The circadian to ultradian power ratio changed with time for HR (black), less for mean arterial BP (gray) and locomotor activity (white). The data are expressed as mean ± s.e.m.; LD—control LD week; S01, S05, S10 and S11—weeks 1, 5, 10 and 11 of PAS, respectively; Y axis—ratio of circadian (24 h) to ultradian harmonic (12, 8, 6, 4.8 and 4 h) period power. Columns with different superscript letters are statistically different. Error bars indicate s.e.m. 

Contexts in source publication

Context 1

... decline in MAP was less pronounced and diminished values (p < 0.05) were recorded for week 10 in comparison with the first week ( figure 2(B)). The circadian to ultradian spectral power ratio for HR decreased to a half after the first week and to a quarter of initial power values during week 11 of PAS exposure ( figure 4). This decline of CUPR reflects diminished circadian variability in spectral power while ultradian spectral power was not changed (figures 2(D), (E), (F)). ...

Context 2

... device (Data Science International, St Paul, Minnesota, USA) that allows continuous measurement of BP, HR and locomotor activity in freely moving animals. The implementation procedure for the device is as previously validated at our department (Molcan et al 2009) and is as follows. Before the surgery the rats were anesthetized by a ketamine hydrochloride (75 mg kg − 1 ) and xylazine hydrochloride (10 mg kg − 1 ) mixture. The pressure radiotelemetric transmitter TA11PA-C40 (DSI, USA) was surgically implanted into the abdominal aorta just above its bifurcation (Brockway et al 1991). The catheter was then stabilized to the aorta with tissue glue (3M Vetbond; DSI, USA) and a cellulose patch (Cellulose Patch Kit—Small Animals; DSI, USA). The transmitter battery was then secured to the muscular wall. The animals were included into the experiment 2 weeks after the surgical procedure. Data were acquired by scheduled sampling interval of 10 s with segment duration of 30 s for BP, HR and locomotor activity. At first, the rats were kept for 1 week under control LD conditions. Afterwards, they were exposed for 12 weeks to 8 h PAS three times per week. Radiotelemetric sensors were ON during weeks 1, 5, 10 and 11 of the experiment when the PAS were applied (figure 1). We evaluated HR, mean BP (mean arterial pressure (MAP)) and locomotor activity from the acquired data. The paired t -test and repeated measures ANOVA with the Fisher LSD post-hoc test were used for the evaluation of differences between groups. Values are presented as mean ± the standard error of the mean (s.e.m.). Circadian and ultradian rhythm analysis of the individual measured data was performed with a Lomb–Scargle periodogram using Chronos- Fit software (Zuther et al 2009). The circadian to ultradian power rhythm ratio (CUPR) was calculated from the original filtered data as a ratio of circadian (24 h) and the average of ultradian (12, 8, 6, 4.8 and 4 h) periods. Since the Shapiro–Wilk normality test of power spectra rejected the null hypothesis for a normal data distribution, the non-parametric Friedman test followed by the Wilcoxon test for multiple comparisons was used. Due to catheter closing in two rats during the experiment, six animals were used for evaluation of long-term differences among weeks while the evaluation of LD differences during the control lighting regimen was performed with eight rats. Rats exposed to control LD conditions exhibited distinct circadian rhythms in HR, with higher values during the active (D) in comparison with the passive (L) phase of the day (L: 315 ± 6 beats min –1 ; D: 355 ± 8 beats min –1 ; t = 11.658; n = 8; p < 0.001). Similarly, both MAP (L: 96 ± 2 mm Hg; D: 100 ± 2 mm Hg; t = 5.852; n = 8; p < 0.01) and locomotor activity (L: 0.9 ± 0.1 counts min –1 ; D: 3 ± 0.4 counts min –1 ; t = 6.094; n = 8; p < 0.001) reached higher levels during the dark phase than during the light phase. Significant dominance of circadian rhythm power over harmonic ultradian rhythm power was calculated for the entrained rhythms of HR ( t 6.704; n 8; p 0.001), MAP ( t 3.573; n 7; p 0.05) and locomotor activity ( t = 5.951; n = 8; p < 0.001) under the LD 12:12 regimen (figure 2). The repeated exposure of rats to PAS decreased mean HR ( F (4,40) = 81.796; p < 0.001) as well as resulted in differences between L and D values (table 1). During the first week of PAS we found negative D − L values after three shift days while on week 10 or 11 a positive D − L ratio was calculated for all measured parameters (figure 3). 11 weeks of PAS exposure failed to affect MAP values as compared to the BP measured in rats kept under control LD conditions (LD: 99.2 ± 1.1 mm Hg versus PAS week 11: 98.6 ± 0.7 mm Hg). The spectral power of circadian rhythms in HR decreased markedly during the first 5 weeks of PAS exposure (figure 2(A)) in comparison with the initial LD values ( p < 0.05). The decrease of spectral power of circadian rhythms for locomotor activity ( p < 0.01; figure 2(C)) paralleled the pattern in HR. The decline in MAP was less pronounced and diminished values ( p < 0.05) were recorded for week 10 in comparison with the first week (figure 2(B)). The circadian to ultradian spectral power ratio for HR decreased to a half after the first week and to a quarter of initial power values during week 11 of PAS exposure (figure 4). This decline of CUPR reflects diminished circadian variability in spectral power while ultradian spectral power was not changed (figures 2(D), (E), (F)). CUPR for MAP ( p = 0.11) and locomotor activity ( p < 0.05) exhibited a similar declining pattern as for HR ( p < 0.01) after PAS exposure but the decrease was less pronounced. The Wilcoxon multiple comparison test of CUPR for MAP revealed a significant ( p < 0.05) decrease in comparison to LD values only in week 5 of PAS exposure. Finally, CUPR for locomotor activity decreased significantly ( p < 0.05) for weeks 5 and 10 in comparison with the first PAS week values (figure 4). Rats exposed to regular 12L:12D conditions exhibited the expected differences in HR, MAP and locomotor activity between the active (D) and passive (L) phases of the daily cycle, with higher values occurring during the D in comparison to the L phase. This finding is in accordance with previously published data (Witte et al 1998). The experimental design involving repeated 8 h PAS three times per week, which lasted for 12 weeks, resulted in a decrease of HR but no significant changes of MAP and locomotor activity values. Similar decreases in HR have also been previously observed in rats exposed to photoperiod manipulation by advancing the dark phase by 4 h or by advancing and delaying the dark phase by 2 h (Zhang et al 2000). The decrease of HR may result either from increased parasympathetic tone activity or decreased sympathetic tone activity induced by the photoperiod changes. Different patterns of HR and locomotor activity over the 12 week period clearly show that the locomotor activity profile cannot explain the observed alterations in hemodynamic variables. The expected circadian rhythms of measured variables were observed in rats exposed to control lighting cycles. Specifically, the highest circadian power was shown for HR, which was more than 20 times higher in comparison with the power of harmonic ultradian rhythms. Approximately eight times higher power of circadian over ultradian period has been shown for MAP and locomotor activity. These results are in line with data obtained in rats exposed to a normal LD cycle (Witte and Lemmer 1995). The circadian power of HR, MAP and locomotor activity was diminished after PAS exposure. The circadian pattern was well detectable for HR, MAP and locomotor activity during the first week of PAS. During the next weeks of PAS exposure (weeks 5, 10 and 11), CUPR decreased. Daily changes of MAP represent an output of several control centres and, at least in humans, ultradian rhythms oscillate independently from 24 h rhythm parameters (Kawamura et al 2003, Hadtstein et al 2004). Therefore, the generation and regulation of ultradian rhythms must be able to be influenced independently of the circadian rhythm control centre (Perez-Lloret et al 2004). For example, suprachiasmatic nucleus lesions of rats kept under 12L:12D resulted in only an incomplete abolishing of day–night variations (Witte et al 1998) and rats after ablation of suprachiasmatic nuclei were still able to discriminate between a morning and an afternoon feeding session (Mistlberger et al 1996). A complex interaction model (neuronal, endocrine, excretion) is involved in the control of circadian and ultradian rhythms in BP. However, the ultradian changes in the functions of the autonomic nervous system have been assumed to be responsible for the ultradian oscillations of BP (Benton and Yates 1989). Since higher BP or non-dipping status leads to target-organ damage (Syrseloudis et al 2011), good control of BP is important in order to keep BP in a distinct range over a day. Therefore, stable and multilevel regulations are necessary for BP control while a rapid and relatively simple control system is needed for HR control. HR is controlled mainly via sinoatrial node pacemaker cells and autonomous nervous system branches (Mighiu and Heximer 2012) which are modulated directly by the suprachiasmatic nuclei (Buijs et al 2003, Scheer et al 2003). The circadian pattern of HR has been shown to be completely abolished in rats with suprachiasmatic nuclei ablation (Warren et al 1994, Sheward et al 2010). Moreover, the suprachiasmatic nucleus itself contains interacting nodes that together with the intrinsic cardiac nodes are responsible for scale invariance of HR fluctuations (Hu et al 2008). In our experiment, rats entrained to LD exhibited a pronounced 24 h pattern, more so for HR than for MAP. Since the number of factors and the resulting interactions involved in the generation of circadian and ultradian rhythms of BP are higher than those for HR, (1) exposure to LD conditions resulted in smaller CUPR for MAP than for HR and (2) long-term PAS exposure induced a smaller decrease in CUPR for MAP as compared with CUPR for HR. However, our experimental design did not allow us to differentiate whether the rhythmicity in cardiovascular parameters was due to periodic masking effects or truly reflected the activity of the endogenous pacemaker. We assume that the irregular LD conditions disturbed circadian outputs from the suprachiasmatic nuclei which influenced the circadian rhythmicity of HR, MAP and locomotor activity. Our results demonstrate that circadian rhythms in HR are more sensitive to disturbances caused by PAS than BP. Since both ultradian and circadian rhythms can help the cardiovascular system to adapt to changing environmental conditions, disturbed daily variability of cardiovascular parameters could be involved in an inadequate response to stress conditions. Under unpredictable conditions the ...

Context 3

... and irregular lighting cycles. Normotensive mature male Wistar rats ( n 8; 356 8 g) were kept under controlled temperature, 21 ± 1 ◦ C, conditions under a regular 12L:12D cycle, with lights on from 06:00. Light intensity was 150 lux as measured with an automatic datalogger (KIMO KH100, Chevrier Instruments Inc., Canada). The rats were housed singly with food and water ad libitum . The experiment was approved by the Ethical Committee for the Care and Use of Laboratory Animals at the Comenius University in Bratislava, Slovak Republic, and the State Veterinary Authority. The cardiovascular parameters were measured with a radiotelemetry device (Data Science International, St Paul, Minnesota, USA) that allows continuous measurement of BP, HR and locomotor activity in freely moving animals. The implementation procedure for the device is as previously validated at our department (Molcan et al 2009) and is as follows. Before the surgery the rats were anesthetized by a ketamine hydrochloride (75 mg kg − 1 ) and xylazine hydrochloride (10 mg kg − 1 ) mixture. The pressure radiotelemetric transmitter TA11PA-C40 (DSI, USA) was surgically implanted into the abdominal aorta just above its bifurcation (Brockway et al 1991). The catheter was then stabilized to the aorta with tissue glue (3M Vetbond; DSI, USA) and a cellulose patch (Cellulose Patch Kit—Small Animals; DSI, USA). The transmitter battery was then secured to the muscular wall. The animals were included into the experiment 2 weeks after the surgical procedure. Data were acquired by scheduled sampling interval of 10 s with segment duration of 30 s for BP, HR and locomotor activity. At first, the rats were kept for 1 week under control LD conditions. Afterwards, they were exposed for 12 weeks to 8 h PAS three times per week. Radiotelemetric sensors were ON during weeks 1, 5, 10 and 11 of the experiment when the PAS were applied (figure 1). We evaluated HR, mean BP (mean arterial pressure (MAP)) and locomotor activity from the acquired data. The paired t -test and repeated measures ANOVA with the Fisher LSD post-hoc test were used for the evaluation of differences between groups. Values are presented as mean ± the standard error of the mean (s.e.m.). Circadian and ultradian rhythm analysis of the individual measured data was performed with a Lomb–Scargle periodogram using Chronos- Fit software (Zuther et al 2009). The circadian to ultradian power rhythm ratio (CUPR) was calculated from the original filtered data as a ratio of circadian (24 h) and the average of ultradian (12, 8, 6, 4.8 and 4 h) periods. Since the Shapiro–Wilk normality test of power spectra rejected the null hypothesis for a normal data distribution, the non-parametric Friedman test followed by the Wilcoxon test for multiple comparisons was used. Due to catheter closing in two rats during the experiment, six animals were used for evaluation of long-term differences among weeks while the evaluation of LD differences during the control lighting regimen was performed with eight rats. Rats exposed to control LD conditions exhibited distinct circadian rhythms in HR, with higher values during the active (D) in comparison with the passive (L) phase of the day (L: 315 ± 6 beats min –1 ; D: 355 ± 8 beats min –1 ; t = 11.658; n = 8; p < 0.001). Similarly, both MAP (L: 96 ± 2 mm Hg; D: 100 ± 2 mm Hg; t = 5.852; n = 8; p < 0.01) and locomotor activity (L: 0.9 ± 0.1 counts min –1 ; D: 3 ± 0.4 counts min –1 ; t = 6.094; n = 8; p < 0.001) reached higher levels during the dark phase than during the light phase. Significant dominance of circadian rhythm power over harmonic ultradian rhythm power was calculated for the entrained rhythms of HR ( t 6.704; n 8; p 0.001), MAP ( t 3.573; n 7; p 0.05) and locomotor activity ( t = 5.951; n = 8; p < 0.001) under the LD 12:12 regimen (figure 2). The repeated exposure of rats to PAS decreased mean HR ( F (4,40) = 81.796; p < 0.001) as well as resulted in differences between L and D values (table 1). During the first week of PAS we found negative D − L values after three shift days while on week 10 or 11 a positive D − L ratio was calculated for all measured parameters (figure 3). 11 weeks of PAS exposure failed to affect MAP values as compared to the BP measured in rats kept under control LD conditions (LD: 99.2 ± 1.1 mm Hg versus PAS week 11: 98.6 ± 0.7 mm Hg). The spectral power of circadian rhythms in HR decreased markedly during the first 5 weeks of PAS exposure (figure 2(A)) in comparison with the initial LD values ( p < 0.05). The decrease of spectral power of circadian rhythms for locomotor activity ( p < 0.01; figure 2(C)) paralleled the pattern in HR. The decline in MAP was less pronounced and diminished values ( p < 0.05) were recorded for week 10 in comparison with the first week (figure 2(B)). The circadian to ultradian spectral power ratio for HR decreased to a half after the first week and to a quarter of initial power values during week 11 of PAS exposure (figure 4). This decline of CUPR reflects diminished circadian variability in spectral power while ultradian spectral power was not changed (figures 2(D), (E), (F)). CUPR for MAP ( p = 0.11) and locomotor activity ( p < 0.05) exhibited a similar declining pattern as for HR ( p < 0.01) after PAS exposure but the decrease was less pronounced. The Wilcoxon multiple comparison test of CUPR for MAP revealed a significant ( p < 0.05) decrease in comparison to LD values only in week 5 of PAS exposure. Finally, CUPR for locomotor activity decreased significantly ( p < 0.05) for weeks 5 and 10 in comparison with the first PAS week values (figure 4). Rats exposed to regular 12L:12D conditions exhibited the expected differences in HR, MAP and locomotor activity between the active (D) and passive (L) phases of the daily cycle, with higher values occurring during the D in comparison to the L phase. This finding is in accordance with previously published data (Witte et al 1998). The experimental design involving repeated 8 h PAS three times per week, which lasted for 12 weeks, resulted in a decrease of HR but no significant changes of MAP and locomotor activity values. Similar decreases in HR have also been previously observed in rats exposed to photoperiod manipulation by advancing the dark phase by 4 h or by advancing and delaying the dark phase by 2 h (Zhang et al 2000). The decrease of HR may result either from increased parasympathetic tone activity or decreased sympathetic tone activity induced by the photoperiod changes. Different patterns of HR and locomotor activity over the 12 week period clearly show that the locomotor activity profile cannot explain the observed alterations in hemodynamic variables. The expected circadian rhythms of measured variables were observed in rats exposed to control lighting cycles. Specifically, the highest circadian power was shown for HR, which was more than 20 times higher in comparison with the power of harmonic ultradian rhythms. Approximately eight times higher power of circadian over ultradian period has been shown for MAP and locomotor activity. These results are in line with data obtained in rats exposed to a normal LD cycle (Witte and Lemmer 1995). The circadian power of HR, MAP and locomotor activity was diminished after PAS exposure. The circadian pattern was well detectable for HR, MAP and locomotor activity during the first week of PAS. During the next weeks of PAS exposure (weeks 5, 10 and 11), CUPR decreased. Daily changes of MAP represent an output of several control centres and, at least in humans, ultradian rhythms oscillate independently from 24 h rhythm parameters (Kawamura et al 2003, Hadtstein et al 2004). Therefore, the generation and regulation of ultradian rhythms must be able to be influenced independently of the circadian rhythm control centre (Perez-Lloret et al 2004). For example, suprachiasmatic nucleus lesions of rats kept under 12L:12D resulted in only an incomplete abolishing of day–night variations (Witte et al 1998) and rats after ablation of suprachiasmatic nuclei were still able to discriminate between a morning and an afternoon feeding session (Mistlberger et al 1996). A complex interaction model (neuronal, endocrine, excretion) is involved in the control of circadian and ultradian rhythms in BP. However, the ultradian changes in the functions of the autonomic nervous system have been assumed to be responsible for the ultradian oscillations of BP (Benton and Yates 1989). Since higher BP or non-dipping status leads to target-organ damage (Syrseloudis et al 2011), good control of BP is important in order to keep BP in a distinct range over a day. Therefore, stable and multilevel regulations are necessary for BP control while a rapid and relatively simple control system is needed for HR control. HR is controlled mainly via sinoatrial node pacemaker cells and autonomous nervous system branches (Mighiu and Heximer 2012) which are modulated directly by the suprachiasmatic nuclei (Buijs et al 2003, Scheer et al 2003). The circadian pattern of HR has been shown to be completely abolished in rats with suprachiasmatic nuclei ablation (Warren et al 1994, Sheward et al 2010). Moreover, the suprachiasmatic nucleus itself contains interacting nodes that together with the intrinsic cardiac nodes are responsible for scale invariance of HR fluctuations (Hu et al 2008). In our experiment, rats entrained to LD exhibited a pronounced 24 h pattern, more so for HR than for MAP. Since the number of factors and the resulting interactions involved in the generation of circadian and ultradian rhythms of BP are higher than those for HR, (1) exposure to LD conditions resulted in smaller CUPR for MAP than for HR and (2) long-term PAS exposure induced a smaller decrease in CUPR for MAP as compared with CUPR for HR. However, our experimental design did not allow us to differentiate whether the rhythmicity in cardiovascular parameters was due to periodic masking effects or ...