Steven C. Dennis

Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists

Abstract Skeletal muscle buffering capacity (βm), enzyme activities and exercise performance were measured before and after 4 weeks of high-intensity, sub maximal␣interval training (HIT) undertaken by six well-trained competitive cyclists [mean maximal oxygen consumption (O2max) = 66.2 ml · kg−1 · min−1]. HIT replaced a portion of habitual endurance training and consisted of six sessions, each of six to eight repetitions of 5 min duration at 80% of peak sustained power output (PPO) separated by 1 min of recovery. βm increased from 206.6 (17.9) to 240.4 (34.1) μmol H+ · g muscle dw−1 · pH−1 after HIT (P = 0.05). PPO, time to fatigue at 150% PPO (TF150) and 40-km cycle time trial performance (TT40) all significantly improved after HIT (P < 0.05). In contrast, there was no change in the activity of either phosphofructokinase or citrate synthase. In addition, βm correlated significantly with TT40 performance before HIT (r = −0.82, P < 0.05) and the relationship between change in βm and change in TT40 was close to significance (r = −0.74). βm did not correlate with TF150. These results indicate that βm may be an important determinant of relatively short-duration (< 60 min) endurance cycling activity and responds positively to just six sessions of high-intensity, submaximal interval training.

Reduction of ischemic K+ loss and arrhythmias in rat hearts. Effect of glibenclamide, a sulfonylurea.

Glibenclamide, one of the antidiabetic sulfonylureas, is known to block ATP-dependent K+ channels. We used this drug to determine to what extent K+ loss from acutely ischemic myocardium is mediated via these channels. We also investigated whether glibenclamide would influence ischemic arrhythmias. Isolated rat hearts rendered globally ischemic showed no correlation between early lactate and K+ efflux rates. Cumulative K+ loss during 11 minutes of global ischemia (0.5 ml min-1 g-1) was reduced, from 3.2 +/- 0.3 to 2.5 +/- 0.1 mueq/g (p less than 0.025) by 1 microM glibenclamide and from 3.3 +/- 0.2 to 1.9 +/- 0.2 mueq/g (p less than 0.005) by 10 microM glibenclamide, while lactate efflux was unaltered by the drug. Glibenclamide also exhibited potent antifibrillatory activity, abolishing irreversible ventricular fibrillation during regional ischemia (0/6 vs. 5/6 controls; p less than 0.02) and during global ischemia (0/7 vs. 9/9 controls; p less than 0.01). Heart rate, coronary flow rate, peak systolic pressure, and myocardial oxygen consumption were unaltered by the drug (1 microM). Similarly, glibenclamide (1 microM) did not alter myocardial ATP, phosphocreatine or lactate content, or glucose utilization. Ventricular fibrillation threshold during normoxia was also unaltered by glibenclamide (1 microM). We conclude that K+ loss during acute myocardial ischemia is mediated partly by ATP-dependent K+ channels, and not by a tightly coupled co-efflux with anionic lactate.

Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

AbstractThese studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake (

Effects of different interval-training programs on cycling time-trial performance

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Metabolic and performance adaptations to interval training in endurance-trained cyclists

O2max), high-intensity exercise (HIE)] and 50% of peak power output [60%

Metabolic adaptations to a high-fat diet in endurance cyclists

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