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We examined the effect of differences in exercise intensity on the time constant (tc) of phosphocreatine (PCr) resynthesis after exercise and the relationships between tc and maximal oxygen uptake (VO2max) in endurance-trained runners (n = 5) and untrained controls (n = 7) (average VO2max = 66.2 and 52.0 ml.min-1.kg-1, respectively). To measure the metabolism of the quadriceps muscle using phosphorus nuclear magnetic resonance spectroscopy, we developed a device which allowed knee extension exercise inside a magnet. All the subjects performed four types of exercise: light, moderate, severe and exhausting. The end-exercise PCr: [PCr+inorganic phosphate (P(i))] ratio decreased significantly with the increase in the exercise intensity (P < 0.01). Although there was little difference in the end-exercise pH, adenosine diphosphate concentration ([ADP]) and the lowest intracellular pH during recovery between light and moderate exercise, significant changes were found at the two higher intensities (P < 0.01). These changes for runners were smaller than those for the controls (P < 0.05). The tc remained constant after light and moderate exercise and then lengthened in proportion to the increase in intensity (P < 0.05). The runners had a lower tc at the same PCr and pH than the controls, particularly at the higher intensity (P < 0.05). There was a significant correlation between tc and [ADP] in light exercise and between tc and both end-exercise PCr and pH in severe and exhausting exercise (P < 0.05). The threshold of changes in pH and tc was a PCr: (PCr+P(i)) ratio of 0.5. There was a significant negative correlation between the VO2max and tc after all levels of exercise (P < 0.05). However, in the controls a significant correlation was found in only light and moderate exercise (P < 0.05). These findings suggest the validity of the use of tc at an end-exercise PCr: (PCr+P(i)) ratio of more than 0.5 as a stable index of muscle oxidative capacity and the correlation between local and general aerobic capacity. Moreover, endurance-trained runners are characterized by the faster PCr resynthesis at the same PCr and intracellular pH.

To investigate the time-course of changes in transverse relaxation time (T2) and cross-sectional area (CSA) of the quadriceps muscle after a single session of eccentric exercise, magnetic resonance imaging was performed on six healthy male volunteers before and at 0, 7, 15, 20, 30 and 60 min and 12, 24, 36, 48, 72 and 168 h after exercise. Although there was almost no muscle soreness immediately after exercise, it started to increase 1 day after, peaking 1-2 days after the exercise (P < 0.01). Immediately after exercise, T2 increased significantly in the rectus femoris, vastus lateralis and intermedius muscles (P < 0.05) and decreased quickly continuing until 60 min after exercise. At and after the 12th h, a significant increase was perceived again in the T2 values of the vastus lateralis and intermedius muscles (P < 0.01) [maximum 9.3 (SEM 2.8)% and 10.9 (SEM 2.2)%, respectively]. The maximal values were exhibited at 24-36 h after exercise. In contrast, the rectus femoris muscle showed no delayed-stage increase. Also, in CSA, an increase after 12 h was observed in addition to the one immediately after exercise in the vastus lateralis, intermedius and medialis and quadriceps muscles as a whole (P < 0.01), reaching the maximal values at 12-24 h after exercise. The plasma creatine kinase activity remained unchanged up to 24 h after and then increased significantly 48 h after exercise (P < 0.05). Beginning 12 h after exercise, the subjects whose T2 and CSA increased less than the others displayed a faster decrease in muscle soreness.(ABSTRACT TRUNCATED AT 250 WORDS)

We examined whether oropharyngeal stimulation by drinking released the dehydration-induced suppression of cutaneous vasodilatation and decreased mean arterial pressure (MAP) in exercising subjects, and assessed the effects of hypovolaemia or hyperosmolality alone on these responses. Seven young males underwent four hydration conditions. These were two normal plasma volume (PV) trials: normal plasma osmolality (P osmol , control trial) and hyperosmolality (∆P osmol = +11 mosmol (kg H 2 O) −1 ); and two low PV trials: isosmolality (∆PV = −310 ml) and hyperosmolality (∆PV = −345 ml; ∆P osmol = +9 mosmol (kg H 2 O) −1 ), attained by combined treatment with furosemide (frusemide), hypertonic saline and/or 24 h water restriction. In each trial, the subjects exercised at 60% peak aerobic power for ∼50 min at 30• C atmospheric temperature and 50% relative humidity. When oesophageal temperature (T oes ) reached a plateau after ∼30 min of exercise, the subjects drank 200 ml water at 37.5• C within a minute. Before drinking, forearm vascular conductance (FVC), calculated as forearm blood flow divided by MAP, was lowered by 20-40% in hypovolaemia, hyperosmolality, or both, compared with that in the control trial, despite increased T oes . After drinking, FVC increased by ∼20% compared with that before drinking (P < 0.05) in both hyperosmotic trials, but it was greater in normovolaemia than in hypovolaemia (P < 0.05). However, no increases occurred in either isosmotic trial. MAP fell by 4-8 mmHg in both hyperosmotic trials (P < 0.05) after drinking, but more rapidly in normovolaemia than in hypovolaemia. PV and P osmol did not change during this period. Thus, oropharyngeal stimulation by drinking released the dehydration-induced suppression of cutaneous vasodilatation and reduced MAP during exercise, and this was accelerated when PV was restored.

We attempted to determine the change in total excess volume of CO2 output (CO2 excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO2 excess and distance-running performance. Six male endurance runners, aged 19-22 years, were subjects. Maximal oxygen uptake (VO2max), oxygen uptake (VO2) at anaerobic threshold (AT), CO2 excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for CO2 excess per unit of body mass per unit of blood lactate accumulation (delta la-) in exercise (CO2 excess.mass-1.delta la-), 12-min ERP, VO2 at AT (AT-VO2) and VO2max on average were 0.8 ml.kg-1.l-1.mmol-1, 97.8 m, 4.4 ml.kg-1. min-1 and 7.3 ml.kg-1.min-1, respectively. The percentage change in CO2 excess.mass-1.delta la- (15.7%) was almost same as those of VO2max (13.7%) and AT-VO2 (13.2%). It was found to be a high correlation between the absolute amount of change in CO2 excess.mass-1.delta la-, and the absolute amount of change in AT-VO2 (r = 0.94, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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Four well-trained combination skiers were studied through pre- and post-training for the effects of short-term intermittent training during hypoxia on muscle energetics during submaximal exercise as measured by Phosphorus-31 nuclear magnetic resonance and maximal aerobic power (VO2max). The hypoxia and training in the cold was conducted in a hypobaric chamber and comprised 60-min aerobic exercise (at an intensity equivalent to the blood lactate threshold), using a cycle ergometer or a treadmill twice a day for 4, consecutive days at 5 degrees C, in conditions equivalent to an altitude of 2000 m (593 mm Hg). No change in VO2max was observed over the training period, while in the muscle energetics during submaximal exercise, the values of phosphocreatine/(phosphocreatine+inorganic phosphate) and intracellular pH were found to be significantly increased by training during hypoxia. During recovery, the time constant of phosphocreatine was found to have been significantly reduced [pre, 27.9 (SD 6.7) s; post, 22.5 (SD 4.7) s, P < 0.01]. The observed inhibition of phosphocreatine as well as that of intracellular pH changes after training during hypoxia and quicker recovery of phosphocreatine in submaximal exercise tests, may indicate improved oxidative capacity (i.e. a high adenosine 5'-triphosphate formation rate) despite the short-term hypoxia training.