Training and performance characteristics among Norwegian international rowers 1970-2001.

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.

Exogenous GSH protection during hypoxia-reoxygenation of the isolated rat heart: impact of hypoxia duration.

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.

Vitamin E concentration in rat skeletal muscle and liver after exercise.

The purpose of this study was to determine whether submaximal exercise significantly changes the concentration of vitamin E (alphaToc) in rat liver and skeletal muscle and to establish a time course for the return to basal levels. Male Sprague-Dawley rats, age 8 to 10 weeks, were randomly divided into sedentary control (Con) (n = 7) and exercise (n = 17) groups. Exercised animals ran 100 min on a motorized treadmill at approximately 70% VO2max for 3 consecutive days. They were then sacrificed immediately postexercise (0Post), 24 hr post (24Post), or 72 hr post (72Post). The gastrocnemius, red vastus lateralis (RV), white vastus lateralis (WV), and liver were excised and analyzed for alphaToc concentration by high-performance liquid chromotography utilizing electrochemical detection. We found that after 3 consecutive days of exercise, alphaToc was reduced in RV and WV at 0Post and 24Post but returned to control values by 72Post. Liver alphaToc content was not changed at 0Post but was significantly reduced at 24Post and 72Post. No significant changes in alphaToc were observed in the gastrocnemius in response to exercise. The data indicate that following an exercise-related decrease, skeletal muscle vitamin E concentration requires more than 24 hr to return to the preexercise concentration, and that the replenishment process may involve redistribution of vitamin E from liver to muscle.

Gender differences in rowing performance and power with aging.

PURPOSE AND METHODS: Competitive indoor rowing performance times of 2487 men ages 24 to 93, and 1615 women ages 24-84 collected from a composite ranking of regional, national, and international indoor rowing competitions were analyzed to determine the impact of age and gender on ergometer rowing performance. RESULTS: For all subjects age was only modestly correlated with performance in men or women (r = 0.58 and 0.46, respectively). When regression analysis was restricted to only the 95th percentile of each 2-yr age increment (119 men, 79 women), age was a powerful predictor of performance variance in men and women (approximately 90%). In the top men, the pattern of performance decline was curvilinear. Between ages 24 and 50, performance decline was only 3% per decade, compared to 7% from ages 50 to 74. The pattern of performance decline in women was essentially linear across the same 50-yr age span. CONCLUSION: Performance time to power output conversion revealed that men and women lose absolute power at a similar rate across the age span analyzed. However, their different starting positions on the exponential power-velocity curve create distinct differences in the pattern of performance decline and the maintenance of relative power. These data suggest that differences in the effect of aging on performance across different endurance sports are caused more by physics than physiology.

Myocardial injury after hypoxia in immature, adult and aged rats.

We evaluated the abilities of isolated perfused hearts from immature (IM) (2.5-3 months), ADULT (11-13 months) and OLD (24-26 months) Fischer 344 rats to tolerate and recover from oxygen deprivation. Hearts were perfused at 60 mmHg for a 30-minute prehypoxic period with oxygenated buffer supplemented with 10 mM glucose (+insulin) and 2 mM acetate, then 30 minutes with substrate-free, hypoxic buffer gassed with 95% N2:5% CO2, and finally reoxygenated for an additional 45 minutes with the same buffer used during the prehypoxic period. During prehypoxia, all groups were similar in ventricular mechanical function, glycogen content, high-energy phosphates (HEP), reduced glutathione (GSH), Ca+2 content, and mitochondrial state 3 rates. At the end of the hypoxic period, glycogen levels were similar and almost completely depleted in all groups, HEP were lower (p < 0.05) in ADULT vs other groups, mitochondrial state 3 rates were decreased (24%, p < 0.05) only in ADULT, and GSH was depleted by 34% in IM vs only 13% in OLD (p < 0.05). After 45 minutes of reoxygenation, IM and OLD had recovered 48% and 45% of their respective prehypoxic function which was two-fold greater than the 23% recovery by ADULT. Loss of cytosolic enzymes, an indicator of sarcolemmal damage, was estimated by measuring lactate dehydrogenase (LDH) release. LDH release and Ca+2 content during reoxygenation in IM were only about half of that observed in ADULT or OLD. We conclude that immature and aged hearts tolerate and recover from hypoxia better than hearts from adults, and that the sarcolemmal membranes of immature rat hearts are less susceptible to damage from hypoxic stress than those of either older group.

Exogenous glutathione attenuates stunning following intermittent hypoxia in isolated rat hearts.

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.

Intrinsic myocardial function and oxidative stress after exhaustive exercise.

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.

Effect of perfusion pressure at reoxygenation on reflow and function in isolated rat hearts.

The effect of coronary perfusion pressure during reoxygenation on recovery of endocardial flow, arrhythmogenesis, and mechanical function was investigated in the isolated rat heart. Hearts were subjected to 30 min of substrate-free hypoxia followed by 30 min reoxygenation at either 80 or 150 cmH2O perfusion pressure. No flow areas were quantified by 0.3% phthalocyanine blue injection after 30 min of hypoxia, 30 min reoxygenation at 80 cmH2O, or 30 min reoxygenation at 150 cmH2O. After hypoxia, 31 +/- 2% of the myocardium was unperfused. After 80 cmH2O reoxygenation, 13 +/- 4% of the heart remained unperfused. Ten of 12 (83%) 80-cmH2O hearts were in sustained fibrillation after 10 min of reoxygenation. Reoxygenation at 150 cmH2O resulted in complete reperfusion of the myocardium. Fibrillation was absent in all hearts reoxygenated at this higher pressure. Functional recovery after 30 min reoxygenation (% of normoxic heart rate x left ventricular developed pressure) was significantly (P less than 0.05) higher in 150 cmH2O vs. 80 cmH2O (60 +/- 5 vs. 42 +/- 8%). Elevating perfusion pressure upon reoxygenation appears to counter the vascular compression caused by contracture and leads to a more rapid and homogeneous restoration of coronary flow during the transition from the hypoxic to the normoxic state.

Fructose-1,6-bisphosphate improves efficiency of work in isolated perfused rat hearts.

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)