Stress-associated cardiovascular reaction masks heart rate dependence on physical load in mice.

When tested on the treadmill mice do not display a graded increase of heart rate (HR), but rather a sharp shift of cardiovascular indices to high levels at the onset of locomotion. We hypothesized that under test conditions cardiovascular reaction to physical load in mice is masked with stress-associated HR increase. To test this hypothesis we monitored mean arterial pressure (MAP) and heart rate in C57BL/6 mice after exposure to stressful stimuli, during spontaneous locomotion in the open-field test, treadmill running or running in a wheel installed in the home cage. Mice were treated with ß1-adrenoblocker atenolol (2mg/kg ip, A), cholinolytic ipratropium bromide (2mg/kg ip, I), combination of blockers (A+I), anxiolytic diazepam (5mg/kg ip, D) or saline (control trials, SAL). MAP and HR in mice increased sharply after handling, despite 3weeks of habituation to the procedure. Under stressful conditions of open field test cardiovascular parameters in mice were elevated and did not depend on movement speed. HR values did not differ in I and SAL groups and were reduced with A or A+I. HR was lower at rest in D pretreated mice. In the treadmill test HR increase over speeds of 6, 12 and 18m/min was roughly 1/7-1/10 of HR increase observed after placing the mice on the treadmill. HR could not be increased with cholinolytic (I), but was reduced after sympatholytic (A) or A+I treatment. Anxiolytic (D) reduced heart rate at lower speeds of movement and its overall effect was to unmask the dependency of HR on running speed. During voluntary running in non-stressful conditions of the home cage HR in mice linearly increased with increasing running speeds. We conclude that in test situations cardiovascular reactions in mice are governed predominantly by stress-associated sympathetic activation, rendering efforts to evaluate HR and MAP reactions to workload unreliable.

[Optimization of training: development of a new partial load mode of strength training].

Hypertrophic effect of strength training is known to originate from mechanical and metabolic stimuli. During exercise with restricted blood supply ofworking muscles, that is under conditions of intensified metabolic shifts, training effect may be achieved with much lower external loads (20% of one repetition maximum (1 RM)). The aim of the study was to compare the effects of 8 wks high-intensity (80-85% MVC) strength training and low-intensity (50% 1 RM) training without relaxation. The high-intensity strength training leads to somewhat higher increments in strength and size of trained muscles than training without relaxation. During high-intensity training an increase of area occupied by type II fibers at muscle cross section prevails while during training without relaxation - an increase of area occupied by type I fibers takes place. An exercise session without relaxation leads to a more pronounced increase in secretion of growth hormone, IGF-1 and cortisol. Expression of gene regulating myogenesis (Myostatin) is changed in different ways after high-intensity strength exercise session and after exercise session without relaxation. Low-intensity strength training (50% 1 RM) without relaxation is an effective way for inducing increases of strength and size of trained muscles. This low intensive type of training may be used in restorative medicine, sports and physical culture.

Metabolism in rats during antiorthostatic hypokinesia.

O2 consumption and CO2 release in 3 groups of awake rats were studied on a MM-100 metabolic monitor system (CWE Inc.). The animals of 2 groups were preadapted to 4-h maintenance in special boxes (2 weeks). The rats could perform rotational movements and limited movements in the rostrocaudal direction (hypokinesia). The animals of one group were daily exposed to 4-h antiorthostatic load (

[Acute effects of eccentric work on a bicycle ergometer].

The dynamics of delayed onset of muscle soreness after exercise on an electrically driven cycle ergometer with floating seat under preferentially concentric and eccentric conditions (forward and backward rotation of the pedals) has been evaluated using three different tests. The delayed onset of muscle soreness was determined using three different procedures: two with active contraction of the tested muscle group in multi-joint (going downstairs) and single-joint (knee extension) movements and one with passive pressure applied to the central part of m. vastus lateralis. With the use of two active tests, the maximum delayed onset of muscle soreness was recorded on the 1st-3rd days after intensive bicycle exercise without significant differences between the groups. Under conditions of passive testing, a tendency to a slower development (both an increase and a decrease) of delayed onset of muscle soreness was recorded. A positive correlation between the relative tension and the delayed onset of muscle soreness was found. Relative tension was determined as a decrease of strength during recovery related to the initial level. No relationship between volume/duration of exercise and the delayed onset of muscle soreness was found.

Effects of corticoliberin fragment CRF(4-6) on sexual behavior in male rats [corrected].

Centrally administered doses of the tripeptide corticoliberin fragment CRF(4-6) (Pro-Pro-Ile) suppressed mating behavior in male rats. Doses of 1 and 2 microg of the tripeptide produced dose-dependent increases in the latent periods of mounting, intromission, and ejaculation. Changes in measures of sexual behavior demonstrated that the corticoliberin fragment CRF(4-6) suppressed both sexual motivation and sexual performance.

[Influence of corticotropin-releasing factor fragment CRF(4-6) on male rat sexual behaviour].

Centrally administered corticotrophin-releasing factor fragment CRF(4-6) (Pro-Pro-Ile) inhibits components of male rat sexual behaviour. Administration of 1 and 2 microg of tripeptide leads to dose-dependent increase in mount, intromission and ejaculation latencies. Alterations of sexual behaviour parameters suggest suppression of both sexual motivation and sexual performance.

[Corticoliberin fragment CRF4-6 modifies rat behavior in opposite ways under stressing and non-stressing conditions].

The effects of tripeptide corticoliberin fragment CRF4-6 (icv; 6, 30, and 150 nmol/head) on behaviour of rats were investigated under non-stressing and stressing conditions. CRF4-6 activated rat behaviour under non-stressing conditions (home cage): the duration of locomotion and exploratory behaviour was increased whereas the duration of passive behaviour and sleep was decreased. On the other hand, CRF4-6 suppressed the rat exploratory behaviour under stressing conditions (elevated plus-maze): the duration of non-exploratory behaviour was increased; numbers of rearings and leanings out to open arms were reduced. All observed effects of the tripeptide CRF4-6 were dose-dependent. Behavioural effects of the tripeptide were similar to the well-known action of the whole corticoliberin molecule. Therefore we suggest that CRF4-6 is located in the active part of CRF or it can be a physiologically active corticoliberin derivative.