Intensity and physiological strain of competitive ultra-endurance exercise in humans.
ABSTRACT The aim of this study was to determine the magnitude and pattern of intensity, and physiological strain, of competitive exercise performed across several days, as in adventure racing. Data were obtained from three teams of four athletes (7 males, 5 females; mean age 36 years, s = 11; cycling .VO(2 peak) 53.9 ml . kg(-1) . min(-1), s = 6.3) in an international race (2003 Southern Traverse; 96 - 116 h). Heart rates (HR) averaged 64% (95% confidence interval: +/- 4%) of heart rate range [%HRR = (HR - HR(min))/(HR(max) - HR(min)) x 100] during the first 12 h of racing, fell to 41% (+/-4%) by 24 h, and remained so thereafter. The level and pattern of heart rate were similar across teams, despite one leading and one trailing all other teams. Core temperature remained between 36.0 and 39.2 degrees C despite widely varying thermal stress. Venous samples, obtained before, during, and after the race, revealed increased neutrophil, monocyte and lymphocyte concentrations (P < 0.01), and increased plasma volume (25 +/- 10%; P < 0.01) with a stable sodium concentration. Standardized exercise tests, performed pre and post race, showed little change in the heart rate-work rate relationship (P = 0.53), but a higher perception of effort post race (P < 0.01). These results provide the first comprehensive report of physiological strain associated with adventure racing.
- Acta Physiologica Scandinavica 71(2):140-50. · 2.55 Impact Factor
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ABSTRACT: The purpose of this study was to investigate the phenomenon of left ventricular (LV) dysfunction after ultraendurance exercise. Subclinical LV dysfunction in response to endurance exercise up to 24 h duration has been described, but its mechanism remains elusive. We tested 86 athletes before and after the Adrenalin Rush Adventure Race using echocardiography, impedance cardiography, and plasma immunoassay. At baseline, athletes demonstrated physiology characteristic of extreme endurance training. After 90 to 120 h of almost-continuous exercise, LV systolic and diastolic function declined (fractional shortening before the race, 39.6 +/- 0.65%; after, 32.2 +/- 0.84%, p < 0.001; mitral inflow E-wave deceleration time before the race, 133 +/- 5 ms; after, 160 +/- 5 ms, n = 48, p < 0.001) without change in loading conditions as defined by LV end-diastolic dimension and total peripheral resistance estimated by thoracic impedance. There was a compensatory increase in heart rate (before, 55 +/- 1.3 beats/min; after, 59 +/- 1.5 beats/min, p = 0.05), which left cardiac output unchanged, as well as significant-but-subclinical increases in brain natriuretic peptide and troponin I. In addition, we found that athletes who were homozygous for the intron-16 insertion polymorphism of the angiotensin-converting enzyme (ACE) gene exhibited a significantly greater decrease in fractional shortening than athletes who were homozygous for the deletion allele. Heterozygotes showed an intermediate phenotype. In addition, the deletion group manifest an enhanced sympathovagal balance after the race, as evidenced by greater power in the low-frequency component of blood pressure variability. The ACE genotype predicts the extent of reversible subclinical LV dysfunction after prolonged exercise and is associated with a differential postactivity augmentation of sympathetic nervous system function that may explain it.Journal of the American College of Cardiology 08/2006; 48(3):523-31. · 14.09 Impact Factor
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ABSTRACT: Acute loss of sleep produces few apparent physiological effects at rest. Nevertheless, many anecdotes suggest that adequate sleep is essential for optimum endurance athletic performance. To investigate this question, heavy exercise performance after 36 h without sleep was compared with that after normal sleep in eight subjects. During prolonged treadmill walking at about 80% of the VO2 max, sleep loss reduced work time to exhaustion by an average of 11% (p = 0.05). This decrease occurred despite doubling monetary incentives for subjects during work after sleeplessness. Subjects appeared to fall into "resistant" and "susceptible" categories: four showed less than a 5% change in performance after sleep loss, while four others showed decrements in exercise tolerance ranging from 15 to 40%. During the walk, sleep loss resulted in significantly greater perceived exertion (p less than 0.05), even though exercise heart rate and metabolic rate (VO2 and VCO2) were unchanged. Minute ventilation was significantly elevated during exercise after sleep loss ( p less than 0.05). Sleep loss failed to alter the continuous slow rises in VE and heart rate that occurred as work was prolonged. These findings suggest that the psychological effects of acute sleep loss may contribute to decreased tolerance of prolonged heavy exercise.European Journal of Applied Physiology and Occupational Physiology 02/1981; 47(4):345-54.