Heart Rate Variability, Standard of Measurement, Physiological Interpretation and Clinical Use in Mountain Marathon Runners during Sleep and after Acclimatization at 3480 m

Fluctuations in autonomic cardiovascular regulation during exposure to high altitude may increase the risk of heart attack during waking and sleep. This study compared heart rate variability (HVR) and its components during sleep at low altitude and after 30 - 41 hours of acclimatization at high altitude (3480 m) in five mountain marathon runners controlled for diet, drugs, light-dark cycle and jet lag. In comparison to sea level, RR-intervals during sleep at high altitude decreased significantly (P 0.001). The significant increase in sympathetic autonomic cardiovascular modulation at high altitude protects against excessive oxygen deprivation during sleep. Increases in R-R intervals can require longer periods of acclimatization at3480 m to mitigate the effects of altitude/hypoxia on sympathetic tone, thus reducing cardiovascular distress at rest during waking and sleep and probably before during and after athletic performance at altitude.

The cerebellum, the hypothalamus and behavior

The cerebellum has been classically considered as the subcortical center for motor control. However, accumulating experimental evidence has revealed that it also plays an important role in cognition, for instance, in learning and memory, as well as in emotional behavior and nonsomatic activities, such as visceral and immunological responses.

Blood Chemistry, Acid-Base, Electrolyte, Blood Lactate Metabolism and Sleep at 3480 m in Mountain Marathon Runners

Altered blood chemistry, acid-base and electrolyte are suggested determinants of sleep disturbance, with frequent arousal at high altitude even in well and long-trained altitude marathon runners. In this sample of experienced altitude marathon runners with maximal aerobic power at sea level of 61.4 ± 2.7 ml/kg-1·min-1 we found that pO2 and percent of oxygen saturation (%SO2) were lower at2050 mand3480 mthan at sea level;pO2 was higher after 38 - 41 hours than after 30 - 31 hours of acclimatization at3480 m(P 2 decreased (P 2 and (P 2 at a sleeping altitude of3480 mwas lower (P Simple regression analysis disclosed a significant correlation between the changes in TST and the percent of REM sleep and the changes in %SpaO2 recorded during sleep (P 2 at higher altitude and the percent of W and of TST (P 2, tCO2 and [HCO3-] correlated negatively and significantly with the percent of REM sleep changes at high altitude (P 2 and pH and correlated negatively with the changes in %SO2, pCO2, tCO2, and [HCO3-] (P ++] and [BE] and negatively with the changes in buffered bases [BB] and [BEeffective] (P 2 and significantly and negatively with the changes in [K+] (P 2, tCO2, [HCO3-] and [K+]

Behaviour and Degenerative Changes in the Basal Forebrain Systems of Aged Rats (12 Months Old) after Levo-Acetyl-Carnitine Treatments

One group of six male control rats [12 months old] and one group of six male rats of the same age, singularly maintained in a cage, and treated with acetyl-L-carnitine-HCl [(gamma-trimethyl-beta-acetyl-butyrobetaine-HCl: Sigma-Tau code ST200 or ALCAR: 60 mg/kg/day[7]/po)] for six months were tested in the spatial learning/memory Morris mazewater task and for atrophy and cell loss in seven myelo- and cytostructurally defined basal forebrain (BF) cholinergic regions [Freddi et al., 2009]. Coronal sections 25 ?m thick were cut through the BF regions and processed every 200 ?m for choline acetyltransferase (ChAT) immunohistochemistry. The ALCAR-treated rats had significantly shorter exit times on the Morris maze-water task test than the control rats (average ± SD 28.3 ± 12.4 s vs. 61.16 ± 4.67 s;t = 6.07, DOF = 10, P = 0.0001). Degenerative morphological changes in the BF ChAT-positive cells were observed in the substantia innominata pars anterior of the control rats but not in the treated animals (P < 0.05). In the BF, the counted and estimated average number of ChAT + cells in the 12-month-old ALCAR-treated rats (ChAT-ALCAR-12+ [Nos. 2,3,4]) was higher but not significantly (15.288 ± 3281) than that counted and estimated in the 12-month-old control rats [(ChAT-CT-12 [Nos. 1,2,3]) (11.508 ± 3868), t = 1.82, DOF = 10, P = 0.319]. In the substantia innominata pars posterior, the ChAT+ cells were significantly more numerous (P < 0.05) in the 12-month-old ALCAR-treated rats (ChAT-ALCAR-12 + [Nos. 2,3,4]) than in the control rats (ChAT-CT-12 [Nos. 1,2,3]). Above all, these results dem-onstrate that treatment with ALCAR from the age of 6 up to 12 months significantly attenuated spatial learning/memory impairment on the Morris maze-water behavioral task (P < 0.001) and also importantly reduced degeneration in size and number of cholinergic cells in the nucleus basalis magnocellularis of the BF. Accordingly, the surviving cholinergic neurons found in the BF of the ALCAR-treated rats might play an important role in modulating cortical activity and facilitating processes of attention, learning and memory.

Electroencephalographic Changes after a Marathon at 4300 M of Altitude

Running at altitude is gaining greater popularity but it may expose participants to the risk of acute mountain sickness (AMS). The study investigated electroencephalographic (EEG) changes and eventual symptoms suggestive of AMS in 5 well-trained lowland native male runners (average age, 38.2 ? 4.6 years;VO2 peak 61.4 ? 2.7 mL?kg–1?min–1 at sea level;best marathon performance at sea level under 3 hours), who completed a marathon at 4300 m altitude. EEG, percentage of peripheral arterial oxygen saturation (% SpaO2) and heart rate (HR) were recorded during wakefulness at rest (supine position) and in comfort: 1) at sea level;2) at 3600 m after 32 - 38 hours of acute acclimatization;3) at 4300 m after 145 - 153 hours of chronic acclimatization;and 4) at 4300 m immediately after a marathon race. Symptoms of AMS were evaluated with the Lake Louise questionnaire before any ECG recording. There was a significant decrease in low-voltage high-frequency activities at rest after acute hypoxic-hypobaric exposure at 3600 m as compared to sea level. After six days of acclimatization at 4300 m there was a significant increase in the power of low-voltage high-frequency activities, particularly beta and gamma, indicating an aroused waking state and an integrated activity across widely distributed cortical regions. An increase in the power of low-voltage high-frequency activities over the entire cortex was observed, particularly after completion of the marathon at 4300 m. The increase in the high-frequency activities was probably due to direct and indirect reflex activation of the forebrain and reticular activating system involved in behavioral and metabolic integration of autonomic control and arousal and due to residual activation of the somatomotor and parietal cortex after the end of the marathon. Lake Louise score always resulted lower than 3, indicating no signs of AMS in all the runners. The results of this study indicate that in well-trained and acclimatized athletes, arousal has a protective role in preventing excessive oxygen deprivation also after an endurance exercise performed at high altitude. The absence of AMS fond in our study bear out that well trained and acclimatized runners, can safely participate in a marathon at high altitude that gives rise to temporary EEG changes without inducing paroxysmal phenomena.