Implications of moderate altitude training for sea-level endurance in elite distance runners

Bailey, Damian Miles; Davies, Bruce; Romer, Lee M.; Castell, L M; Newsholme, Eric A.; Gandy, G

doi:10.1007/s004210050432

Cited by 68 publications

(61 citation statements)

References 43 publications

(32 reference statements)

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“…This was associated with a 50 % increase in the incidence of self-reported infectious illness, which included physical symptoms such as a sore throat, runny nose, sinusitis, earache and cough (defined as any respiratory infection), myalgia, pyrexia, diarrhoea and vomiting. We also observed a decline in endurance performance (Bailey et al 1998).…”

supporting

confidence: 51%

Human Physiology

1999

The Journal of Physiology

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The purpose of the experiment, which had ethical committee approval, was to investigate for the first time the effect of carbohydrate (CHO) ingestion on post-exercise glycogen resynthesis, measured simultaneously in human liver and skeletal muscle, and subsequent exercise capacity. Ten healthy, well-trained and familiarized males cycled at 70 % maximal oxygen uptake for 83 ± 8 min, on six separate occasions. Subjects then ingested 1 g (kg body massr l (BM) glucose (18'5% w/v; condition A) or sucrose (18'5% w/v; B), or an equivalent volume of placebo (control; C). Over the following 4 h, muscle and liver glycogen content was measured by 13C MRS (occasions 1-3).Liver spectra and volume measurements were obtained pre-and post-exercise, within 30 min after CHO ingestion and hourly thereafter. Muscle spectra and volume measurements were obtained from 30-60 min and hourly thereafter. Subsequent exercise capacity was measured on occasions 4-6. To do this, the above procedures were repeated with the omission of the glycogen measurements and, at the end of the 4 h recovery period, exercise time to exhaustion was measured. Values are given as means ± S.E.M. Data were analysed by two-way repeated measures ANOVA. Liver and muscle glycogen content declined during the initial bout of exercise by ~60 % in all trials (P < 0'05). No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident following glucose (13 ± 8 g) and sucrose (25 ± 5 g) ingestion, both of which were different from control (P < 0'01).A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150 and 210 min of recovery (r = 0'59-0'79, P < 0'05). Furthermore, a modest relationship existed between the change in liver glycogen content (g) and subsequent exercise capacity. Significant changes in muscle glycogen resynthesis were not demonstrated, due perhaps to the small CHO load and the large inter-individual variation in glycogen measurements.Peak blood glucose was highest following glucose ingestion (P < 0'05). Ammonia production tended to be lower during exercise bout 2 following CHO ingestion (P = 0'069). No significant difference in exercise capacity was found (C: 35 ± 5; A: 40 ± 5; B: 46 ± 6 min).Therefore, 1 g (kg BMr 1 glucose or sucrose is sufficient to initiate post-exercise liver glycogen resynthesis, which Journal of Physiology (1999) It has been reported than an increase in cellular creatine (Cl') availability can increase lean tissue mass (Kreider et al. 1988) and stimulate mitochondrial respiration (Wyss et al. 1992). As a decrease in cellular Cr availability has been implicated in the disruption of energy metabolism in failing myocardium (Conway et al. 1998), this raises the possibility that Cr supplementation may be beneficial in cardiac disease states. However, there are presently little or no data available concerning the effects of Cr supplementation on myocardial creatine accumulation and creatine transporter mRNA (CrT mRNA) content. Therefore, the aim of t...

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supporting

confidence: 51%

Human Physiology

1999

The Journal of Physiology

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“…However, the efficiency of such training is controversial (Levine and Stray-Gundersen, 1992;Bailey et al, 1998). Since the beginning of the 1990s, new methods combining endurance training and intermittent hypoxia exposure have been proposed: 'living high-training low' (Levine et al, 1991) and 'living low-training high' (Emonson et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Effects of exercise and training in hypoxia on antioxidant/pro-oxidant balance

Pialoux¹,

Mounier²,

Ponsot

et al. 2006

Eur J Clin Nutr

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Objective: The aim was to investigate the effects of acute exercise under hypoxic condition and the repetition of such exercise in a 'living low-training high' training on the antioxidant/prooxidant balance. Design: Randomized, repeated measures design. Setting: Faculté de Médecine, Clermont-Ferrand, France. Subjects: Fourteen runners were randomly divided into two groups. A 6-week endurance training protocol integrated two running sessions per week at the second ventilatory threshold into the usual training. Intervention: A 6-week endurance training protocol integrated two running sessions per week at the second ventilatory threshold into the usual training. The first hypoxic group (HG, n ¼ 8) carried out these sessions under hypoxia (3000 m simulated altitude) and the second normoxic group (NG, n ¼ 6) in normoxia. In control period, the runners were submitted to two incremental cycling tests performed in normoxia and under hypoxia (simulated altitude of 3000 m). Plasma levels of advanced oxidation protein products (AOPP), malondialdehydes (MDA) and lipid oxidizability, ferric-reducing antioxidant power (FRAP), lipid-soluble antioxidants (a-tocopherol and b-carotene) normalized for triacyglycerols and cholesterol were measured before and after the two incremental tests and at rest before and after training. Results: No significant changes of MDA and AOPP level were observed after normoxic exercise, whereas hypoxic exercise induced a 56% rise of MDA and a 44% rise of AOPP. Plasma level of MDA and arterial oxygen hemoglobin desaturations after the acute both exercises were highly correlated (r ¼ 0.73). a-Tocopherol normalized for cholesterol and triacyglycerols increased only after hypoxic exercise (10-12%, Po0.01). After training, FRAP resting values (À21%, Po0.05) and a-tocopherol/ triacyglycerols ratio (À24%, Po0.05) were diminished for HG, whereas NG values remained unchanged. Conclusions: Intense exercise and hypoxia exposure may have a cumulative effect on oxidative stress. As a consequence, the repetition of such exercise characterizing the 'living low-training high' model has weakened the antioxidant capacities of the athletes. Sponsorship: International Olympic Committee and the Direction Régionale de la Jeunesse et des Sports de la Région Auvergne.

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“…Svedenhag et al found that 2 weeks of altitude (2000 m) training improved RPE during exercise compared to sea-level training [33] but there are currently no studies comparing the perceived exertion of responders with non-responders. Bailey et al also reported that 4 weeks of altitude training (1500-2000 m) improved RPE when performing a submaximal exercise test at sea-level in elite distance runners [34]. A high correlation between RPE and HR was reported by Borg et al in a variety of work tasks (cycling and treadmill) and under varying exercise conditions (moderate to heavy intensity) [35].…”

Section: Subjective Variablesmentioning

confidence: 91%

Live High-Train Low Altitude Training: Responders and Non- Responders

Hamlin¹,

Manimmanakorn²,

Creasy³

et al. 2015

J Athl Enhancement

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Objective: Investigate differences between athletes that responded (improved performance) compared to those that did not, after a 20-day "live high-train low" (LHTL) altitude training camp. Methods:Ten elite triathletes completed 20 days of live high (1545-1650 m), train low (300 m) training. The athletes underwent (i), two 800-m swimming time trials at sea-level (1 week prior to and 1 week after the altitude camp) and (ii) two 10-min standardised submaximal cycling tests at altitude on day 1 and day 20 of the altitude camp. Acute mountain sickness (AMS) was also measured during the camp. Based on their 800-m swimming time trial performances, athletes were divided into responders (improved by 3.2 ± 2.2%, mean ± SD, n=6) and non-responders (decreased by 1.8 ± 1.2%, n=4).Results: Compared to non-responders, the responders had lower exercise heart rates (-6.3 ± 7.8%, mean ± 90% CL, and higher oxygen saturations (1.2 ± 1.3%) at the end of the 10-min submaximal test after the camp. Compared to the responders, the non-responders had substantially higher VE and VE/VO 2 during the submaximal test on day 1 of the altitude training camp, and a substantially higher RER during the submaximal test on day 20 of the camp. As a result of the altitude training, exercise economy of the non-responders compared to the responders deteriorated (i.e., non-responders required more oxygen per watt). Non-responders were 3.0 times (90% CL=0.5-16.6) more likely to suffer symptoms of acute mountain sickness during first 5 days of altitude compared to responders. Conclusion:Changes in SpO 2 , heart rate and some respiratory variables during exercise and resting AMS scores may help determine athletes that respond to LHTL altitude training camps from athletes that fail to respond to such training.

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Implications of moderate altitude training for sea-level endurance in elite distance runners

Cited by 68 publications

References 43 publications

Human Physiology

Human Physiology

Effects of exercise and training in hypoxia on antioxidant/pro-oxidant balance

Live High-Train Low Altitude Training: Responders and Non- Responders

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