This study was designed to quantify the daily distribution of training intensity in a group of well-trained junior crosscountry skiers and compare the results of three different methods of training intensity quantification. Eleven male athletes performed treadmill tests to exhaustion to determine heart rate and VO 2 corresponding to ventilatory thresholds (VT 1 , VT 2 ), maximal oxygen consumption (VO 2max ), and maximal heart rate. VT 1 and VT 2 were used to delineate three intensity zones. During the same time period, all training sessions (N 5 384, 37 strength training, 347 endurance) performed over 32 consecutive days were quantified using continuous heart rate registration and session Rating of Perceived Exertion (RPE). In addition, a subset of 60 consecutive training sessions was quantified using blood lactate measurements. Intensity distribution across endurance training sessions (n 5 318) was similar when based on heart rate analysis (75 AE 3%, zone 1; 8 AE 3%, zone 2; 17 AE 4%, zone 3) or session RPE (76 AE 4%, zone 1; 6 AE 5%, zone 2; 18 AE 7%, zone 3). Similarly, from measurements of 60 consecutive sessions, 71% were performed with 2.0 mM blood lactate, 7% between 2 and 4 mM, and 22% with over 4 mM (mean 5 9.5 AE 2.8 mM). In this group of nationally competitive junior skiers, training was organized after a polarized pattern, with most sessions performed clearly below (about 75%) or with substantial periods above (15-20%) the lactate accommodation zone, which is bounded by VT 1 and VT 2 . The pattern quantified here is similar to that reported in observational studies of elite endurance athletes across several sports. It appears that elite endurance athletes train surprisingly little at the lactate threshold intensity.

This study quantified changes in training volume, organization, and physical capacity among Norwegian rowers winning international medals between 1970 and 2001. Twenty-eight athletes were identified (27 alive). Results of physiological testing and performance history were available for all athletes. Twenty-one of 27 athletes responded to a detailed questionnaire regarding their training during their internationally competitive years. Maximal oxygen uptake (VO2 max) increased 12% (6.5+/- 0.4 vs. 5.8+/-0.2 L min(-1)) from the 1970s to the 1990s. Similarly, 6-min ergometer rowing performance increased almost 10%. Three major changes in training characteristics were identified: (1) training at a low blood lactate (< 2 mM) increased from 30 to 50 h month(-1) and race pace and supra-maximal intensity training (approximately 8-14 mM lactate) decreased from 23 to approximately 7 h month(-1); (2) training volume increased by approximately 20%, from 924 to 1128 h yr(-1); (3) altitude training was used as a pre-competition peaking strategy, but it is now integrated into the winter preparation program as periodic 2-3-week altitude camps. The training organization trends are consistent with data collected on athletes from other sports, suggesting a "polarized" pattern of training organization where a high volume of low intensity training is balanced against regular application of training bouts utilizing 90%-95% of VO2 max.

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The purpose of this study was to determine whether exogenous fructose-1,6-bisphosphate (F-1,6-P2) directly affects myocardial hemodynamics and certain metabolic parameters. Isolated working rat hearts were perfused for 30 min with 10 mM glucose (+insulin) as the exclusive exogenous substrate followed by 15 min with glucose plus one of the following concentrations (in mM) of F-1,6-P2: 1.25, 2.5, 5, or 10, and finally returned to the glucose only buffer. Additions of 2.5 and 5 mM F-1,6-P2 decreased (P less than 0.01) oxygen consumption (VO2) by 10.8 and 17.0% and coronary flow by 8.3 and 10.3%, respectively. No changes were observed in lactate release, cardiac output (CO), peak systolic pressure, heart rate, or pressure work (PW). Efficiency, expressed as PW divided by VO2, increased with F-1,6-P2 by 8.6% with 1.25 mM (P less than 0.05), 13.2% with 2.5 mM (P less than 0.01), and 16.9% with 5 mM (P less than 0.01). F-1,6-P2 at 10 mM produced no further improvements in VO2 or efficiency but was associated with declines (P less than 0.05) in CO and PW. Glucose plus 10 mM fructose had no effects on any of the above parameters, indicating that the F-1,6-P2-induced changes were not due to changes in osmolarity or to end products of F-1,6-P2 hydrolysis. Some chelation of buffer calcium by F-1,6-P2 occurred, but when free calcium was equalized in glucose and glucose plus 5 mM F-1,6-P2 buffers, the decline in VO2 (11.5%) was still far greater than could be explained by exogenous F-1,6-P2 metabolism in the glycolytic pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

The objective of this study was to determine the interaction between duration of myocardial hypoxia and presence of exogenous glutathione (GSH) on functional recovery upon subsequent reoxygenation. Isolated perfused rat hearts were subjected to 20, 30, 40, or 50 min hypoxia (HYP), which resulted in a progressive decline in the amount of contractile recovery (% of normoxic rate-pressure product (RPP) and developed pressure) during 30 min reoxygenation. Supplementation with 5 mM GSH throughout normoxia, hypoxia, and reoxygenation significantly improved contractile recovery during reoxygenation after 20 and 30 min hypoxia (p < 0.05), but had no effect after longer durations of hypoxia when contractile recovery was typically below 40% of RPP and significant areas of no-reflow were observed. ECG analysis revealed that GSH shifted the bell-shaped curve for reperfusion ventricular fibrillation to the right resulting in attenuated fibrillation after 20 and 30 min hypoxia then increased incidences after 40 min when Control hearts were slow to resume electrical activity. ECG conduction velocity was well preserved in all hearts after 20 and 30 min hypoxia, but GSH administration significantly attenuated the decline that occurred with longer durations. GSH supplementation did not attenuate the 35% decline in intracellular thiols during 30 min of hypoxia. When 5 mM GSH was added only during 40 min of hypoxia, RPP recovery after reoxygenation was improved compared to unsupplemented Controls (73% vs. 55% of pre-hypoxia value, p < 0.05). Administration of GSH only during reoxygenation following 40 min of hypoxia did not alter RPP recovery compared to Control hearts. We conclude that cardioprotection by exogenous GSH is dependent on the duration of hypoxia and the functional parameter being evaluated. It is not due to an enhancement of intracellular GSH suggesting that exogenous GSH acts extracellularly to protect sarcolemmal proteins against thiol oxidation during the phase of hypoxia when oxidative stress is a major contributor to cardiac dysfunction. Furthermore, if enough damage accrues during oxygen deprivation, supplementing with GSH during reoxygenation will not impact recovery.

The purposes of this study were to determine the effect of an exhaustive running bout on intrinsic myocardial function by using the isolated working rat heart and to determine whether exhaustive exercise resulted in measurable oxidative stress in the myocardium. Untrained familiarized male rats were run at 18 m/min on a 0% grade until exhausted. Run time to exhaustion was approximately 75 min. Postexhaustion isolated heart measurements of cardiac output, rate-pressure product at low and high workloads, maximum left ventricular pressure, or 50-min performance at 85% of peak rate-pressure product were not different from those of nonexercised perfused control hearts. Exhaustive exercise resulted in a significant decline (174 vs. 224 nmol/g wet wt; P < 0.05) in nonprotein nonglutathione sulfhydryls, a thiol fraction indicative of oxidative stress. However, the magnitude of this measure of oxidative stress appears insufficient to cause alterations in intrinsic myocardial performance. We conclude that healthy untrained rats subjected to exhaustive exercise fail to demonstrate accumulation of a functionally significant level of myocardial oxidative stress.

An isolated rat heart model of intermittent hypoxia was used to investigate the impact of exogenous supplementation of glutathione and two thiol delivery vehicles on functional recovery during reoxygenation and whether efficacy was dependent on enhanced intracellular thiol concentration. Hearts from F344 rats were perfused in the Langendorff mode and exposed to three, 5 minute bouts of global, substrate free, normothermic hypoxia separated by 5 minute reoxygenation periods. Changes in coronary flow, heart rate, systolic and diastolic pressure, and rate pressure product were evaluated throughout in control hearts and compared with hearts in which one of the following was provided during the hypoxic periods: reduced glutathione (GSH, 1 or 10 mM), 10 mM GSH mono-ethyl ester (GSHMEE), or 1 mM L-2-oxothiozolidine-4-carboxylate (OZT). After three hypoxic periods plus reoxygenation, rate pressure product in control hearts was approximately 60% of pre-hypoxic values. Exposing hearts to 1 or 10 mM GSH, 10 mM GSHMEE, or 1 mM OZT significantly (p < 0.05) enhanced post-hypoxic recovery of rate pressure product and attenuated the rise in diastolic pressure during hypoxia. This improvement in function was not associated with an elevated intracellular thiol concentration in treated hearts. Cumulative oxidative changes may occur during intermittent hypoxia via a mechanism localized on or near the sarcolemmal membrane. These changes appear to precede the appearance of significant intracellular oxidative stress and may be due to alterations in the reduced status of critical membrane bound proteins. Exogenously administered thiols attenuate protein alterations via a localized increase in thiol availability without an increase in gross measures of intracellular thiol or glutathione content.