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We studied the influence of heat acclimation (1 to 48 h and 4 to 60 d at 35 +/- 1 degrees C) on certain hepatic carbohydrate-related enzymes and substrates in rats. The results showed a decrease of liver glycogen content and GPho-ase a activity during the period of short-term exposure, followed by normalization to the control level and stabilization to the new level in the period of long-term heat acclimation. Conversely, G-6-P-ase and F-1,6-BP-ase activities increased during the short-term period, followed by a decrease and stabilization to a new, lower level in the prolonged acclimation. The blood glucose level decreased during whole period of acclimation, whereas intermediate substrates increased during the short-term and stabilized at a new, higher level during prolonged acclimation. The time-dependent changes of duration of heat acclimation could be summarized in three phases: short-term heat exposure (1 to 24 h) with intensive glycogenolysis and gluconeogenesis to glucose; a period with temporary changes (24 h to 7 d) with tendency of normalization to control level, and prolonged heat acclimation (7 d to 60 d), which favors both direct and indirect glycogen synthesis.

Based on the observation that heat acclimation is a slowly developing response, evoked by continuous exposure to moderate heat, we investigated the time-dependent acclimatory changes of heart glycogen metabolism. Cardiac levels of key carbohydrate-related enzymes and substrates were studied in the function of the duration of short-term (STHA; 6, 12, 24 and 48 h) and long-term heat acclimation (LTHA; 7, 14, 21 and 30 days) to high environmental temperature (35 ± 1°C). The changes in heart glycogen metabolism during STHA could be separated in two phases: up to 12 h exposure, where significant decrease of the heart glycogen (Glk), glucose-6-phosphate (G6P), hexokinase (HK) activity as well as increase of heart glucose was observed; and from 24 to 48 h exposure, manifested with elevation of Glk, Glu, glycogen phosphorylase a (GPa), phosphofructokinase (PFK) and HK activities. The metabolic changes in the period of LTHA could also be seen as separate phases: in a period of 7-14 days of heat exposure there was an increase of heart Glk, Glu, G6P, HK, as well as a decrease of GPa and PFK, while in the period of 21-28 days there was more intensive rebound of Glk and G6P, increase of GPa activity and non-significant changes of Glu, HK and PFK. The results obtained have showed that acclimation to moderate hyperthermic environment has caused significant changes in examined parameters which differ depending on duration to the exposure: intensive stress-induced glycogenolytic and glycolytic processes in the period of STHA and intensive energy sparing, manifested by Glk deposition in the period of LTHA.

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Adaptation to one environmental stressor sometimes provides protection against additional, more intensive type of stress, a phenomenon called cross-tolerance. We aimed to estimate theprotection provided by acute heat stress (AHS) over carbohydrate disturbances in streptozotocin-diabetic rats. We investigated changes in activity of some hepatic glycolitic and gluconeogenic enzymes, and concentration of some substrates in control and diabetic animals exposed to AHS (41±0.5°C / 1 h), with 1 h and 24 h recovery at room temperature before sacrifice or induction of streptozotocin (STZ)-diabetes, respectively. AHS with 1 h-recovery before sacrifice resulted in intensive glycogenolysis, directed to endogenous glucose production and further utilization of glucose by peripheral tissues, while 24 h recovery resulted in a slight tendency towards normalization of metabolic disturbances caused by AHS. Experimental diabetes caused a significant decrease of substrates and glycolytic enzymes, but an increase of gluconeogenic enzymes. In diabetic animals previously exposed to AHS we measured a less intensive decrease of liver glycogen and glucose-6-phosphate concentration and hexokinase activity, as well as less intensive increase of liver glucose concentration, glucose-6-phosphatase and fructose-1,6-bisphosphatase activity compared to control diabetic animals that had been maintained at room temperature. Prior AHS provided some protection over diabetes-induced alterations in carbohydrate-related parameters (see graphical apstract), indicating a possible development of cross-tolerance phenomenon between the two stressors, AHS and STZ-diabetes.