Canadian journal of applied physiology = Revue canadienne de physiologie appliquee最新文献

The purpose of this study was to determine, in heart failure patients (HF), whether acute or chronic L-arginine supplementation (LAS) might delay the ventilatory threshold (VT) and whether chronic LAS might reduce exercise-induced plasma lactate increase. HF patients undertook 4 cardiopulmonary bicycle exercises tests. The first 3 were maximal without (EX(1)), after acute (EX(2)), or chronic (EX(3)) oral LAS (6 gm twice a day for 6 weeks). The 4th test (EX(4)) performed after chronic LAS, was similar to the first in order to investigate the effect of chronic LAS on circulating lactate levels. Results showed that acute LAS failed to improve both submaximal and maximal exercise capacities. Similarly, maximal exercise capacity remained unmodified after chronic LAS. Nevertheless, chronic LAS delayed significantly the patients' ventilatory threshold. Thus exercise duration prior to VT increased (mean +/- SEM) from 6.04 +/- 0.9 to 7.7 +/- 1.03 min (p = 0.04), resulting in a significant increase in oxygen uptake (1.05 +/- 0.08 to 1.24 +/- 0.12 L.min(-1); p = 0.03), CO(2) release (0.94 +/- 0.10 to 1.2 +/- 0.12 L.min(-1); p = 0.018), minute ventilation (29.31 +/- 2.8 to 34.5 +/- 2.7 L; p = 0.009), and workload (60.7 +/- 9.8 to 78.5 +/- 10.2 watts; p = 0.034). Furthermore, chronic LAS significantly reduced the exercise-induced increase in postexercise plasma lactate concentration (-21 +/- 7%). In conclusion, unlike acute supplementation, chronic LAS significantly delays the ventilatory threshold, and chronic LAS reduces circulating plasma lactate in HF patients. These data suggest that chronic LAS might improve the ability of HF patients to perform their daily-life activities.

The aim of the present study was to investigate potential mechanisms responsible for the improvement in prolonged exercise capacity in hot environments with exogenous carbohydrate. Eight endurance-trained men (VO(2)max 60.5 +/- 2.4 ml.kg(-1).min(-1), mean +/- SE) cycled to exhaustion on three occasions at 60% VO(2)max at an ambient temperature of 35 degrees C. They ingested either a sweet 6.4% carbohydrate solution (SC), a nonsweet 6.4% carbohydrate solution (NSC), or water (W). Exercise capacity was significantly increased with SC and NSC compared to W, the improvements corresponding to 15.8% and 11.8%, respectively. No difference in exercise capacity was seen between SC and NSC solutions. Plasma glucose concentrations were higher during the SC and NSC trials compared to W, significantly so at 10 min and at fatigue. Rates of carbohydrate oxidation were higher in the SC and NSC trials, although the rates never declined below 2.1 +/- 0.2 g.min(-1) in the W trial. There was no difference in the rate of rise of rectal temperature between trials, but there was a trend for subjects to fatigue at higher temperatures during the two carbohydrate trials. In conclusion, exogenous carbohydrate, independent of sweetness, improves exercise capacity in the heat compared to water alone.

The aim of this study was to compare male and female thermal, cardiac, and muscular responses induced by a prolonged run undertaken in a hot environment. Twelve volunteers participated in this study. The first group consisted of 6 men and the second one consisted of 6 women. After determination of their VO(2)max and maximal aerobic velocity (MAV), each athlete completed a 40-min run at 65% MAV in a hot and dry environment (temperature 31-33 degrees C, relative humidity 30%). Immediately before and after the run, each subject performed two different vertical jumps, i.e., a squat jump (SJ) and a counter-movement jump (CMJ) on a force platform. Force, velocity, power, and jump height were measured during each jump. The completion of the run was associated with a significant loss (p < 0.001) of body mass (BM) and significant increases (p < 0.001) in heart rate, tympanic temperature, and lactate concentration ([La]). Muscle power was significantly improved (+9%, p < 0.05) during the SJ only in the women. A significant enhancement of this parameter was also demonstrated during the CMJ in both groups (men: +10%, p < 0.05; women: +8%, p < 0.01). Surprisingly, a comparison of thermal, cardiac, and muscular responses did not reveal any significant differences between the sexes. Moderate dehydration (-2.0 to -2.3% of BM) and a rise in core temperature (above 39.2 degrees C) induced by the 40-min run led to an improvement of muscular strength in both men and women. However, the results of this study did not reveal any significant between-sex differences in thermal, cardiac, and muscular responses after exercising in the heat.

Many researchers have used cycling exercise to evaluate muscle metabolism. Inherent in such studies is an assumption that changes in whole-body respiration are due solely to respiration at the working muscle. Some researchers, however, have speculated that the metabolic cost of torso stabilization may contribute to the metabolic cost of cycling. Therefore, our primary purpose was to determine whether a torso stabilization device would reduce the metabolic cost of producing cycling power. Our secondary purpose was to determine the validity of the ergometer used in this study. Nine male cyclists cycled on a Velotron cycle ergometer at mechanical power outputs intended to elicit 50, 75, and 100% of their ventilatory threshold at 40, 60, and 80 rpm, with and without torso stabilization. Power was controlled by the Velotron in iso-power mode and measured with an SRM powermeter. We determined metabolic cost by indirect calorimetery and recorded power output. Torso stabilization significantly reduced metabolic cost of producing submaximal power (1%), and reduction tended to be greatest at the lower pedaling rates where pedaling force was greatest (1.6% at 40 rpm, 1.2% at 60 rpm, 0.2% at 80 rpm). Power, measured with the SRM powermeter, was strongly correlated with that specified to the Velotron ergometer control unit (R(2) > 0.99). We conclude that muscular contractions associated with torso stabilization elicit significant metabolic costs, which tend to be greatest at low pedaling rates. Researchers who intend to make precise inferences regarding metabolism in the working muscles of the legs may wish to provide torso stabilization as a means of reducing variability, particularly when comparing metabolic data across a wide range of pedaling rates.

Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease.

In discussion of the physiological mechanisms that regulate fat metabolism, and with consideration of the metabolic stimuli that modulate substrate metabolism, the issue of how an acute state of negative lipid balance can be maximized is addressed. The regulation of lipolysis by catecholamines and insulin is reviewed, and the mechanisms of fatty acid mobilization and uptake by muscle are also briefly discussed. The implications of substrate availability and the hormonal response during physiological states such as fasting, exercise, and after food intake are also addressed, with particular regard to the influences on fatty acid mobilization and/or oxidation from eliciting these stimuli conjointly. Finally, a brief discussion is given of both the nature of exercise and the exercising individual, and how these factors influence fat metabolism during exercise. It is also a primary thrust of this paper to underline gaps in the existing literature with regard to exercise timing concerning food ingestion for maximizing acute lipid utilization.

In spite of our knowledge of activity related adaptations in supraspinal neurones and skeletal muscles, very little is known concerning adaptations in alpha-motoneurones to alterations in chronic activity levels. Recent evidence shows that the biophysical properties of alpha-motoneurones are plastic and adapt to both increases and decreases in chronic activation. The nature of the adaptations--in resting membrane potential, spike threshold, afterhyper-polarization amplitude,and rate of depolarization during spike generation--point to involvement of density, type, location, and/or metabolic modulation of ion conductance channels in the motoneuronal membrane. These changes will have significant effects on how motoneurones respond when activated during the generation of movements, and on the effort required to sustain activation during prolonged exercise. Since the adaptations most likely involve structural changes in the motoneurones and changes in protein synthesis, and change the output response of the cells to input, they are considered to be learning responses. Future research directions for examining this issue are outlined.

Human splenic contraction occurs both during apnea and maximal exercise, increasing the circulating erythrocyte volume. We investigated the hematological responses to 3 maximal apneas performed by elite apneic divers, elite cross-country skiers, and untrained subjects. Post-apnea hemoglobin concentration had increased in all groups, but especially in divers. The increases disappeared within 10 min of recovery. Apneic duration across apneas also increased the most in divers. Responses in divers could be more pronounced as a result of apnea training.

During the first few weeks of isometric resistance training there is an increase in maximal muscle force output that cannot be accounted for by muscle hypertrophy. Early on, researchers postulated the existence of neural adaptations to training primarily through the use of surface electromyographic recordings. More recent evidence also suggests that increased excitation may occur at the cortical levels following short-term resistance training. Alterations in synergistic activation and reductions in antagonist activation are neural factors that have been identified as changing during the early stages of resistance training which could contribute to maximal force generation. Neural adaptations that occur during the ramp-up phase of isometric contraction include decreases in motor unit recruitment thresholds, increased motor unit discharge rates, and increases in double discharges. An increase in the maximal rate of force development also occurs during the early stages of resistance training, but whether the neural mechanisms associated with the increase in the rate of rise are also associated with the increase in maximal force has not been elucidated. More work is needed to examine the integration of changes in cortical and spinal excitability with single motor unit firing patterns during this simple form of exercise before we can extend our understanding to different types of training.