Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance (original) (raw)
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The Journal of physiology, 2011
The mechanisms determining exercise intolerance are poorly understood. A reduction in work efficiency in the form of an additional energy cost and oxygen requirement occurs during high-intensity exercise and contributes to exercise limitation. Muscle fatigue and subsequent recruitment of poorly efficient muscle fibres has been proposed to mediate this decline. These data demonstrate in humans, that muscle fatigue, generated in the initial minutes of exercise, is correlated with the increasing energy demands of high-intensity exercise. Surprisingly, however, while muscle fatigue reached a plateau, oxygen uptake continued to increase throughout 8 min of exercise. This suggests that additional recruitment of inefficient muscle fibres may not be the sole mechanism contributing to the decline in work efficiency during high-intensity exercise.
Viewpoint: Fatigue mechanisms determining exercise performance: integrative physiology
2000
Duhamel TA, Green HJ, Stewart RD, Foley KP, Smith IC, Ouyang J. Muscle metabolic, SR Ca 2ϩ -cycling responses to prolonged cycling, with and without glucose supplementation. This study investigated the effects of prolonged exercise, with and without glucose supplementation, on metabolism and sarcoplasmic reticulum (SR) Ca 2ϩ -handling properties in working vastus lateralis muscle. Fifteen untrained volunteers [peak O 2 consumption (V O2peak) ϭ 3.45 Ϯ 0.17 l/min; mean Ϯ SE] cycled at ϳ60% V O2peak on two occasions, during which they were provided with either an artificially sweetened placebo beverage (NG) or a 6% glucose (G) beverage (ϳ1.00 g carbohydrate/kg body mass). Beverage supplementation started at 30 min of exercise and continued every 15 min thereafter. SR Ca 2ϩ handling, metabolic, and substrate responses were assessed in tissue extracted from the vastus lateralis at rest, after 30 min and 90 min of exercise, and at fatigue in both conditions. Plasma glucose during G was 15-23% higher (P Ͻ 0.05) than those observed during NG following 60 min of exercise until fatigue. Cycle time to fatigue was increased (P Ͻ 0.05) by ϳ19% during G (137 Ϯ 7 min) compared with NG (115 Ϯ 6 min). Prolonged exercise reduced (P Ͻ 0.05) maximal Ca 2ϩ -ATPase activity (Ϫ18.4%), SR Ca 2ϩ uptake (Ϫ27%), and both Phase 1 (Ϫ22.2%) and Phase 2 (Ϫ34.2%) Ca 2ϩ -release rates during NG. The exercise-induced reductions in SR Ca 2ϩ -cycling properties were not altered during G. The metabolic responses to exercise were all unaltered by glucose supplementation, since no differences in respiratory exchange ratios, carbohydrate and lipid oxidation rates, and muscle metabolite and glycogen contents were observed between NG and G. These results indicate that the maintenance of blood glucose homeostasis by glucose supplementation is without effect in modifying the muscle metabolic, endogenous glycogen, or SR Ca 2ϩhandling responses. Ca 2ϩ regulation; glucose supplementation; human skeletal muscle; metabolism THE PRIMARY FUNCTION OF THE sarcoplasmic reticulum (SR) in the skeletal muscle cell is the control of cytosolic-free calcium concentration ([Ca 2ϩ ] f ). The regulation of [Ca 2ϩ ] f by the SR is mediated both by the open state of the Ca 2ϩ -release channel (CRC or ryanodine receptor), which controls the release of stored Ca 2ϩ from the SR, and by the activity of the sarco(endo)plasmic reticulum Ca 2ϩ -ATPase (SERCA), the cation pump, which sequesters Ca 2ϩ back into the lumen of the SR (2). In skeletal muscle, the CRC, which consists of a single isoform (ryanodine receptor 1) with a molecular mass of ϳ560 kDa, is composed of a large cytoplasmic foot structure facing and attached to the T tubule and anchored to the junctional SR membrane by 4 -12 transmembrane sequences (51). Calcium release from the SR occurs from the cytoplasmic Downloaded from 15 min, 30min Ͻ 60 min, 90 min, 115 Ϯ 6 min, and 137 Ϯ 7 min. For V CO2, rest Ͻ 15 min, 30 min, 60 min, 90 min, 115 Ϯ 6 min, and 137 Ϯ 7 min. For RER, rest Ͻ 15 min, 30 min Ͼ 60 min, 90 min, 115 Ϯ 6 min, and 137 Ϯ 7 min. 1989 MUSCLE RESPONSE TO CARBOHYDRATE FEEDINGS DURING EXERCISE Downloaded from a main effect (P Ͻ 0.05) of exercise was found. For Phase 1, rest Ͼ 30 min, 90 min, 115 Ϯ 6 min, and 137 Ϯ 7 min; 30 min Ͼ 115 Ϯ 6 min and 137 Ϯ 7 min. For Phase 2, rest Ͼ 30 min, 90 min, 115 Ϯ 6 min, and 137 Ϯ 7 min. 1994 MUSCLE RESPONSE TO CARBOHYDRATE FEEDINGS DURING EXERCISE
Metabolic and hormonal basis of fatigue during exercise
European Journal of Experimental Biology, 2013
Exercise-induced reduction in maximal force production or the inability to continue activity with enough force is defined as fatigue. Although the etiology of fatigue is complex, but it can be divided into two distinct parts: Central and peripheral which are not separated from each other and have close relationship with each other. Different activities cause fatigue and main challenge is identifying the different mechanisms which are involved in various conditions. Seemingly the traditional justification of the intra cellular accumulation of lactic and hydrogen ions, which cause to dysfunction of contractile protein in mammals, particularly humans, has little significance. In one hand most of the studies about fatigue has been done on isolated animal fiber and in another hand the main issue is putting the dispersed information from different studies together in order to understand the fatigue mechanism in human, particularly athletes. Topics which will be discussed in this study would complete our understanding of the metabolic and hormonal fatigue. _____________________________________________________________________________________________ Sporting activities are accompanied by the changes in metabolite levels in which the magnitude of the changes depends on the type of activity. For example, activities with working load more than the critical power results to
Fatigue during high-intensity exercise : relationship to the critical power concept
2013
The hyperbolic power-duration relationship for high-intensity exercise is defined by two parameters: an asymptote (critical power; CP) reflecting the highest sustainable rate of oxidative metabolism, and a curvature constant (W ), which indicates a fixed amount of work that can be completed above CP (W>CP). According to the CP model of bioenergetics, constant work rate exercise above CP depletes the capacity-limited W with fatigue occurring when W is completely expended. The complete depletion of W has been reported to occur when O2max is attained and a critical degree of muscle metabolic perturbation (decline of finite anaerobic substrates and accumulation of fatigue-related metabolites) is reached. However, while the CP model is effective at predicting metabolic perturbation and the tolerable duration of severe-intensity constant work rate (CWR) exercise, it is unclear if metabolic perturbation and exercise performance can be explained by the CP model when different methods of ...
Cardiac fatigue and oxygen kinetics after prolonged exercise
International Journal of Cardiology, 2006
Background: Although the underlying mechanisms responsible for cardiac dysfunction after prolonged exercise remains to be elucidated, it has reported cardiac deterioration following exhaustive exercise in the absence of underlying cardiovascular diseases, which has been attributed to cardiac fatigue. The study was designed to investigate the effects of after fatiguing exercise on oxygen kinetics. Methods: Six athletes have taken examination, firstly by echocardiography, secondly by cardiopulmonary exercise testing and then by nearinfrared spectroscopy (NIRS), before 2 days (pre-race) and after 1 day (post-race) marathon competition. Results: We found decrease in left ventricular systolic and diastolic functions, and peak oxygen consumption while increasing half time of muscular oxygen delivery after race period. Conclusion: Cardiopulmonary exercise testing in conjunction with oxygen kinetics of skeletal muscle measured by NIRS may be a tool for detecting cardiac fatigue. D
Physiological Basis of Exercise
2011
VO , the Best Measure of Cardiovascular Capacity 4. Respiratory Regulation During Exercise 4.1. Increased Alveolar-Capillary P O 2 Gradient, Blood Flow, and CO 2 Removal 4.2. Changes in Respiratory Quotient (RQ) During Exercise 4.3. Control of Ventilation During Exercise 4.4. Exercise Capacity Limiting Factor 5. Fatigue 6. Conclusion Acknowledgement Glossary Bibliography Biographical Sketches His special interests in research are biotransformation and adaptation to chemical loading, biomonitoring of toxicants, comparative biochemical toxicology; muscle metabolism and function; and ergonomics. He has contributed 266 papers to refereed journals, 72 to proceedings, written 55 reviews, and 30 books and book chapters. He serves on the editorial board of four international journals and is at present the European Journal Editor of Pathophysiology. Of his postgraduate students (32 in Biotransformation, 27 in Muscle Metabolism and Physiology, and five others) 12 serve as professors in China, Finland, Greece, Sweden, and the United States.
Locomotor Muscle Fatigue Does Not Alter Oxygen Uptake Kinetics during High-Intensity Exercise
Frontiers in Physiology, 2016
The V O 2 slow component (V O 2 sc) that develops during high-intensity aerobic exercise is thought to be strongly associated with locomotor muscle fatigue. We sought to experimentally test this hypothesis by pre-fatiguing the locomotor muscles used during subsequent high-intensity cycling exercise. Over two separate visits, eight healthy male participants were asked to either perform a non-metabolically stressful 100 intermittent drop-jumps protocol (pre-fatigue condition) or rest for 33 min (control condition) according to a random and counterbalanced order. Locomotor muscle fatigue was quantified with 6-s maximal sprints at a fixed pedaling cadence of 90 rev•min −1. Oxygen kinetics and other responses (heart rate, capillary blood lactate concentration and rating of perceived exertion, RPE) were measured during two subsequent bouts of 6 min cycling exercise at 50% of the delta between the lactate threshold and V O 2 max determined during a preliminary incremental exercise test. All tests were performed on the same cycle ergometer. Despite significant locomotor muscle fatigue (P = 0.03), the V O 2 sc was not significantly different between the pre-fatigue (464 ± 301 mL•min −1) and the control (556 1 ± 223 mL•min −) condition (P = 0.50). Blood lactate response was not significantly different between conditions (P = 0.48) but RPE was significantly higher following the pre-fatiguing exercise protocol compared with the control condition (P < 0.01) suggesting higher muscle recruitment. These results demonstrate experimentally that locomotor muscle fatigue does not significantly alter the V O 2 kinetic response to high intensity aerobic exercise, and challenge the hypothesis that the V O 2 sc is strongly associated with locomotor muscle fatigue.
Physiological responses during exercise to exhaustion at critical power
European Journal of Applied Physiology, 2002
Critical power (CP) is a theoretical construct derived from a series of constant load tests to failure. Many studies have examined the methodological limitations of deriving CP, but few studies have examined the responses to exercise at CP in well-trained individuals. The purpose of the present study was to examine the physiological responses to exercise at CP. Seven male subjects [mean (SD) body mass 75.6 (6.4) kg, maximum oxygen uptake 4.6 (0.7) l min-1 ] performed three constant load tests to derive CP. Subjects then exercised at CP until volitional exhaustion. Heart rate, oxygen consumption and blood lactate concentration were measured throughout. Repeated measures analysis of variance revealed significant differences over time in heart rate 118 (24) to 177(5) beats min-1 , oxygen consumption 3.7 (0.6) to 4.1 (0.5) l min-1 and blood lactate concentration 4.3 (1.8) to 6.5 (2.0) mM. All seven subjects completed 20 min of exercise with the range of time to failure at CP from 20 min 1 s to 40 min 37 s. Time to failure and maximum oxygen consumption were significantly correlated (r=0.779, P<0.05). We conclude, therefore, that CP does not represent a sustainable steady-state intensity of exercise.