Cardiac remodeling and functional adaptations consecutive to altitude training in rats: implications for sea level aerobic performance

2005 ◽  
Vol 98 (1) ◽  
pp. 83-92 ◽  
Author(s):  
C. Reboul ◽  
S. Tanguy ◽  
J. M. Juan ◽  
M. Dauzat ◽  
P. Obert
Keyword(s):  
Sea Level ◽  
Isolated Heart ◽  
Left Ventricular ◽  
Aerobic Performance ◽  
Altitude Training ◽  
Moderate Altitude ◽  
Ventricular Performance ◽  
Morphological Adaptations ◽  
Before And After ◽  
And Training

This study questioned the effect of living and training at moderate altitude on cardiac morphological and functional adaptations and tested the incidences of potential specific adaptations compared with aerobic sea level training on maximal left ventricular performance. Sea level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Cardiac adaptations were evaluated throughout the study period by Doppler echocardiography. Maximal stroke volume (LVSVmax) was measured during volume overloading before and after the study period. Finally, at the end of the study period, passive pressure-volume relationships on isolated heart and cardiac weighing were obtained. Altitude training resulted in a specific left ventricular (LV) remodeling compared with NT, characterized by an increase in wall thicknesses without any alteration in internal dimensions. These morphological adaptations associated with hypoxia-induced alterations in pulmonary outflow and preload conditions led to a decrease in LV filling and subsequently no improvement in LV performance during resting physiological conditions in CHT compared with NT. Such a lack of improvement was confirmed during volume overloading that simulated maximal effort (LVSVmax pretest: NT = 0.58 ± 0.05, CHT = 0.57 ± 0.08 ml; posttest: NT = 0.72 ± 0.06, CHT = 0.58 ± 0.07 ml; NT vs. CHT in posttest session, P < 0.05). Maximal aerobic velocities increased to the same extent in NT and CHT rats despite marked polycythemia in the latter. The lack of LVSVmax improvement resulting from altitude training-induced cardiac morphological and functional adaptations could be responsible for this phenomenon.

scholarly journals “Living high-training low”: effect of moderate-altitude acclimatization with low-altitude training on performance

1997 ◽  
Vol 83 (1) ◽  
pp. 102-112 ◽  
Author(s):  
Benjamin D. Levine ◽  
James Stray-Gundersen
Keyword(s):  
Sea Level ◽  
Cell Mass ◽  
Altitude Training ◽  
Moderate Altitude ◽  
Altitude Acclimatization ◽  
Red Cell Mass ◽  
Low Altitude ◽  
Mass Volume ◽  
Trained Runners ◽  
And Training

Levine, Benjamin D., and James Stray-Gundersen.“Living high-training low”: effect of moderate-altitude acclimatization with low-altitude training on performance. J. Appl. Physiol. 83(1): 102–112, 1997.—The principal objective of this study was to test the hypothesis that acclimatization to moderate altitude (2,500 m) plus training at low altitude (1,250 m), “living high-training low,” improves sea-level performance in well-trained runners more than an equivalent sea-level or altitude control. Thirty-nine competitive runners (27 men, 12 women) completed 1) a 2-wk lead-in phase, followed by 2) 4 wk of supervised training at sea level; and 3) 4 wk of field training camp randomized to three groups: “high-low” ( n = 13), living at moderate altitude (2,500 m) and training at low altitude (1,250 m); “high-high” ( n = 13), living and training at moderate altitude (2,500 m); or “low-low” ( n = 13), living and training in a mountain environment at sea level (150 m). A 5,000-m time trial was the primary measure of performance; laboratory outcomes included maximal O2 uptake (V˙o 2 max), anaerobic capacity (accumulated O2 deficit), maximal steady state (MSS; ventilatory threshold), running economy, velocity at V˙o 2 max, and blood compartment volumes. Both altitude groups significantly increased V˙o 2 max(5%) in direct proportion to an increase in red cell mass volume (9%; r = 0.37, P < 0.05), neither of which changed in the control. Five-kilometer time was improved by the field training camp only in the high-low group (13.4 ± 10 s), in direct proportion to the increase inV˙o 2 max( r = 0.65, P < 0.01). Velocity atV˙o 2 max and MSS also improved only in the high-low group. Four weeks of living high-training low improves sea-level running performance in trained runners due to altitude acclimatization (increase in red cell mass volume and V˙o 2 max) and maintenance of sea-level training velocities, most likely accounting for the increase in velocity atV˙o 2 max and MSS.

Individual variation in response to altitude training

1998 ◽  
Vol 85 (4) ◽  
pp. 1448-1456 ◽  
Author(s):  
Robert F. Chapman ◽  
James Stray-Gundersen ◽  
Benjamin D. Levine
Keyword(s):  
Cell Volume ◽  
Sea Level ◽  
Interval Training ◽  
Training Model ◽  
Individual Response ◽  
Altitude Training ◽  
Moderate Altitude ◽  
Red Cell ◽  
Red Cell Volume ◽  
The Individual

Moderate-altitude living (2,500 m), combined with low-altitude training (1,250 m) (i.e., live high-train low), results in a significantly greater improvement in maximal O2 uptake (V˙o 2 max) and performance over equivalent sea-level training. Although the mean improvement in group response with this “high-low” training model is clear, the individual response displays a wide variability. To determine the factors that contribute to this variability, 39 collegiate runners (27 men, 12 women) were retrospectively divided into responders ( n = 17) and nonresponders ( n = 15) to altitude training on the basis of the change in sea-level 5,000-m run time determined before and after 28 days of living at moderate altitude and training at either low or moderate altitude. In addition, 22 elite runners were examined prospectively to confirm the significance of these factors in a separate population. In the retrospective analysis, responders displayed a significantly larger increase in erythropoietin (Epo) concentration after 30 h at altitude compared with nonresponders. After 14 days at altitude, Epo was still elevated in responders but was not significantly different from sea-level values in nonresponders. The Epo response led to a significant increase in total red cell volume andV˙o 2 max in responders; in contrast, nonresponders did not show a difference in total red cell volume or V˙o 2 maxafter altitude training. Nonresponders demonstrated a significant slowing of interval-training velocity at altitude and thus achieved a smaller O2 consumption during those intervals, compared with responders. The acute increases in Epo and V˙o 2 maxwere significantly higher in the prospective cohort of responders, compared with nonresponders, to altitude training. In conclusion, after a 28-day altitude training camp, a significant improvement in 5,000-m run performance is, in part, dependent on 1) living at a high enough altitude to achieve a large acute increase in Epo, sufficient to increase the total red cell volume andV˙o 2 max, and 2) training at a low enough altitude to maintain interval training velocity and O2 flux near sea-level values.

An evaluation of the concept of living at moderate altitude and training at sea level

2001 ◽  
Vol 128 (4) ◽  
pp. 777-789 ◽  
Author(s):  
Allan G Hahn ◽  
Christopher J Gore ◽  
David T Martin ◽  
Michael J Ashenden ◽  
Alan D Roberts ◽  
...  
Keyword(s):  
Sea Level ◽  
Moderate Altitude ◽  
And Training

Ventricular performance, pressure-volume relationships, and O2 consumption during hypothermia

1964 ◽  
Vol 206 (1) ◽  
pp. 67-73 ◽  
Author(s):  
R. G. Monroe ◽  
R. H. Strang ◽  
C. G. LaFarge ◽  
J. Levy
Keyword(s):  
Peak Pressure ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Heart Rates ◽  
Performance Pressure ◽  
Air Chamber ◽  
Lower Temperature

Left ventricular performance in the isolated heart of a dog was observed at normal temperatures (37.7 C) and under hypothermia (32.2 C) at comparable heart rates. The peak pressure of isovolumic contractions at the same ventricular end-diastolic pressures averaged 40% higher at the lower temperature. Diastolic pressure-volume relationships were similar at both temperatures. In studies in which the ventricle ejected fluid and performed work the hypothermic ventricle was capable of performing greater work at comparable heart rates, left ventricular end-diastolic pressures, and loading. When the ventricle was allowed to perform work by compressing air into a chamber of constant volume left ventricular oxygen consumption (Vo2) increased with the peak systolic pressure as the temperature was lowered. If the peak systolic pressure was maintained constant by increasing the volume of the air chamber as the temperature was lowered no consistent relationship could be shown between left ventricular Vo2 and the integral of systolic pressure in time which invariably increased with hypothermia.

Enhanced left ventricular shortening during chronic volume overload in conscious dogs

1980 ◽  
Vol 238 (2) ◽  
pp. H126-H133 ◽  
Author(s):  
M. M. LeWinter ◽  
R. L. Engler ◽  
J. S. Karliner
Keyword(s):  
Volume Overload ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Stimulation ◽  
Ventricular Performance ◽  
Blood Pressure Elevation ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ejection Phase

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Cardiac and respiratory effects of digitalis during chronic hypoxia in intact conscious dogs

1975 ◽  
Vol 229 (2) ◽  
pp. 270-274 ◽  
Author(s):  
GA Beller ◽  
SR Giamber ◽  
SB Saltz ◽  
TW Smith
Keyword(s):  
Sea Level ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Left Ventricular ◽  
Control Group ◽  
Continuous Exposure ◽  
Ventricular Performance ◽  
Toxic Dose ◽  
Respiratory Effects ◽  
Significant Difference

The arrhythmogenic and respiratory effects of ouabain during chronic hypoxia were studied in 10 unanesthetized dogs in a hypobaric chamber (446 mmHg) following 7-19 (mean 14.7) days of continuous exposure at this altitude. Another 15 dogs studied at sea level comprised the normoxic control group. In both groups, a 7.5-mug/kg loading dose of ouabain was followed by infusion of ouabain at 3.0 mug/kg per min to ECG evidence of toxicity. Mean arterial Po2 was 46 +/- 5 mmHg in chronically hypoxic dogs as compared to 86 +/- 7 mmHg in normoxic animals (P less than 0.001). Mean hematocrit was 54 +/- 1% in hypoxic and 43 +/- 2% in normoxic groups (P less than 0.001). In five dogs studied first at sea level and subsequently under conditions of chronic hypoxia, mean maximum left ventricular dP/dt and peak (dP/dt)P-1 were unchanged. Marked hyperventilation during ouabain infusion was observed. In normoxic dogs mean arterial pH rose from 7.43 +/- 0.05 to 7.70 +/- 0.02 U, and Pco2 fell from 41 +/- 4 to 15 +/- 1 mmHg during ouabain administration (P less than 0.001). Similar changes were observed in hypoxic dogs. There was no significant difference in the mean toxic dose of ouabain in chronically hypoxic (71 +/- 11 mug/kg) versus normoxic (78 +/- 12 mug/kg) animals. Thus, in contrast to acute hypoxia, chronic hypoxia in unanesthetized dogs was not associated with a significant reduction in the dose of ouabain required to produce toxic arrhythmias. Chronic hypoxia was also not associated with alterations in left ventricular performance.

Defining the “dose” of altitude training: how high to live for optimal sea level performance enhancement

2014 ◽  
Vol 116 (6) ◽  
pp. 595-603 ◽  
Author(s):  
Robert F. Chapman ◽  
Trine Karlsen ◽  
Geir K. Resaland ◽  
R.-L. Ge ◽  
Matthew P. Harber ◽  
...  
Keyword(s):  
Sea Level ◽  
Performance Enhancement ◽  
Cell Mass ◽  
Time Trial ◽  
Individual Variability ◽  
Altitude Training ◽  
Distance Runners ◽  
Before And After ◽  
And Performance ◽  
Level Performance

Chronic living at altitudes of ∼2,500 m causes consistent hematological acclimatization in most, but not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a given altitude show substantial individual variability. We hypothesized that athletes living at higher altitudes would experience greater improvements in sea level performance, secondary to greater hematological acclimatization, compared with athletes living at lower altitudes. After 4 wk of group sea level training and testing, 48 collegiate distance runners (32 men, 16 women) were randomly assigned to one of four living altitudes (1,780, 2,085, 2,454, or 2,800 m). All athletes trained together daily at a common altitude from 1,250–3,000 m following a modified live high-train low model. Subjects completed hematological, metabolic, and performance measures at sea level, before and after altitude training; EPO was assessed at various time points while at altitude. On return from altitude, 3,000-m time trial performance was significantly improved in groups living at the middle two altitudes (2,085 and 2,454 m), but not in groups living at 1,780 and 2,800 m. EPO was significantly higher in all groups at 24 and 48 h, but returned to sea level baseline after 72 h in the 1,780-m group. Erythrocyte volume was significantly higher within all groups after return from altitude and was not different between groups. These data suggest that, when completing a 4-wk altitude camp following the live high-train low model, there is a target altitude between 2,000 and 2,500 m that produces an optimal acclimatization response for sea level performance.

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