Intermittent Hypoxia Erythropoiesis Mitochondrial Biogenesis Effects on Behavior Including Endurance in Athletics essay

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Intermittent Hypoxia, Erythropoiesis, Mitochondrial Biogenesis, Effects on Behavior (including Endurance in Athletics

A test of fourteen senior male national squad rowers was conducted by Telford and co-workers (1994) in order to ascertain whole blood viscosity at higher 100 s-1 (WBVH) shear rate and low 0.1 s-1 (WBVL), red blood cell mean cell volume, white and red blood cell count, blood parameters of haemoglobin concentration. In order to evaluate the performance of rower, rowing ergometer was used for the 2500 m continuous effort. The results of rowers included Hb 15.5 g.dL-1, Hct 45.5%, WBVL 64.1 cP, WBVH 4.2 cP, and a BMI (Body Mass Index) of 24.6. WBVH demonstrated by the rowers was significantly (p<.001) and had a negative correlation with rowing ergometer performance (2500m) (Telford et al., 1994).

Significant correlation was found of WBVH in rowers with rowing performance (p<.001) after making certain alterations in Hb concentration. Significant Relationship was absent in rowers between Hb concentration and WBVL or rowing performance (2500 m) and WBVL. It has been mentioned by Telford and colleagues in the former study that at higher shear rate (100 s-1), rather than lower shear rate (0.1 s-1), we can find a significant relationship between rowing performance and WBV (as cited in Telford et al., 1994).

Considering that WBVH is greatly influenced by haematocrit, plasma viscosity, and erythrocyte deformability then rowers' better performance can be attributed to decreased plasma viscosity and increased "red blood cell deformability." Viscosity is increased when the red blood cell aggregation is increased, which dampens the effect of haematocrit, plasma viscosity, and "red blood cell deformability" on the whole body, particularly at lower shear rates (Telford et al., 1994). Hence this paper will not only look at the aforementioned aspects but also pay primary attention at the influential aspects of intermittent hypoxia, erythropoiesis, mitochondrial biogenesis and RBC production on the athlete's overall performance and endurance.

Living High-Training Low

Levine et al. (1991) in their study, as well as Levine and Stray-Gundersen (1992) in their respective study, initiated an innovative path to training at altitudes for athletes to increase their endurance or performance. Levine and his colleagues suggested that the 'most effective' plan in training could be to live at some altitude, either by living at that height or by using a simulator of height resembling the altitude of around 2500 meters, and to minimize the training at sea-level. The plus points of normally living in an environment comparatively low in oxygen are increase in the density and count of RBCs, without really giving up an increase in VO2 max and recovery time. But one negative point in training at heights is decrease in the excellence and power of training because of living and doing training at such elevated heights. Intermittent Hypoxic Exposure or IHE is the rule of training of 'living high' at the altitude of 2500 meters and at sea-level ie. 'training low.'

The presumptive theory of "living at high altitude and training at low altitude (high-low)" was applied on nine aggressive and able runners in an experimental period of training for four weeks to see its impact on their endurance and performance. The high-low group was made to live at 2500 m but both the groups, control ("low-low") and the "high-low," were trained at 1300 m. In the "high-low" group there was a noteworthy increase of 5% in VO2max. "High-low" group was also able to enhance their running time trial of 5 km at normal sea-level radically, by 30 seconds. No particular alterations were seen in running time trial of 5 km in low-low group. There was an increase of 500ml of total volume of blood in "high-low" group as compared to "low-low" group. Problems associated with decrease in excellence and power of training normally seen at elevated heights, were somewhat circumvented by training of both groups at decreased altitude i.e. 1300 m.

Stray-Gundersen and Levin (1994), and Stray-Gundersen et al. (1995) initiated their role as training supervisors by supervising 6 weeks of continuous training at sea level after subsequent studies had been done on subjects like 'living high' and 'training low'. The athletes then underwent a 4-week training on subjects - 'high-low' (2500/1300) and 'high-high' (2500). On the other hand a focus group underwent the same training to improve endurance and performance but at sea level. Groups which underwent training on 2 subjects, 'high-high' and 'high-low', recorded an increase in serum EPO at altitude and a substantial increase in RBC mass and sea-level VO2 max. The serum EPO, sea level VO2 max and RBC mass remained the same for the focused group sea level. 'High-high', high-low' and low-low groups did not record a substantial statistical difference in the sea level performance of 5 km running time on the running track.

From the time of these studies, Finnish researchers like Rusko et al. 1995 built a peculiar 'altitude house' in which with the use of normobaric displacement of nitrogen and the content of oxygen in the air could be brought down. These 'altitude houses' had a distinguishing feature that it permitted the athletes to sleep and 'live' under normobaric hypoxic conditions of simulated altitude, however, simultaneously train them with their standard sea level regime. This was again done in effort to improve athlete's endurance and performance. Impressed with these houses, Australia with the help of Australian Institute of Sport built up a similar structure of an altitude house.

The consequences of a hypoxic normobaric environment and normoxic mormobaric environment were looked into at the two studies that were done at the Australian Institute of Sport by Ashenden (1999a and 1999b) on chosen dependant variables. Under this study, the majorly trained cyclists, female (Ashenden 1999a) and majorly trained runners, male (Ashenden 1999b), slept in normobaric hypoxia simulating a 2650 m altitude. A focus group of athletes was included in every study that underwent the same training but slept at 600m. No change in Hbmass or VO2 max was observed in an exercise that lasted 4 minutes.

The group of highly trained runners - 400 m was disclosed to a normobaric hypoxia environment (~2200m) in a Live-High Train-Low rule for ten days and beneficial results of performance were observed (Nummela and Rusko 2000). The control group as compared to the runners who were disclosed to the hypoxia did not show any change however the time for such runners fell in 400 m race time.

For more knowledge on the prevailing trends in altitude training, read the follow-ups done by Wilber (2001) and Levine (2002). To sum it up, according to Levine et al. 1991, as well as other researchers like Nummela and Rusko 2000, and Stray-Gunderson and Levine 1994, the Live High Train Low rule is more of an advantage to sea level VO2man and time trial performance of the athletes. On the other hand Stray-Gundersen and Levine (1994) and Stray-Gundersen et al. (1995) think of the same rules as a disadvantage.

Significant individual behavior variability exists in the magnitude of betterment in spite of the favorable position of the live-high train-low over traditional altitude or sea level training (Levine 2002). According to him the reason behind the variability of studies is because of the lack of iron. He also said that a major reason for the decline in iron stones in bone marrows in 40% distance runners which comprises of 20% male and 60% female runners is only due to the existence of serum ferritin. Such athletes do not grow and increase erythrocyte volume, RBC volume or VO2nab whenever they seek altitude training.

Mechanisms IHE

There is no available resource which explains about the reticulocyte counts, the plasma concentration of transferrin receptors and erythroprotein as the RBC count was never calculated in any study (Julian et al., 2004; Hinckson et al., 2007) and that IHE increases the red cell mass. Economy cannot be changed by IHE (Julian et al., 2004; Tadibi et al., 2007), and the buffering property cannot be changed by unaltered anaerobic performance (Tadibi et a., 2007).

After passing seven days, an increase in hypoxic ventilatory response is not possible (Fagenholz et al., 2007) and fourteen days of IHE (Serebrovskaya et al., 1999) observed in untrained athletes as advancement of performance is also highly unlikely. It can be stated, that intermittent hypoxic exposure cannot affect any mechanism which are responsible for improvement of athlete performance by height or hypoxia (Bartsch, 2008).

An advanced peek in the writings shows no proof of any studies on association between total blood viscosity, RBC colume and ability to function. However, the facts point towards the suggestion that "fitness level" and resting WBV have an inverse relationship (Brun et al. 1994 and Ernst et al. 1985c). As mentioned by Letcher et al. 1981, there are various rationales for this inverse relationship which include a change in deformation of red blood cell. The definite solution lies in spreading up of plasma volume with ongoing exercise.

The process behind increase in plasma volume due to training is considered to engage the concentrations of vasopressin, renin, albumin and…[continue]

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"Intermittent Hypoxia Erythropoiesis Mitochondrial Biogenesis Effects On Behavior Including Endurance In Athletics" (2011, March 28) Retrieved December 6, 2016, from http://www.paperdue.com/essay/intermittent-hypoxia-erythropoiesis-mitochondrial-120420

"Intermittent Hypoxia Erythropoiesis Mitochondrial Biogenesis Effects On Behavior Including Endurance In Athletics" 28 March 2011. Web.6 December. 2016. <http://www.paperdue.com/essay/intermittent-hypoxia-erythropoiesis-mitochondrial-120420>

"Intermittent Hypoxia Erythropoiesis Mitochondrial Biogenesis Effects On Behavior Including Endurance In Athletics", 28 March 2011, Accessed.6 December. 2016, http://www.paperdue.com/essay/intermittent-hypoxia-erythropoiesis-mitochondrial-120420


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