycled (74% peak O2 uptake) to exhaustion in a hot and wet (37 degrees C and 48% relative humidity) environment. For G, plasma volume was expanded (P < 0.05) during rehydration and remained higher than W (P < 0.05) during exercise. Exercise time to exhaustion during G (33 +/- 4 min) was longer (P < 0.05) compared with both W (27 +/- 3 min) and NF (19 +/- 3 min). Cutaneous vascular conductance was significantly elevated (P < 0.05) during G, but G provided no other thermoregulatory or cardiovascular benefits compared with W and NF. Fluid-regulating hormones (vasopressin, aldosterone, atriopeptin, and plasma renin activity) decreased during rehydration and increased during exercise (except atriopeptin), but there were no differences between G and W. These data indicated that glycerol had little or no major effect on fluid-regulating factors during rehydration or exercise, and the improved exercise capacity in G was likely due to a greater plasma volume during exercise.

Heat acclimation and physical training adaptations of young women using different contraceptive hormones.

Although endogenous and exogenous steroid hormones affect numerous physiological processes, the interactions of reproductive hormones, chronic exercise training, and heat acclimation are unknown. This investigation evaluated the responses and adaptations of 36 inactive females [age 21 +/- 3 (SD) yr] as they undertook a 7- to 8-wk program [heat acclimation and physical training (HAPT)] of indoor heat acclimation (90 min/day, 3 days/wk) and outdoor physical training (3 days/wk) while using either an oral estradiol-progestin contraceptive (ORAL, n = 15), a contraceptive injection of depot medroxyprogesterone acetate (DEPO, n = 7), or no contraceptive (EU-OV, n = 14; control). Standardized physical fitness and exercise-heat tolerance tests (36.5 degrees C, 37% relative humidity), administered before and after HAPT, demonstrated that the three subject groups successfully (P < 0.05) acclimated to heat (i.e., rectal temperature, heart rate) and improved muscular endurance (i.e., sit-ups, push-ups, 4.6-km run time) and body composition characteristics. The stress of HAPT did not disrupt the menstrual cycle length/phase characteristics, ovulation, or plasma hormone concentrations of EU-OV. No between-group differences (P > 0.05) existed for rectal and skin temperatures or metabolic, cardiorespiratory, muscular endurance, or body composition variables. A significant difference post-HAPT in the onset temperature of local sweating, ORAL (37.2 +/- 0.4 degrees C) vs. DEPO (37.7 +/- 0.2 degrees C), suggested that steroid hormones influenced this adaptation. In summary, virtually all adaptations of ORAL and DEPO were similar to EU-OV, suggesting that exogenous reproductive hormones neither enhanced nor impaired the ability of women to complete 7-8 wk of strenuous physical training and heat acclimation.

AMP-activated protein kinase activates transcription of the UCP3 and HKII genes in rat skeletal muscle.

AMP-activated protein kinase (AMPK) has recently emerged as a key signaling protein in skeletal muscle, coordinating the activation of both glucose and fatty acid metabolism in response to increased cellular energy demand. To determine whether AMPK signaling may also regulate gene transcription in muscle, rats were given a single subcutaneous injection (1 mg/g) of the AMP analog 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside (AICAR). AICAR injection activated (P < 0.05) AMPK-alpha 2 ( approximately 2.5-fold) and transcription of the uncoupling protein-3 (UCP3, approximately 4-fold) and hexokinase II (HKII, approximately 10-fold) genes in both red and white skeletal muscle. However, AICAR injection also elicited (P < 0.05) an acute drop (60%) in blood glucose and a sustained (2-h) increase in blood lactate, prompting concern regarding the specificity of AICAR on transcription. To maximize AMPK activation in muscle while minimizing potential systemic counterregulatory responses, a single-leg arterial infusion technique was employed in fully conscious rats. Relative to saline-infused controls, single-leg arterial infusion of AICAR (0.125, 0.5, and 2.5 micro g. g(-1). min(-1) for 60 min) induced a dose-dependent increase (2- to 4-fold, P < 0.05) in UCP3 and HKII transcription in both red and white skeletal muscle. Importantly, AICAR infusion activated transcription only in muscle from the infused leg and had no effect on blood glucose or lactate levels. These data provide evidence that AMPK signaling is linked to the transcriptional regulation of select metabolic genes in skeletal muscle.

Central nervous system control of heat acclimation adaptations: an emerging paradigm.

The role of the central nervous system (CNS) in the control of human heat acclimation (HA) and HA adaptations at the ultrastructural and biochemical level are not well described, although empirical evidence demonstrates that the hypothalamus adjusts thermoregulation subsequent to 8-14 days of exercise in a hot environment. Therefore, numerous investigations and concepts are presented in this paper that 1) describe plausible mechanisms for the development and CNS control of physiological adaptations and enhanced performance during heat acclimation, 2) include adaptations of neuron morphology and biochemical pathways, 3) account for situations in which homeostatic control during exercise in heat is inadequate, and 4) describe applications to other phenomena in physiology and medicine. The resulting paradigm incorporates information storage, temperature-sensitive neurons in the brain, and neural plasticity.

The effect of endurance-type exercise training on growth mediators and inflammatory cytokines in pre-pubertal and early pubertal males.

Recent studies demonstrate an unexpected reduction in circulating levels of IGF-I after 5 wk of endurance-type exercise training in adolescent boys and girls and prepubertal girls. We hypothesized that the reduction in IGF-I would be accompanied by a training-associated stimulation of proinflammatory cytokines IL-1beta, IL-6, or tumor necrosis factor-alpha (TNF-alpha), each of which can inhibit the GH-->IGF-I axis. Healthy boys (age range 9-11 y old, mean Tanner 1.7) volunteered for the study and were randomized to control (n = 14) and training groups (n = 12) for 5 wk. After the intervention, significant increase in fitness was observed in the training group but not control group. Although IGF-I was correlated at baseline to peak oxygen consumption in all subjects, there was a significant decrease in IGF-I and IGF binding protein-3 in the training subjects (-12.8 +/- 7.3% and -17.5 +/- 7%, respectively, p < 0.05). In contrast, IGF binding protein-2, known to inhibit anabolic effects of IGF-I, increased in the training subjects (27.8 +/- 11%, p < 0.02) as did IL-1beta and TNF-alpha (51.5 +/- 30.22%, p < 0.02, and 44.5 +/- 23.2%, p < 0.02, respectively). Finally, we also found that GHBP was inversely correlated with fitness, suggesting altered GH function in more-sedentary boys. Thus, these data support the hypothesis that a sustained increase in physical activity can stimulate proinflammatory cytokines, which may contribute to suppression of the GH-->IGF-I axis. Physical activity can influence growth and development through its influence on anabolic and catabolic mediators.