Showing papers on "Exercise physiology published in 1998"
TL;DR: There is now extensive epidemiological evidence demonstrating that long-term regular physical exercise can significantly reduce the risk of developing non-insulin-dependent diabetes mellitus.
Abstract: Physical exercise can be an important adjunct in the treatment of both non-insulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus. Over the past several years, considerable progress has been made in understanding the molecular basis for these clinically important effects of physical exercise. Similarly to insulin, a single bout of exercise increases the rate of glucose uptake into the contracting skeletal muscles, a process that is regulated by the translocation of GLUT4 glucose transporters to the plasma membrane and transverse tubules. Exercise and insulin utilize different signaling pathways, both of which lead to the activation of glucose transport, which perhaps explains why humans with insulin resistance can increase muscle glucose transport in response to an acute bout of exercise. Exercise training in humans results in numerous beneficial adaptations in skeletal muscles, including an increase in GLUT4 expression. The increase in muscle GLUT4 in trained individuals contributes to an increase in the responsiveness of muscle glucose uptake to insulin, although not all studies show that exercise training in patients with diabetes improves overall glucose control. However, there is now extensive epidemiological evidence demonstrating that long-term regular physical exercise can significantly reduce the risk of developing non-insulin-dependent diabetes mellitus.
1,077 citations
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01 Apr 1998
TL;DR: The conceptual basis for coronary artery disease risk factor assessment in clinical practice epidemiology of physical activity, physical fitness, and selected chronic diseases diet and chronic disease tobacco exposure and chronic illness influence of emotional distress on chronic illness integration of lifestyle behaviours are considered.
Abstract: Section one Lifestyle and health: conceptual basis for coronary artery disease risk factor assessment in clinical practice epidemiology of physical activity, physical fitness, and selected chronic diseases diet and chronic disease tobacco exposure and chronic illness influence of emotional distress on chronic illness integration of lifestyle behaviours Section two Anatomy: cardiovascular anatomy respiratory anatomy musculoskeletal anatomy surface anatomy Section three Biomechanics: mechanical load on the body biomechanics and physiology of posture and gait low back exercises - prescription for the healthy back and when recovering from injury Section four Exercise physiology: fundamentals of exercise metabolism normal cardiorespiratory esponses to acute exercise abnormal cardiorespiratory responses to acute exercise cardiorespiratory adaptations to exercise factors affecting the acute neuromuscular responses to resistance exercise chronic musculoskeletal adaptations to resistance training mechanisms of muscular fatigue detraining and retention of adaptations induced by endurance training deconditioning and bed rest - induced effects on bone health deconditioning and bed rest - musculoskeletal response environmental considerations - heat and cold exercise and the environment - altitude and air pollution Section five Coronary artery disease: coronary atherosclerosis manifestations of coronary atherosclerosis diagnosis of coronary artery disease medical and invasive interventions in the management of coronary artery disease Appendix: Drugs-resource list comprehensive cardiovascular risk reduction in patients with coronary artery disease (Part contents)
707 citations
TL;DR: It is shown that the respiratory muscle work normally expended during maximal exercise has two significant effects on the cardiovascular system: up to 14-16% of the CO is directed to the respiratory muscles; and local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.
Abstract: We have recently demonstrated that changes in the work of breathing during maximal exercise affect leg blood flow and leg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Peg...
441 citations
TL;DR: Analysis of instantaneous R-R interval variability from Poincaré plots at rest and during exercise in a population of healthy males shows that poor physical fitness is associated with an impairment of cardiac vagal function during exercise, whereas aging itself results in more evident impairment of vagalfunction at rest.
Abstract: This study was designed to assess the effects of age and physical fitness on vagal modulation of heart rate (HR) during exercise by analyzing the instantaneous R-R interval variability from Poincar...
432 citations
TL;DR: It was concluded that exercise-heat tolerance in this uncompensable heat-stress environment is not influenced by short-term heat acclimation but is significantly improved by long-term aerobic fitness.
Abstract: The purpose of the present study was to determine the separate and combined effects of aerobic fitness, short-term heat acclimation, and hypohydration on tolerance during light exercise while wearing nuclear, biological, and chemical protective clothing in the heat (40 degrees C, 30% relative humidity). Men who were moderately fit [(MF); 55 ml . kg-1 . min-1 maximal O2 consumption; n = 8] were tested while they were euhydrated or hypohydrated by approximately 2.5% of body mass through exercise and fluid restriction the day preceding the trials. Tests were conducted before and after 2 wk of daily heat acclimation (1-h treadmill exercise at 40 degrees C, 30% relative humidity, while wearing the nuclear, biological, and chemical protective clothing). Heat acclimation increased sweat rate and decreased skin temperature and rectal temperature (Tre) in HF subjects but had no effect on tolerance time (TT). MF subjects increased sweat rate but did not alter heart rate, Tre, or TT. In both MF and HF groups, hypohydration significantly increased Tre and heart rate and decreased the respiratory exchange ratio and the TT regardless of acclimation state. Overall, the rate of rise of skin temperature was less, while DeltaTre, the rate of rise of Tre, and the TT were greater in HF than in MF subjects. It was concluded that exercise-heat tolerance in this uncompensable heat-stress environment is not influenced by short-term heat acclimation but is significantly improved by long-term aerobic fitness.
388 citations
TL;DR: The view that different priorities are placed on lipid and carbohydrate oxidation during exercise in men and women is supported and that these gender-based differences extend to the catecholamine response to exercise.
Abstract: This study aimed to determine gender-based differences in fuel metabolism in response to long-duration exercise. Fuel oxidation and the metabolic response to exercise were compared in men (n = 14) ...
347 citations
TL;DR: It is concluded that blood flow to the exercising muscles declines significantly with dehydration, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction, and the progressive increase in oxygen consumption during exercise is confined to the active muscles.
Abstract: 1. The present study examined whether the blood flow to exercising muscles becomes reduced when cardiac output and systemic vascular conductance decline with dehydration during prolonged exercise in the heat. A secondary aim was to determine whether the upward drift in oxygen consumption (VO2) during prolonged exercise is confined to the active muscles. 2. Seven euhydrated, endurance-trained cyclists performed two bicycle exercise trials in the heat (35 C; 40-50 % relative humidity; 61 +/- 2 % of maximal VO2), separated by 1 week. During the first trial (dehydration trial, DE), they bicycled until volitional exhaustion (135 +/- 4 min, mean +/- s.e.m.), while developing progressive dehydration and hyperthermia (3.9 +/- 0.3 % body weight loss; 39.7 +/- 0.2 C oesophageal temperature, Toes). In the second trial (control trial), they bicycled for the same period of time while maintaining euhydration by ingesting fluids and stabilizing Toes at 38.2 +/- 0.1 C after 30 min exercise. 3. In both trials, cardiac output, leg blood flow (LBF), vascular conductance and VO2 were similar after 20 min exercise. During the 20 min-exhaustion period of DE, cardiac output, LBF and systemic vascular conductance declined significantly (8-14 %; P < 0.05) yet muscle vascular conductance was unaltered. In contrast, during the same period of control, all these cardiovascular variables tended to increase. After 135 +/- 4 min of DE, the 2.0 +/- 0.6 l min-1 lower blood flow to the exercising legs accounted for approximately two-thirds of the reduction in cardiac output. Blood flow to the skin also declined markedly as forearm blood flow was 39 +/- 8 % (P < 0.05) lower in DE vs. control after 135 +/- 4 min. 4. In both trials, whole body VO2 and leg VO2 increased in parallel and were similar throughout exercise. The reduced leg blood flow in DE was accompanied by an even greater increase in femoral arterial-venous O2 (a-vO2) difference. 5. It is concluded that blood flow to the exercising muscles declines significantly with dehydration, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction. Furthermore, the progressive increase in oxygen consumption during exercise is confined to the exercising skeletal muscles.
322 citations
TL;DR: Exercise training increases parasympathetic tone at rest in both the healthy older and young men, which may contribute to the reduction in mortality associated with regular exercise.
Abstract: Heart rate variability (HRV) (SD of the RR interval), an index of parasympathetic tone, was measured at rest and during exercise in 13 healthy older men (age 60 to 82 years) and 11 healthy young men (age 24 to 32 years) before and after 6 months of aerobic exercise training. Before exercise training, the older subjects had a 47% lower HRV at rest compared with the young subjects (31 +/- 5 ms vs 58 +/- 4 ms, p = 0.0002). During peak exercise, the older subjects had less parasympathetic withdrawal than the young subjects (-45% vs -84%, p = 0.0001). Six months of intensive aerobic exercise training increased maximum oxygen consumption by 21% in the older group and 17% in the young group (analysis of variance: overall training effect, p = 0.0001; training effect in young vs old, p = NS). Training decreased the heart rate at rest in both the older (-9 beats/min) and the young groups (-5 beats/min, before vs after, p = 0.0001). Exercise training increased HRV at rest (p = 0.009) by 68% in the older subjects (31 +/- 5 ms to 52 +/- 8 ms) and by 17% in the young subjects (58 +/- 4 ms to 68 +/- 6 ms). Exercise training increases parasympathetic tone at rest in both the healthy older and young men, which may contribute to the reduction in mortality associated with regular exercise.
279 citations
TL;DR: It is concluded that muscle triacylglycerol concentrations are not diminished during exhaustive glycogen-depleting exercise, however, in the postex exercise recovery period, muscle glycogen resynthesis has high metabolic priority, resulting in postexercise lipid combustion despite a high carbohydrate intake.
Abstract: The utilization of muscle triacylglycerols was studied during and after prolonged bicycle ergometer exercise to exhaustion in eight healthy young men. Two days before exercise and in the postexerci...
278 citations
TL;DR: The time course of cytokine production, the close association with muscle damage, and the finding of mRNA-IL-6 in skeletal muscle biopsies after intense exercise all support the idea that during eccentric exercise myofibers are mechanically damaged and that this process stimulates the local production of inflammatory cytokines.
Abstract: Strenuous exercise is accompanied by an increase in circulating proinflammatory and inflammation responsive cytokines, having some similarities with the response to sepsis and trauma. The sequential release of tumour necrosis factor-alpha, interleukin (IL) 1 beta, IL-6, and IL-1 receptor antagonist (IL-1ra) in the blood is comparable to that observed in relation to bacterial diseases. Eccentric exercise is associated with an increase in serum IL-6 concentrations and is significantly correlated with the concentration of creatine kinase (CK) in the following days, whereas no changes are found after the concentric exercise; this demonstrates a close association between exercise-induced muscle damage and increased serum levels of IL-6. The time course of cytokine production, the close association with muscle damage, and the finding of mRNA-IL-6 in skeletal muscle biopsies after intense exercise all support the idea that during eccentric exercise myofibers are mechanically damaged and that this process stimulates the local production of inflammatory cytokines. It remains to be shown whether systemic endotoxemia during exercise is also a cause of elevated levels of cytokines in the plasma. The present review also discusses the possible roles of protein breakdown, delayed onset muscle soreness, and clinical implications of the acute-phase response following exercise.
250 citations
TL;DR: It appears that the primary determinants of sustained exercise hyperemia in skeletal muscle are metabolic vasodilation and increased vascular conductance via the muscle pump and sympathetic neural control is important in regulating muscle blood flow during exercise.
Abstract: For exercise to be sustained, it is essential that adequate blood flow be provided to skeletal muscle. The local vascular control mechanisms involved in regulating muscle perfusion during exercise include metabolic control, endothelium-mediated control, propagated responses, myogenic control, and the muscle pump. The primary determinant of muscle perfusion during sustained exercise is the metabolic rate of the muscle. Metabolites from contracting muscle diffuse to resistance arterioles and act directly to induce vasodilation, or indirectly to inhibit noradrenaline release from sympathetic nerve endings and oppose alpha-adrenoreceptor-mediated vasoconstriction. The vascular endothelium also releases vasodilator substances (e.g., prostacyclin and nitric oxide) that are prominent in establishing basal vascular tone, but these substances do not appear to contribute to the exercise hyperemia in muscle. Endothelial and smooth muscle cells may also be involved in propagating vasodilator signals along arterioles to parent and daughter vessels. Myogenic autoregulation does not appear to be involved in the exercise hyperemia in muscle, but the rhythmic propulsion of blood from skeletal muscle veins facilitates venous return to the heart and muscle perfusion. It appears that the primary determinants of sustained exercise hyperemia in skeletal muscle are metabolic vasodilation and increased vascular conductance via the muscle pump. Additionally, sympathetic neural control is important in regulating muscle blood flow during exercise.
TL;DR: It is concluded that the elevation in blood flow with the first duty cycle(s) is due to muscle mechanical factors, but vasodilators initiate a more potent amplification within the second to fourth contraction.
Abstract: To evaluate the temporal relationship between blood flow, blood pressure, and muscle contractions, we continuously measured femoral arterial inflow with ultrasound Doppler at onset of passive exerc...
TL;DR: In this paper, the threshold of exercise energy expenditure necessary to change blood lipid and lipoprotein concentrations and Lipoprotein lipase activity (LPLA) in healthy, trained men was determined.
Abstract: The purpose of this study was to determine the threshold of exercise energy expenditure necessary to change blood lipid and lipoprotein concentrations and lipoprotein lipase activity (LPLA) in healthy, trained men. On different days, 11 men (age, 26.7 +/- 6.1 yr; body fat, 11.0 +/- 1.5%) completed four separate, randomly assigned, submaximal treadmill sessions at 70% maximal O2 consumption. During each session 800, 1,100, 1,300, or 1,500 kcal were expended. Compared with immediately before exercise, high-density lipoprotein cholesterol (HDL-C) concentration was significantly elevated 24 h after exercise (P < 0.05) in the 1,100-, 1,300-, and 1,500-kcal sessions. HDL-C concentration was also elevated (P < 0.05) immediately after and 48 h after exercise in the 1,500-kcal session. Compared with values 24 h before exercise, LPLA was significantly greater (P < 0.05) 24 h after exercise in the 1,100-, 1,300-, and 1,500-kcal sessions and remained elevated 48 h after exercise in the 1,500-kcal session. These data indicate that, in healthy, trained men, 1,100 kcal of energy expenditure are necessary to elicit increased HDL-C concentrations. These HDL-C changes coincided with increased LPLA.
TL;DR: During vigorous exercise, carbohydrate, in the form of muscle glycogen and blood glucose, is the primary energy source, whereas fatty acids play a secondary, carbohydrate-sparing role, which plays a major role in determining how long vigorous endurance exercise can be performed if other causes of fatigue are avoided.
Abstract: The rate of carbohydrate utilization during prolonged, strenuous exercise is closely geared to the energy needs of the working muscles. In contrast, fat utilization during exercise is not tightly regulated, as there are no mechanisms for closely matching availability and metabolism of fatty acids to the rate of energy expenditure. As a result, the rate of fat oxidation during exercise is determined by the availability of fatty acids and the rate of carbohydrate utilization. Blood glucose and muscle glycogen are essential for prolonged strenuous exercise, and exhaustion can result either from development of hypoglycemia or depletion of muscle glycogen. Both absolute and relative (i.e. % of maximal O2 uptake) exercise intensities play important roles in the regulation of substrate metabolism. The absolute work rate determines the total quantity of fuel required, while relative exercise intensity plays a major role in determining the proportions of carbohydrate and fat oxidized by the working muscles. As relative exercise intensity is increased, there is a decrease in the proportion of the energy requirement derived from fat oxidation and an increase in that provided by carbohydrate oxidation. During moderately strenuous exercise of an intensity that can be maintained for 90 minutes or longer ( approximately 55-75% of VO2max), there is a progressive decline in the proportion of energy derived from muscle glycogen and a progressive increase in plasma fatty acid oxidation. The adaptations induced by endurance exercise training result in a marked sparing of carbohydrate during exercise, with an increased proportion of the energy being provided by fat oxidation. The mechanisms by which training decreases utilization of blood glucose are not well understood. However, the slower rate of glycogenolysis can be explained on the basis of lower concentrations of inorganic phosphate (Pi) in trained, as compared to untrained, muscles during exercise of the same intensity. The lower Pi level is a consequence of the increase in muscle mitochondria induced by endurance exercise training. A large increase in muscle glycogen concentration, far above the level found in the well-fed sedentary state, occurs in response to carbohydrate feeding following glycogen depleting exercise. It was recently found that this muscle "glycogen supercompensation" is markedly enhanced by endurance exercise training that induces an increase in the GLUT4 isoform of the glucose transporter in skeletal muscle.
TL;DR: The hypothesis of a hypothalamo-pituitary dysregulation during OT expressed by an impaired response of pituitary hormones to exhaustive short-endurance exercise is confirmed.
Abstract: The aim of the present prospective longitudinal study was to investigate the hormonal response in overtrained athletes at rest and during exercise consisting of a short-term exhaustive endurance test on a cycle ergometer at an intensity 10% above the individual anaerobic threshold. Over a period of 19+/-1 months, 17 male endurance athletes (cyclists and triathletes; age 23.4+/-1.6 yr; VO2max. 61.2+/-1.8 mL x min(-1) x kg(-1); means+/-SEM) were examined five times on two separate days under standardized conditions. Short-term overtraining states (OT, N=15) were primarily induced by an increase of frequency of high-intensive bouts of exercise or competitions without increase of the total amount of training. OT was compared with normal training states intraindividually (NS, N=62). During OT, the time to exhaustion of the exercise test was significantly decreased by 27% on average. At rest and during exercise, the concentrations in plasma and the nocturnal excretion in urine of free epinephrine and norepinephrine were not significantly changed during OT. At physical rest, the concentrations of (free) testosterone, cortisol, luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, growth hormone, and insulin during OT were comparable with those during NS. A significantly (P < 0.025) lower maximal exercise-induced increase of the adrenocorticotropic hormone and growth hormone, as well as a trend for a decrease of cortisol (P=0.060) and insulin (P=0.036), was measured. The response of free catecholamines as well as the ergometric performance of an all-out 30-s test was unchanged. Serum urea, uric acid, ferritin, and activity of creatine kinase showed no differences between conditions. In conclusion, the results confirm the hypothesis of a hypothalamo-pituitary dysregulation during OT expressed by an impaired response of pituitary hormones to exhaustive short-endurance exercise.
TL;DR: A new physiological model is proposed in which skeletal muscle recruitment is regulated by a central "governor" specifically to prevent the development of a progressive myocardial ischemia that would precede theDevelopment of skeletal muscle anaerobiosis during maximum exercise.
Abstract: Bassett and Howley contend that the 1996 J. B. Wolffe lecture is erroneous because: 1) A. V. Hill did establish the existence of the "plateau phenomenon," 2) the maximum oxygen consumption (VO2max) is limited by the development of anaerobiosis in the active muscle, and 3) endurance performance is also determined by skeletal muscle anaerobiosis because the VO2max is the best predictor of athletic ability. As a result, 4) cardiovascular and not skeletal muscle factors determine endurance performance. They further contend that Hill's "scientific hunches were correct," requiring "only relatively minor refinements" in the past 70 yr. But the evidence presented in this rebuttal shows that Hill neither sought nor believed in either the "plateau phenomenon" or the concept of the individual maximum oxygen consumption. These twin concepts were created by Taylor et al. (97) in 1955 and erroneously attributed to Hill. Rather Hill believed that there was a universal human VO2max of 4 L x min(-1). His error resulted from his incorrect belief that the real VO2 unmeasurable because it includes a large "anaerobic component," rose exponentially at running speeds greater than 13.2 km x h(-1). But Hill and his colleagues were indeed the first to realize the danger that a plateau in cardiac output (CO) and hence in VO2 would pose for the heart itself. For unlike skeletal muscle, the pumping capacity of the heart is both dependent on, but also the determinant of, its own blood supply. Thus, if the CO reaches a peak causing the "plateau phenomenon," the immediate cause of that peak will have been a plateau in myocardial oxygen delivery, causing a developing myocardial ischemia. The ischemia must worsen as exercise continues beyond the supposed VO2 "plateau." To accommodate this dilemma, Hill and his colleagues proposed a governor "either in the heart muscle or in the nervous system" necessary to prevent myocardial ischemia developing during maximal exercise. This governor would cause maximal exercise to terminate before the development of a plateau in either coronary flow, CO, or VO2, or the onset of skeletal muscle anaerobiosis. Accordingly, a new physiological model is proposed in which skeletal muscle recruitment is regulated by a central "governor" specifically to prevent the development of a progressive myocardial ischemia that would precede the development of skeletal muscle anaerobiosis during maximum exercise. As a result cardiovascular function "limits" maximum exercise capacity, probably as a result of a limiting myocardial oxygen delivery. The model is compatible with all the published findings of cardiovascular function during exercise in hypobaric hypoxia, in which there is a greater likelihood that myocardial hypoxia will develop.
TL;DR: This review focuses on the response of "stress" hormones to heat, exercise (single or repeated bouts), and combinations of these stimuli, with particular reference to their impact upon immune function.
Abstract: This review focuses on the response of "stress" hormones to heat, exercise (single or repeated bouts), and combinations of these stimuli, with particular reference to their impact upon immune function. Very hot conditions induce a typical stress response, with secretion of catecholamines and cortisol. The catecholamines induce a demargination of leukocytes, and cortisol subsequently causes cells to migrate to lymphoid tissue. Sustained exercise, even in a thermally comfortable environment, induces a larger hormonal response than moderate thermal stress. With moderate exercise, increases in leukocyte numbers are related mainly to plasma norepinephrine concentrations, but with more intense exercise epinephrine concentrations assume a major importance. As exercise continues, plasma cortisol levels also rise, inducing an influx of neutrophils from bone marrow and an efflux of other leukocyte subsets. A combination of exercise and heat stress augments both hormonal and leukocyte responses. But these changes seem to be reversed if temperatures are clamped by exercising in cold water. If a second bout of exercise is performed with an inter-test interval of 30-45 min, neither hormone concentrations nor immune responses show any great cumulative effect under temperate conditions. However, in a hot environment the second exercise bout induces a larger and more persistent neutrophilia. Training influences these various responses mainly by decreasing the stress imposed when exercising at a given absolute work-rate.
TL;DR: Short-term creatine supplementation appears to increase body mass in males, although the initial increase is most likely water, and chronic creatine supplementation, in conjunction with physical training involving resistance exercise, may increase lean body mass, however, confirmatory research data are needed.
Abstract: Creatine, a natural nutrient found in animal foods, is alleged to be an effective nutritional ergogenic aid to enhance sport or exercise performance. Research suggests that oral creatine monohydrate supplementation may increase total muscle creatine [TCr], including both free creatine [FCr] and phosphocreatine [PCr]. Some, but not all, studies suggest that creatine supplementation may enhance performance in high-intensity, short-term exercise tasks that are dependent primarily on PCr (i.e., < 30 seconds), particularly laboratory tests involving repeated exercise bouts with limited recovery time between repetitions; additional corroborative research is needed regarding its ergogenic potential in actual field exercise performance tasks dependent on PCr. Creatine supplementation has not consistently been shown to enhance performance in exercise tasks dependent on anaerobic glycolysis, but additional laboratory and field research is merited. Additionally, creatine supplementation has not been shown to enhance performance in exercise tasks dependent on aerobic glycolysis, but additional research is warranted, particularly on the effect of chronic supplementation as an aid to training for improvement in competitive performance. Short-term creatine supplementation appears to increase body mass in males, although the initial increase is most likely water. Chronic creatine supplementation, in conjunction with physical training involving resistance exercise, may increase lean body mass. However, confirmatory research data are needed. Creatine supplementation up to 8 weeks has not been associated with major health risks, but the safety of more prolonged creatine supplementation has not been established. Creatine is currently legal and its use by athletes is not construed as doping.
TL;DR: In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension, however, in contrast to exercise at 50 and 80%, exercise at 30% ofVO2peak decreased post-Exercise HR and RP.
Abstract: To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 +/- 314 vs R5-30 = 7150 +/- 326, R35-60 = 6794 +/- 349, and R65-90 = 6628 +/- 311, P < 0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 +/- 267 vs 9818 +/- 366, P < 0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP.
TL;DR: In young women, whole body lipolysis (glycerol Ra) during exercise is not significantly impacted by training, and training-induced increases in plasma FFA oxidation are the main contributor to elevated total F FA oxidation during exercise exertion after training.
Abstract: We examined the effects of exercise intensity and training [12 wk, 5 days/wk, 1 h, 75% peak oxygen consumption (V˙o 2 peak)] on lipolysis and plasma free fatty acid (FFA) flux in women (n = 8; 24.3...
TL;DR: Two methods of inducing a short-term energy deficit had markedly different effects on appetite: the low-energy breakfast presumably fails to generate the inhibitory satiety signals induced by the 500 kcal breakfast, whereas the metabolic effects of an exercise session failed to generate excitatory signals to hunger and food intake.
TL;DR: The results of this study indicate that glycogen phosphorylase transformation is independent of increasing power outputs, despite increasing glycogenolytic flux, suggesting that flux through glycogen phosphate is matched to the demand for energy by posttransformational factors, such as free Pi and AMP.
Abstract: This study investigated the transformational and posttransformational control of skeletal muscle glycogen phosphorylase and pyruvate dehydrogenase (PDH) at three exercise power outputs [35, 65, and...
TL;DR: A single bout of resistance exercise is capable of modifying the sensation of experimentally induced pain and changes in pain perception were accompanied by changes in heart rate, systolic blood pressure, and body awareness after exercise.
Abstract: OBJECTIVES: The main objective was to assess the influence of resistance exercise on pain threshold and pain ratings. Secondary objectives included measuring state anxiety, body awareness, systolic blood pressure, diastolic blood pressure, and heart rate responses. METHODS: Pressure (3 kg force) was applied to the middle digit of the left hand for two minutes using a Forgione-Barber pain stimulator before and after (five minute and 15 minutes) resistance exercise and quiet rest. Resistance exercise consisted of 45 minutes of lifting three sets of 10 repetitions at 75% of an individual's one repetition maximum. Quiet rest consisted of sitting quietly in a room free from distractions. RESULTS: Data were analysed by repeated measures analysis of variance for multifactor experiments. Pain threshold was significantly higher (p<0.05) and pain ratings were significantly lower (p<0.05) five minutes after resistance exercise. Changes in pain perception were accompanied by changes in heart rate, systolic blood pressure, and body awareness after exercise. CONCLUSION: A single bout of resistance exercise is capable of modifying the sensation of experimentally induced pain.
TL;DR: Carbohydrate ingestion during exercise, in the form of CHO-electrolyte beverages, leads to performance benefits during prolonged submaximal and variable intensity exercise, however, the mechanism underlying this ergogenic effect is less clear.
Abstract: Carbohydrate (CHO) ingestion during exercise, in the form of CHO-electrolyte beverages, leads to performance benefits during prolonged submaximal and variable intensity exercise. However, the mechanism underlying this ergogenic effect is less clear. Euglycaemia and oxidation of blood glucose at high rates late in exercise and a decreased rate of muscle glycogen utilisation (i.e. glycogen 'sparing') have been proposed as possible mechanisms underlying the ergogenic effect of CHO ingestion. The prevalence of one or the other mechanism depends on factors such as the type and intensity of exercise, amount, type and timing of CHO ingestion, and pre-exercise nutritional and training status of study participants. The type and intensity of exercise and the effect of these on blood glucose, plasma insulin and catecholamine levels, may play a major role in determining the rate of muscle glycogen utilisation when CHO is ingested during exercise. The ingestion of CHO (except fructose) at a rate of > 45 g/h, accompanied by a significant increase in plasma insulin levels, could lead to decreased muscle glycogen utilisation (particularly in type I fibres) during exercise. Endurance training and alterations in pre-exercise muscle glycogen levels do not seem to affect exogenous glucose oxidation during submaximal exercise. Thus, at least during low intensity or intermittent exercise, CHO ingestion could result in reduced muscle glycogen utilisation in well trained individuals with high resting muscle glycogen levels. Further research needs to concentrate on factors that regulate glucose uptake and energy metabolism in different types of muscle fibres during exercise with and without CHO ingestion.
TL;DR: Exercise training improves tolerance to exercise in the heat by increasing the sensitivity of the sweat rate/core temperature relationship, decreasing the core temperature threshold for sweating and increasing total blood volume.
Abstract: During strenuous exercise the body's heat production may exceed 1000 W. Some of the heat produced is stored, raising body core temperature by a few degrees. Rises in body temperature are sensed by central and skin thermoreceptors and this sensory information is processed by the hypothalamus to trigger appropriate effector responses. Other sensory inputs from baroreceptors and osmoreceptors can modify these responses. Evaporation of sweat and increased skin blood flow are effective mechanisms for the dissipation of heat from the body but dehydration impairs the capacity to sweat and lose body heat. Hot, humid environments or inappropriate clothing may compromise the ability to lose heat from the body. Exercise training improves tolerance to exercise in the heat by increasing the sensitivity of the sweat rate/core temperature relationship, decreasing the core temperature threshold for sweating and increasing total blood volume.
TL;DR: There is no evidence that protein intakes in the range suggested will have adverse effects in healthy individuals, and future longitudinal studies are needed to confirm these recommendations and asses whether these protein intakes can enhance exercise performance.
Abstract: This paper reviews the factors (exercise intensity, carbohydrate availability, exercise type, energy balance, gender, exercise training, age, and timing of nutrient intake or subsequent exercise sessions) thought to influence protein need. Although there remains some debate, recent evidence suggests that dietary protein need increases with rigorous physical exercise. Those involved in strength training might need to consume as much as 1.6 to 1.7 g protein x kg(-1) x day(-1) (approximately twice the current RDA) while those undergoing endurance training might need about 1.2 to 1.6 g x kg(-1) x day(-1) (approximately 1.5 times the current RDA). Future longitudinal studies are needed to confirm these recommendations and asses whether these protein intakes can enhance exercise performance. Despite the frequently expressed concern about adverse effects of high protein intake, there is no evidence that protein intakes in the range suggested will have adverse effects in healthy individuals.
TL;DR: The results demonstrate that the differences in phosphocreatine concentration with varied FIO2 are not the result of different V(O2) onset kinetics, as this was eliminated by the experimental design, and demonstrate that changes in intracellular oxygenation result in significant changes in cell homeostasis.
Abstract: There is evidence that the concentration of the high-energy phosphate metabolites may be altered during steady-state submaximal exercise by the breathing of different fractions of inspired O2( F I ...
TL;DR: By improving insulin sensitivity, circuit-type resistance training may postpone the manifestations of NIDDM in these high-risk individuals and should therefore be included in an exercise program for IGT subjects.
Abstract: The role of physical activity in the prevention of non-insulin-dependent diabetes mellitus (NIDDM) is of utmost importance. The aim of the present study was to evaluate the metabolic effects of aerobic endurance exercise and circuit-type resistance training in subjects with impaired glucose tolerance (IGT). Twenty-two individuals participated in the study. Fourteen subjects were enrolled in the aerobic endurance exercise part of the study; seven exercised regularly for six months, while seven served as controls. Maximal aerobic capacity (VO2max) was measured and insulin sensitivity and insulin secretion were assessed by a frequently sampled intravenous glucose tolerance test (FSIVGTT). Eight subjects participated in a circuit-type resistance training program for three months. Insulin sensitivity and substrate oxidation were then assessed using the euglycemic insulin clamp technique combined with indirect calorimetry. The aerobic endurance exercise program caused in increase in VO2max (21.6 +/- 1.9 to 25.4 +/- 2.4 ml/kg.min; p < 0.05) and HDL-cholesterol (1.14 +/- 0.06 to 1.23 +/- 0.08 mmol/l; p < 0.05), but no change in insulin sensitivity nor insulin secretion occurred. However, comparing the changes between the intervention and control group, the differences disappeared. Circuit-type resistance training increased insulin sensitivity (glucose disposal) by 23% (p < 0.05), primarily due to a 27% increase in non-oxidative glucose metabolism. Both circuit-type resistance training and aerobic endurance exercise seem to have beneficial effects in subjects with impaired glucose tolerance. However, by improving insulin sensitivity, circuit-type resistance training may postpone the manifestations of NIDDM in these high-risk individuals and should therefore be included in an exercise program for IGT subjects.
TL;DR: It is suggested that lactate extrusion from exercising muscles is increased after training, and this may be associated with the increase in skeletal muscle MCT1.
Abstract: We examined the effects of increasing a known lactate transporter protein, monocarboxylate transporter 1 (MCT1), on lactate extrusion from human skeletal muscle during exercise. Before and after short-term bicycle ergometry training [2 h/day, 7 days at 65% maximal oxygen consumption (VO2max)], subjects (n = 7) completed a continuous bicycle ergometer ride at 30% VO2max (15 min), 60% VO2max (15 min), and 75% VO2max (15 min). Muscle biopsy samples (vastus lateralis) and arterial and femoral venous blood samples were obtained before exercise and at the end of each workload. After 7 days of training the MCT1 content in muscle was increased (+18%; P < 0.05). The concentrations of both muscle lactate and femoral venous lactate were reduced during exercise (P < 0.05) that was performed after training. High correlations were observed between muscle lactate and venous lactate before training (r = 0.92, P < 0.05) and after training (r = 0.85, P < 0.05), but the slopes of the regression lines between these variables differed markedly. Before training, the slope was 0.12 +/- 0.01 mM lactate.mmol lactate-1.kg muscle dry wt-1, and this was increased by 33% after training to 0.18 +/- 0.02 mM lactate.mmol lactate-1.kg muscle dry wt-1. This indicated that after training the femoral venous lactate concentrations were increased for a given amount of muscle lactate. These results suggest that lactate extrusion from exercising muscles is increased after training, and this may be associated with the increase in skeletal muscle MCT1.
TL;DR: The results of this study indicate that exercise may detrimentally affect the quantity of saliva produced, but not the quality of saliva and when exercise is to exhaustion, the intensity of the bout does not appear to influence the saliva response.
Abstract: The quality and quantity of saliva may be important in defending against pathogens transmitted via the buccal cavity. The aim of the present study was to examine the effect of cycling to exhaustion at moderate and high intensity on various salivary parameters and the time course of recovery. Eighteen male subjects of mixed physical fitness took part in the study. Subjects performed two bouts of exercise on separate occasions at least one week apart. Following an overnight fast, subjects cycled on an electrically braked cycle ergometer at a work rate equivalent to 80% VO2max until exhaustion. On another occasion they cycled on the same ergometer at 55% VO2max for 3 h or to fatigue (whichever was sooner). The order of the rides was randomised. Timed, unstimulated saliva samples were collected pre-exercise, during exercise, at cessation of exercise and at 1, 2.5, 5 and 24 h post-exercise. Saliva samples were analysed for IgA, total protein and osmolality. Saliva flow rate was significantly reduced by exercise (P < 0.01). Saliva IgA concentration, secretion rate and ratio to osmolality increased during exercise (P < 0.01). IgA to protein ratio did not change significantly during exercise. Since saliva protein secretion rate increased during exercise (P < 0.01) it appears that correcting for loss of saliva water by expressing IgA relative to protein is misleading. IgA secretion rate and IgA to osmolality ratio are more appropriate measures and neither parameter was lowered by exercise. The results of this study indicate that exercise may detrimentally affect the quantity of saliva produced, but not the quality of saliva. Furthermore, when exercise is to exhaustion, the intensity of the bout does not appear to influence the saliva response. Neither exercise protocol had any long term effect on saliva as all variables recovered within 1 h post-exercise.