Showing papers on "Exercise physiology published in 2003"
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01 Jan 2003
TL;DR: Our biological heritage includes the cell and its regulatory mechanisms, the muscle and its contraction, motor function, body fluids, blood, and circulation, respiratory system, and skeletal system.
Abstract: Our biological heritage -- The cell and its regulatory mechanisms -- The muscle and its contraction -- Motor function -- Body fluids, blood, and circulation -- Respiration -- Skeletal system -- Physical performance -- Evaluation of physical performance on the basis of tests -- Body dimensions and muscular exercise -- Physical training -- Nutrition and physical performance -- Temperature regulation -- Factors affecting performance -- Fatigue -- Applied sport physiology -- Applied work physiology -- Physical activity and health.
1,123 citations
TL;DR: Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary, and athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1–2 days following intense DOMS-inducing exercise.
Abstract: Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted. A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1–2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.
1,121 citations
TL;DR: It is demonstrated that exercise induces a dramatic transient increase in PGC‐1α transcription and mRNA content in human skeletal muscle, consistent with its role as a transcriptional coactivator, and suggest that PGC•1α may coordinate the activation of metabolic genes in human muscle in response to exercise.
Abstract: Endurance exercise training induces mitochondrial biogenesis in skeletal muscle. The peroxisome proliferator activated receptor co-activator 1α (PGC-1α) has recently been identified as a nuclear factor critical for coordinating the activation of genes required for mitochondrial biogenesis in cell culture and rodent skeletal muscle. To determine whether PGC-1α transcription is regulated by acute exercise and exercise training in human skeletal muscle, seven male subjects performed 4 weeks of one-legged knee extensor exercise training. At the end of training, subjects completed 3 h of two-legged knee extensor exercise. Biopsies were obtained from the vastus lateralis muscle of both the untrained and trained legs before exercise and after 0, 2, 6 and 24 h of recovery. Time to exhaustion (2 min maximum resistance), as well as hexokinase II (HKII), citrate synthase and 3-hydroxyacyl-CoA dehydrogenase mRNA, were higher in the trained than the untrained leg prior to exercise. Exercise induced a marked transient increase (P 40-fold) and mRNA content (7- to 10-fold), peaking within 2 h after exercise. Activation of PGC-1α was greater in the trained leg despite the lower relative workload. Interestingly, exercise did not affect nuclear respiratory factor 1 (NRF-1) mRNA, a gene induced by PGC-1α in cell culture. HKII, mitochondrial transcription factor A, peroxisome proliferator activated receptor α, and calcineurin Aα and Aβ mRNA were elevated (≈2- to 6-fold; P < 0.05) at 6 h of recovery in the untrained leg but did not change in the trained leg. The present data demonstrate that exercise induces a dramatic transient increase in PGC-1α transcription and mRNA content in human skeletal muscle. Consistent with its role as a transcriptional coactivator, these findings suggest that PGC-1α may coordinate the activation of metabolic genes in human muscle in response to exercise.
895 citations
TL;DR: The muscle mitochondrial response to 4 months of aerobic exercise training was similar in all age-groups, although the older people did not have an improvement in insulin sensitivity, and insulin sensitivity improved in younger people but not in middle-aged or older groups.
Abstract: Insulin resistance increases and muscle oxidative capacity decreases during aging, but lifestyle changes-especially physical activity-may reverse these trends. Here we report the effect of a 16-week aerobic exercise program (n = 65) or control activity (n = 37) performed by men and women aged 21-87 years on insulin sensitivity and muscle mitochondria. Insulin sensitivity, measured by intravenous glucose tolerance test, decreased with age (r = -0.32) and was related to abdominal fat content (r = -0.65). Exercise increased peak oxygen uptake (VO(2peak); 10%), activity of muscle mitochondrial enzymes (citrate synthase and cytochrome c oxidase, 45-76%) and mRNA levels of mitochondrial genes (COX4, ND4, both 66%) and genes involved in mitochondrial biogenesis (PGC-1alpha, 55%; NRF-1, 15%; TFAM, 85%). Exercise also increased muscle GLUT4 mRNA and protein (30-52%) and reduced abdominal fat (5%) and plasma triglycerides (25%). None of these changes were affected by age. In contrast, insulin sensitivity improved in younger people but not in middle-aged or older groups. Thus, the muscle mitochondrial response to 4 months of aerobic exercise training was similar in all age-groups, although the older people did not have an improvement in insulin sensitivity.
635 citations
TL;DR: It is suggested that moderate-intensity aerobic exercise augments endothelium-dependent vasodilation in humans through the increased production of nitric oxide and that high-intensity exercise possibly increases oxidative stress.
Abstract: Background— Aerobic exercise enhances endothelium-dependent vasodilation in hypertensive patients, patients with chronic heart failure, and healthy individuals. However, it is unclear how the intensity of exercise affects endothelial function in humans. The purpose of the present study was to determine the effects of different intensities of exercise on endothelium-dependent vasodilation in humans. Methods and Results— We evaluated the forearm blood flow responses to acetylcholine, an endothelium-dependent vasodilator, and isosorbide dinitrate, an endothelium-independent vasodilator, before and after different intensities of exercise (mild, 25% Vo2max; moderate, 50% Vo2max; and high, 75% Vo2max; bicycle ergometers, 30 minutes, 5 to 7 times per week for 12 weeks) in 26 healthy young men. Forearm blood flow was measured using a mercury-filled Silastic strain-gauge plethysmograph. Twelve weeks of moderate-intensity exercise, but not mild- or high-intensity exercise, significantly augmented acetylcholine-i...
592 citations
TL;DR: Regular exercise has a statistically and clinically significant effect on VO2max in Type 2 diabetic individuals and higher intensity exercise could have additional benefits on cardiorespiratory fitness and HbA1c.
Abstract: Low cardiorespiratory fitness is a powerful and independent predictor of mortality in people with diabetes. Several studies have examined the effects of exercise on cardiorespiratory fitness in Type 2 diabetic individuals. However, these studies had relatively small sample sizes and highly variable results. Therefore the aim of this study was to systematically review and quantify the effects of exercise on cardiorespiratory fitness in Type 2 diabetic individuals. MEDLINE, EMBASE, and four other databases were searched up to March 2002 for randomized, controlled trials evaluating effects of structured aerobic exercise interventions of 8 weeks or more on cardiorespiratory fitness in adults with Type 2 diabetes. Cardiorespiratory fitness was defined as maximal oxygen uptake (VO2max) during a maximal exercise test. Seven studies, presenting data for nine randomized trials comparing exercise and control groups (overall n=266), met the inclusion criteria. Mean exercise characteristics were as follows: 3.4 sessions per week, 49 min per session for 20 weeks. Exercise intensity ranged from 50% to 75% of VO2max. There was an 11.8% increase in VO2max in the exercise group and a 1.0% decrease in the control group (post intervention standardized mean difference =0.53, p<0.003). Studies with higher exercise intensities tended to produce larger improvements in VO2max. Exercise intensity predicted post-intervention weighted mean difference in HbA1c (r=−0.91, p=0.002) to a larger extent than did exercise volume (r=−0.46, p=0.26). Regular exercise has a statistically and clinically significant effect on VO2max in Type 2 diabetic individuals. Higher intensity exercise could have additional benefits on cardiorespiratory fitness and HbA1c.
531 citations
TL;DR: Long-term endurance training significantly influences how the autonomic nervous system controls heart function, and increases parasympathetic activity and decreases sympathetic activity in the human heart at rest.
Abstract: Long-term endurance training significantly influences how the autonomic nervous system controls heart function. Endurance training increases parasympathetic activity and decreases sympathetic activity in the human heart at rest. These two training-induced autonomic effects, coupled with a possible reduction in intrinsic heart rate, decrease resting heart rate. Long-term endurance training also decreases submaximal exercise heart rate by reducing sympathetic activity to the heart. Physiological ageing is associated with a reduction in parasympathetic control of the heart; this decline in parasympathetic activity can be reduced by regular endurance exercise. Some research has indicated that females have increased parasympathetic and decreased sympathetic control of heart rate. These gender-specific autonomic differences probably contribute to a decreased cardiovascular risk and increased longevity observed in females.
479 citations
TL;DR: Whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and the relationship between this peak VO2 (V(O2 peak) and that determined from one, or several, maximal constant-load tests is ascertained and the peak value attained was not different from the plateau in the plot of VO2 vs. work rate.
Abstract: The quantification of maximum oxygen uptake (Vo2 max), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (Vo2) to ...
438 citations
TL;DR: The data in young subjects indicate that the MGF and IGF‐IEa isoforms are differentially regulated in human skeletal muscle, and an attenuated MGF response to high resistance exercise in the older subjects is indicative of age‐related desensitivity to mechanical loading.
Abstract: The mRNA expression of two splice variants of the insulin-like growth factor-I (IGF-I) gene, IGF-IEa and mechano growth factor (MGF), were studied in human skeletal muscle. Subjects (eight young, aged 25–36 years, and seven elderly, aged 70–82 years) completed 10 sets of six repetitions of single legged knee extensor exercise at 80 % of their one repetition maximum. Muscle biopsy samples were obtained from the quadriceps muscle of both the control and exercised legs 2.5 h after completion of the exercise bout. Expression levels of the IGF-I mRNA transcripts were determined using real-time quantitative RT-PCR with specific primers. The resting levels of MGF were significantly (≈100-fold) lower than those of the IGF-IEa isoform. No difference was observed between the resting levels of the two isoforms between the two subject groups. High resistance exercise resulted in a significant increase in MGF mRNA in the young, but not in the elderly subjects. No changes in IGF-IEa mRNA levels were observed as a result of exercise in either group. The mRNA levels of the transcription factor MyoD were greater at rest in the older subjects (P < 0.05), but there was no significant effect of the exercise bout. Electrophoretic separation of myosin heavy chain (MHC) isoforms showed the older subjects to have a lower (P < 0.05) percentage of MHC-II isoforms than the young subjects. However, no association was observed between the composition of the muscle and changes in the IGF-I isoforms with exercise. The data from this study show an attenuated MGF response to high resistance exercise in the older subjects, indicative of age-related desensitivity to mechanical loading. The data in young subjects indicate that the MGF and IGF-IEa isoforms are differentially regulated in human skeletal muscle.
428 citations
TL;DR: The constant muscle oxygenation during the initial phase of the on-transition indicates a tight coupling between increases in O2 delivery and O2 utilization and adequacy of O2 availability in relation to needs.
Abstract: Near-infrared spectroscopy (NIRS) was utilized to gain insights into the kinetics of oxidative metabolism during exercise transitions. Ten untrained young men were tested on a cycle ergometer durin...
423 citations
TL;DR: It is suggested that acute bouts of cardiovascular exercise affect neuroelectric processes underlying executive control through the increased allocation of neuroelectric resources and through changes in cognitive processing and stimulus classification speed.
01 Aug 2003
TL;DR: It is suggested that exercise produces energetic benefits in other components of the daily energy budget, thus generating a net effect on energy balance much greater than the direct energy cost of the exercise alone.
Abstract: The direct effects of physical activity interventions on energy expenditure are relatively small when placed in the context of total daily energy demands. Hence, the suggestion has been made that exercise produces energetic benefits in other components of the daily energy budget, thus generating a net effect on energy balance much greater than the direct energy cost of the exercise alone. Resting metabolic rate (RMR) is the largest component of the daily energy budget in most human societies and, therefore, any increases in RMR in response to exercise interventions are potentially of great importance. Animal studies have generally shown that single exercise events and longer-term training produce increases in RMR. This effect is observed in longer-term interventions despite parallel decreases in body mass and fat mass. Flight is an exception, as both single flights and long-term flight training induce reductions in RMR. Studies in animals that measure the effect of voluntary exercise regimens on RMR are less commonly performed and do not show the same response as that to forced exercise. In particular, they indicate that exercise does not induce elevations in RMR. Many studies of human subjects indicate a short-term elevation in RMR in response to single exercise events (generally termed the excess post-exercise O2 consumption; EPOC). This EPOC appears to have two phases, one lasting < 2 h and a smaller much more prolonged effect lasting up to 48 h. Many studies have shown that long-term training increases RMR, but many other studies have failed to find such effects. Data concerning long-term effects of training are potentially confounded by some studies not leaving sufficient time after the last exercise bout for the termination of the long-term EPOC. Long-term effects of training include increases in RMR due to increases in lean muscle mass. Extreme interventions, however, may induce reductions in RMR, in spite of the increased lean tissue mass, similar to the changes observed in animals in response to flight.
TL;DR: It appears that trained individuals have a more rapid return of post-exercise metabolism to resting levels after exercising at either the same relative or absolute work rate; however, studies after more strenuous exercise bouts are needed.
Abstract: In the recovery period after exercise there is an increase in oxygen uptake termed the ‘excess post-exercise oxygen consumption’ (EPOC), consisting of a rapid and a prolonged component. While some studies have shown that EPOC may last for several hours after exercise, others have concluded that EPOC is transient and minimal. The conflicting results may be resolved if differences in exercise intensity and duration are considered, since this may affect the metabolic processes underlying EPOC. Accordingly, the absence of a sustained EPOC after exercise seems to be a consistent finding in studies with low exercise intensity and/or duration. The magnitude of EPOC after aerobic exercise clearly depends on both the duration and intensity of exercise. A curvilinear relationship between the magnitude of EPOC and the intensity of the exercise bout has been found, whereas the relationship between exercise duration and EPOC magnitude appears to be more linear, especially at higher intensities. Differences in exercise mode may potentially contribute to the discrepant findings of EPOC magnitude and duration. Studies with sufficient exercise challenges are needed to determine whether various aerobic exercise modes affect EPOC differently. The relationships between the intensity and duration of resistance exercise and the magnitude and duration of EPOC have not been determined, but a more prolonged and substantial EPOC has been found after hardversus moderate-resistance exercise. Thus, the intensity of resistance exercise seems to be of importance for EPOC. Lastly, training status and sex may also potentially influence EPOC magnitude, but this may be problematic to determine. Still, it appears that trained individuals have a more rapid return of post-exercise metabolism to resting levels after exercising at either the same relative or absolute work rate; however, studies after more strenuous exercise bouts are needed. It is not determined if there is a sex effect on EPOC. Finally, while some of the mechanisms underlying the more rapid EPOC are well known (replenishment of oxygen stores, adenosine triphosphate/creatine phosphate resynthesis, lactate removal, and increased body temperature, circulation and ventilation), less is known about the mechanisms underlying the prolonged EPOC component. A sustained increased circulation, ventilation and body temperature may contribute, but the cost of this is low. An increased rate of triglyceride/fatty acid cycling and a shift from carbohydrate to fat as substrate source are of importance for the prolonged EPOC component after exhaustive aerobic exercise. Little is known about the mechanisms underlying EPOC after resistance exercise.
TL;DR: Suggestions have been made that carbohydrate availability is the main limiting factor for glycogen synthesis when large quantities of glucose are ingested following exercise.
Abstract: The pattern of muscle glycogen synthesis following glycogen-depleting exercise occurs in two phases. Initially, there is a period of rapid synthesis of muscle glycogen that does not require the presence of insulin and lasts about 30–60 minutes. This rapid phase of muscle glycogen synthesis is characterised by an exercise-induced translocation of glucose transporter carrier protein-4 to the cell surface, leading to an increased permeability of the muscle membrane to glucose. Following this rapid phase of glycogen synthesis, muscle glycogen synthesis occurs at a much slower rate and this phase can last for several hours. Both muscle contraction and insulin have been shown to increase the activity of glycogen synthase, the rate-limiting enzyme in glycogen synthesis. Furthermore, it has been shown that muscle glycogen concentration is a potent regulator of glycogen synthase. Low muscle glycogen concentrations following exercise are associated with an increased rate of glucose transport and an increased capacity to convert glucose into glycogen. The highest muscle glycogen synthesis rates have been reported when large amounts of carbohydrate (1.0–1.85 g/kg/h) are consumed immediately post-exercise and at 15.60 minute intervals thereafter, for up to 5 hours post-exercise. When carbohydrate ingestion is delayed by several hours, this may lead to ∼50% lower rates of muscle glycogen synthesis. The addition of certain amino acids and/ or proteins to a carbohydrate supplement can increase muscle glycogen synthesis rates, most probably because of an enhanced insulin response. However, when carbohydrate intake is high (≥1.2 g/kg/h) and provided at regular intervals, a further increase in insulin concentrations by additional supplementation of protein and/or amino acids does not further increase the rate of muscle glycogen synthesis. Thus, when carbohydrate intake is insufficient ( 1 g/min) of glucose are ingested following exercise.
TL;DR: Current evidence supports a 10% per decade decline in V̇O2max in men and women regardless of activity level, and aging most likely plays a role as studies have demonstrated that training maintenance becomes more difficult with advancing age.
Abstract: Because of the influence of cardiorespiratory fitness on functional independence, quality of life, and cardiovascular disease and all-cause mortality, tremendous interest has been directed towards describing the age-related change in maximal oxygen consumption (VO(2max)). Current evidence supports a 10% per decade decline in VO(2max) in men and women regardless of activity level. High-intensity exercise may reduce this loss by up to 50% in young and middle-aged men, but not older men, if maintained long term. Middle-aged and older women do not appear to be able to reduce loss rates in VO(2max) to less than 10% per decade, which may be related to estrogen status. However, maintaining high-intensity training seems limited to approximately one decade at best and to a select few individuals. While the factors limiting the ability to maintain high-intensity training are not completely known, aging most likely plays a role as studies have demonstrated that training maintenance becomes more difficult with advancing age. Age-related loss of VO(2max) seems to occur in a non-linear fashion in association with declines in physical activity. In sedentary individuals, this non-linear decline generally occurs during the twenties and thirties whereas athletic individuals demonstrate a non-linear decline upon decreasing or ceasing training. Non-linear loss rates are also demonstrated in individuals over the age of 70 years. The decline in VO(2max) seems to be due to both central and peripheral adaptations, primarily reductions in maximal heart rate (HR(max)) and lean body mass (LBM). Exercise training does not influence declines in HR(max), while LBM can be maintained to some degree by exercise. Recommendations for exercise training should include aerobic activities utilising guidelines established by the American College of Sports Medicine for improving CV fitness and health, as well as strength training activities for enhancing LBM.
TL;DR: It is demonstrated that lower extremity resistance exercise can improve muscle structure and function in those with limited exercise tolerance and because low energy cost is coupled to high force production with eccentric exercise, this intervention may be useful for patients that are otherwise unable to achieve high muscle forces with traditional resistance exercise.
Abstract: Background. The objective of this study was to determine if a chronic eccentric training intervention, i.e., negative work, could limit or even reverse sarcopenia and its related impairments and functional limitations. Is high-force eccentric training tolerable by elderly people and will it result in improved muscle size, strength, balance, and fall risk? Methods. 21 frail elderly subjects (mean age, 80 years) experienced 11 weeks of lower extremity resistance training. The experimental eccentric (ECC) group (n ¼ 11) performed negative work while exercising on a high-force eccentric ergometer. The active ‘‘controls’’ performed traditional (TRAD) (n ¼ 10) lower extremity resistance exercises (weight training). Muscle fiber cross-sectional area and strength, balance, stair descending abilities, and fall risk were assessed prior to and following this intervention. Results. All ECC subjects who started the negative work intervention completed the study and reported the training to be relatively effortless; they experienced minimal and transient muscle soreness. Both groups experienced a significant increase in muscle fiber cross-sectional area (ECC ¼ 60%, TRAD ¼ 41%). Only the ECC group experienced significant improvements in strength (60%), balance (7%), and stair descent (21%) abilities. The timed up and go task improved in both groups, but only the ECC group went from a high to a low fall risk. Conclusions. These data demonstrate that lower extremity resistance exercise can improve muscle structure and function in those with limited exercise tolerance. The greater strength increase following negative work training resulted in improved balance, stair descent, and fall risk only in the ECC group. Because low energy cost is coupled to high force production with eccentric exercise, this intervention may be useful for a number of patients that are otherwise unable to achieve high muscle forces with traditional resistance exercise.
TL;DR: It is followed that in exercise unto comparable degrees of exhaustion and muscular fatigue, superimposed 26’Hz vibration appears to elicit an alteration in neuromuscular recruitment patterns, which apparently enhance neuromUScular excitability.
Abstract: Summary The effects of hard squatting exercise with (VbX+) and without (VbX)) vibration on neuromuscular function were tested in 19 healthy young volunteers. Before and after the exercise, three different tests were performed: maximum serial jumping for 30 s, electromyography during isometric knee extension at 70% of the maximum voluntary torque, and the quantitative analysis of the patellar tendon reflex. Between VbX+ and VbX) values, there was no difference found under baseline conditions. Time to exhaustion was significantly shorter in VbX+ than in VbX) (349 ± 338 s versus 515 ± 338 s), but blood lactate (5AE49 ± 2AE73 mmol l )1 versus 5AE00 ± 2AE26 mmol l )1 ) and subjectively perceived exertion (rate of perceived exertion values 18AE 1±1 AE2 versus 18AE 6±1 AE6) at the termination of exercise indicate comparable levels of fatigue. After the exercise, comparable effects were observed on jump height, ground contact time, and isometric torque. The vastus lateralis mean frequency during isometric torque, however, was higher after VbX+ than after VbX). Likewise, the tendon reflex amplitude was significantly greater after VbX+ than after VbX) (4AE34 ± 3AE63 Nm versus 1AE68 ± 1AE32 Nm). It is followed that in exercise unto comparable degrees of exhaustion and muscular fatigue, superimposed 26 Hz vibration appears to elicit an alteration in neuromuscular recruitment patterns, which apparently enhance neuromuscular excitability. Possibly, this effect may be exploited for the design of future training regimes.
TL;DR: The occurrence of contractile fatigue during exercise may explain why bronchodilation fails to improve exercise tolerance in some COPD patients.
Abstract: We evaluated whether contractile fatigue of the quadriceps occurs after cycling exercise in patients with chronic obstructive pulmonary disease (COPD) and whether it could contribute to exercise limitation. Eighteen COPD patients performed two constant work-rate cycling exercises up to exhaustion. These tests were preceded by nebulization of placebo or 500 microg of ipratropium bromide. Muscle fatigue was defined as a postexercise reduction in quadriceps twitch force of more than 15% of the resting value. There was an increase in endurance time postipratropium compared with placebo nebulization (440 +/- 244 seconds vs. 322 +/- 188 seconds, p = 0.06). Nine patients developed contractile fatigue after placebo exercise. In these patients, ipratropium did not increase the endurance time (394 +/- 220 seconds with placebo vs. 400 +/- 119 seconds with ipratropium) despite an 11% improvement in FEV1. In the nine patients who did not fatigue after placebo exercise, endurance time increased from 249 +/- 124 seconds with placebo to 479 +/- 298 seconds with ipratropium (p < 0.05). There was a significant correlation between the improvement in endurance time with ipratropium and quadriceps twitch force at 10 minutes after placebo exercise (r = 0.59, p = 0.01). The occurrence of contractile fatigue during exercise may explain why bronchodilation fails to improve exercise tolerance in some COPD patients.
TL;DR: The ability to maintain habitual physical activity levels with advancing age appears to be a critical determinant of changes in PFC in part via modulation of maximal aerobic capacity.
Abstract: Physiological functional capacity (PFC) is defined here as the ability to perform the physical tasks of daily life and the ease with which these tasks can be performed. For the past decade, we have sought to determine the effect of primary (healthy) adult human aging on PFC and the potential modulatory influences of gender and habitual aerobic exercise status on this process by studying young adult and Masters athletes. An initial approach to determining the effects of aging on PFC involved investigating changes in peak exercise performance with age in highly trained and competitive athletes. PFC, as assessed by running and swimming performance, decreased only modestly until age 60-70 yr but declined exponentially thereafter. A progressive reduction in maximal O2 consumption (Vo2 max) appears to be the primary physiological mechanism associated with declines in endurance running performance with advancing age, along with a reduction in the exercise velocity at lactate threshold. Because Vo2 max is impor...
TL;DR: An alternative model explaining the limitation of exercise endurance thus proposes that the central nervous system integrates input from various sources all related to the exercise and limits the intensity and duration of recruitment of limb skeletal muscle to prevent jeopardizing the integrity of the organism.
Abstract: Classically the limit to endurance of exercise is explained in terms of metabolic capacity. Cardio-respiratory capacity and muscle fatigue are thought to set the limit and the majority of studies on factors limiting endurance exercise discuss issues such as maximal oxygen uptake (VO2max), aerobic enzyme capacity, cardiac output, glycogen stores, etc. However, this paradigm does not explain the limitation to endurance exercise with large muscle groups at altitude, when at exhaustion exercise is ended without limb locomotor muscle fatigue and with sub-maximal cardiac output. A simple fact provides a basis for an explanation. Voluntary exercise starts and ends in the brain. It starts with spatial and temporal recruitment of motor units and ends with their de-recruitment. A conscious decision precedes a voluntary effort. The end of effort is again volitional and a forced conscious decision to stop precedes it, but it is unknown what forces the off-switch of recruitment at exhaustion although sensation of exertion certainly plays a role. An alternative model explaining the limitation of exercise endurance thus proposes that the central nervous system integrates input from various sources all related to the exercise and limits the intensity and duration of recruitment of limb skeletal muscle to prevent jeopardizing the integrity of the organism. This model acknowledges the cardio-respiratory and muscle metabolic capacities as prime actors on the performance scene, while crediting the central nervous system for its pivotal role as the ultimate site where exercise starts and ends.
TL;DR: These findings suggest that regularly menstruating female athletes, competing in strength-specific sports and intense anaerobic/aerobic sports, do not need to adjust for menstrual cycle phase to maximise performance.
Abstract: This article reviews the potential effects of the female steroid hormone fluctuations during the menstrual cycle on exercise performance. The measurement of estrogen and progesterone concentration to verify menstrual cycle phase is a major consideration in this review. However, even when hormone concentrations are measured, the combination of differences in timing of testing, the high inter- and intra-individual variability in estrogen and progesterone concentration, the pulsatile nature of their secretion and their interaction, may easily obscure possible effects of the menstrual cycle on exercise performance. When focusing on studies using hormone verification and electrical stimulation to ensure maximal neural activation, the current literature suggests that fluctuations in female reproductive hormones throughout the menstrual cycle do not affect muscle contractile characteristics. Most research also reports no changes over the menstrual cycle for the many determinants of maximal oxygen consumption (VO2max), such as lactate response to exercise, bodyweight, plasma volume, haemoglobin concentration, heart rate and ventilation. Therefore, it is not surprising that the current literature indicates that VO2max is not affected by the menstrual cycle. These findings suggest that regularly menstruating female athletes, competing in strength-specific sports and intense anaerobic/aerobic sports, do not need to adjust for menstrual cycle phase to maximise performance. For prolonged exercise performance, however, the menstrual cycle may have an effect. Even though most research suggests that oxygen consumption, heart rate and rating of perceived exertion responses to sub-maximal steady-state exercise are not affected by the menstrual cycle, several studies report a higher cardiovascular strain during moderate exercise in the mid-luteal phase. Nevertheless, time to exhaustion at sub-maximal exercise intensities shows no change over the menstrual cycle. The significance of this finding should be questioned due to the low reproducibility of the time to exhaustion test. During prolonged exercise in hot conditions, a decrease in exercise time to exhaustion is shown during the mid-luteal phase, when body temperature is elevated. Thus, the mid-luteal phase has a potential negative effect on prolonged exercise performance through elevated body temperature and potentially increased cardiovascular strain. Practical implications for female endurance athletes may be the adjustment of competition schedules to their menstrual cycle, especially in hot, humid conditions. The small scope of the current research and its methodological limitations warrant further investigation of the effect of the menstrual cycle on prolonged exercise performance.
TL;DR: This study compared the effects of CS on effect size (ES) for body composition (BC) variables (mass and lean body mass), duration and intensity of the exercise task, type of exercise task (single, repetitive, laboratory, field, upper-body, lower-body), CS duration (loading, maintenance), and subject characteristics (gender, training status).
Abstract: Background: Creatine supplementation (CS) has been reported to increase body mass and improve performance in high-intensity, short-duration exercise tasks. Research on CS, most of which has come into existence since 1994, has been the focus of several qualitative reviews, but only one meta-analysis, which was conducted with a limited number of studies. Purpose: This study compared the effects of CS on effect size (ES) for body composition (BC) variables (mass and lean body mass), duration and intensity (≤30 s, [ATP-PCr = A]; 30‐150 s [glycolysis = G]; >150 s, [oxidative phosphorylation = O]) of the exercise task, type of exercise task (single, repetitive, laboratory, field, upper-body, lowerbody), CS duration (loading, maintenance), and subject characteristics (gender, training status). Methods: A search of MEDLINE and SPORTDiscus using the phrase “creatine supplementation” revealed 96 English-language, peer-reviewed papers (100 studies), which included randomized group formation, a placebo control, and human subjects who were blinded to treatments. ES was calculated for each body composition and performance variable. Results: Small, but significant (ES > 0, p ≤ .05) ES were reported for BC (n = 163, mean ± SE = 0.17 ± 0.03), ATP-PCr (n = 17, 0.24 ± 0.02), G (n = 135, 0.19 ± 0.05), and O (n = 69, 0.20 ± 0.07). ES was greater for change in BC following a loading-only CS regimen (0.26 ± 0.03, p = .0003) compared to a maintenance regimen (0.04 ± 0.05), for repetitive-bout (0.25 ± 0.03, p = .028) compared to single-bout (0.18 ± 0.02) exercise, and for upper-body exercise (0.42 ± 0.07, p < .0001) compared to lower (0.21 ± 0.02) and total body (0.13 ± 0.04) exercise. ES for laboratorybased tasks (e.g., isometric/isotonic/isokinetic exercise, 0.25 ± 0.02) were greater (p = .014) than those observed for field-based tasks (e.g., running, swimming, 0.14 ± 0.04). There were no differences in BC or performance ES between males and females or between trained and untrained subjects. Conclusion: ES was greater for changes in lean body mass following short-term CS, repetitivebout laboratory-based exercise tasks ≤ 30 s (e.g., isometric, isokinetic, and isotonic resistance exercise), and upper-body exercise. CS does not appear to be effective in improving running and swimming performance. There is no evidence in the literature of an effect of gender or training status on ES following CS.
TL;DR: Aerobic training in sedentary subjects results in altered autonomic regulation of HR toward vagal dominance and a moderate training volume is a sufficient intervention to induce these beneficial effects.
Abstract: This study was designed to assess the effects of moderate- and high-volume aerobic training on the time domain and on spectral and fractal heart rate (HR) variability indexes. Sedentary subjects we...
TL;DR: It is concluded that there is a progressive reduction in muscle strength that applies across a range of functional characteristics during exercise that mimics the work rate in soccer.
Abstract: Fatigue represents a reduction in the capability of muscle to generate force. The aim of the present study was to establish the effects of exercise that simulates the work rate of competitive soccer players on the strength of the knee extensors and knee flexors. Thirteen amateur soccer players (age 23.3±3.9 years, height 1.78±0.05 m, body mass 74.8±3.6 kg; mean±s) were tested during the 2000–2001 soccer season. Muscle strength of the quadriceps and hamstrings was measured on an isokinetic dynamometer. A 90 min soccer-specific intermittent exercise protocol, incorporating a 15 min half-time intermission, was developed to provide fatiguing exercise corresponding in work rate to a game of soccer. The exercise protocol, performed on a programmable motorized treadmill, consisted of the different intensities observed during soccer match-play (e.g. walking, jogging, running, sprinting). Muscle strength was assessed before exercise, at half-time and immediately after exercise. A repeated-measures analysis of vari...
TL;DR: It is concluded that IMTG stores form an important substrate source during moderate intensity exercise in endurance‐trained male athletes following an overnight fast, with the oxidation rate of muscle‐ plus lipoprotein‐derived TG being decreased with the duration of exercise.
Abstract: Both stable isotope methodology and fluorescence microscopy were applied to define the use of intramuscular triglyceride (IMTG) stores as a substrate source during exercise on a whole-body as well as on a fibre type-specific intramyocellular level in trained male cyclists. Following an overnight fast, eight subjects were studied at rest, during 120 min of moderate intensity exercise (60 % maximal oxygen uptake capacity (VO2,max)) and 120 min of post-exercise recovery. Continuous infusions of [U-13C]palmitate and [6,6-2H2]glucose were administered at rest and during subsequent exercise to quantify whole-body plasma free fatty acid (FFA) and glucose oxidation rates and the contribution of other fat sources (sum of muscle- plus lipoprotein-derived TG) and muscle glycogen to total energy expenditure. Fibre type-specific intramyocellular lipid content was determined in muscle biopsy samples collected before, immediately after and 2 h after exercise. At rest, fat oxidation provided 66 +/- 5 % of total energy expenditure, with FFA and other fat sources contributing 48 +/- 6 and 17 +/- 3 %, respectively. FFA oxidation rates increased during exercise, and correlated well with the change in plasma FFA concentrations. Both the use of other fat sources and muscle glycogen declined with the duration of exercise, whereas plasma glucose production and utilisation increased (P < 0.001). On average, FFA, other fat sources, plasma glucose and muscle glycogen contributed 28 +/- 3, 15 +/- 2, 12 +/- 1 and 45 +/- 4 % to total energy expenditure during exercise, respectively. Fluorescence microscopy revealed a 62 +/- 7 % net decline in muscle lipid content following exercise in the type I fibres only, with no subsequent change during recovery. We conclude that IMTG stores form an important substrate source during moderate intensity exercise in endurance-trained male athletes following an overnight fast, with the oxidation rate of muscle- plus lipoprotein-derived TG being decreased with the duration of exercise.
TL;DR: The data support the hypothesis that the role of IL-6 released from contracting muscle during exercise is to act in a hormone-like manner to mobilize extracellular substrates and/or augment substrate delivery during exercise.
Abstract: Interleukin-6 (IL-6) is produced locally in working skeletal muscle and can account for the exercise-induced increase in plasma IL-6. The transcription rate for IL-6 in muscle nuclei isolated from muscle biopsies during exercise is very high and is enhanced further when muscle glycogen content is low. Furthermore, cultured human primary muscle cells can increase IL-6 mRNA when incubated with the calcium ionophore ionomycin and it is likely that myocytes produce IL-6 in response to muscle contraction. The biological roles of muscle-derived IL-6 have been investigated in studies in which human recombinant IL-6 was infused in healthy volunteers to mimic closely the IL-6 concentrations observed during prolonged exercise. Using stable isotopes, we have demonstrated that physiological concentrations of IL-6 induce lipolysis. Although we have yet to determine the precise biological action of muscle-derived IL-6, our data support the hypothesis that the role of IL-6 released from contracting muscle during exercise is to act in a hormone-like manner to mobilize extracellular substrates and/or augment substrate delivery during exercise. In addition, IL-6 inhibits low-level TNF-α production, and IL-6 produced during exercise probably inhibits TNF-α-induced insulin resistance in peripheral tissues. Hence, IL-6 produced by skeletal muscle during contraction may play an important role in the beneficial health effects of exercise
TL;DR: It is demonstrated that muscle fibre type is significantly related to both the speed and the amplitudes of the V̇O2 response at the onset of constant-load sub-maximal exercise.
Abstract: The purpose of the present study was to test the hypothesis that muscle fibre type influences the oxygen uptake (.VO(2)) on-kinetic response (primary time constant; primary and slow component amplitudes) during moderate, heavy and severe intensity sub-maximal cycle exercise. Fourteen subjects [10 males, mean (SD) age 25 (4) years; mass 72.6 (3.9) kg; .VO(2peak) 47.9 (2.3) ml kg(-1) min(-1)] volunteered to participate in this study. The subjects underwent a muscle biopsy of the vastus lateralis for histochemical determination of muscle fibre type, and completed repeat "square-wave" transitions from unloaded cycling to power outputs corresponding to 80% of the ventilatory threshold (VT; moderate exercise), 50% (heavy exercise) and 70% (severe exercise) of the difference between the VT and .VO(2peak). Pulmonary .VO(2) was measured breath-by-breath. The percentage of type I fibres was significantly correlated with the time constant of the primary .VO(2) response for heavy exercise (r=-0.68). Furthermore, the percentage of type I muscle fibres was significantly correlated with the gain of the .VO(2) primary component for moderate (r=0.65), heavy (r=0.57) and severe (r=0.57) exercise, and with the relative amplitude of the .VO(2) slow component for heavy (r=-0.74) and severe (r=-0.64) exercise. The influence of muscle fibre type on the .VO(2) on-kinetic response persisted when differences in aerobic fitness and muscle capillarity were accounted for. This study demonstrates that muscle fibre type is significantly related to both the speed and the amplitudes of the .VO(2) response at the onset of constant-load sub-maximal exercise. Differences in contraction efficiency and oxidative enzyme activity between type I and type II muscle fibres may be responsible for the differences observed.
TL;DR: It is demonstrated that glucose ingestion during exercise attenuates leg IL‐6 release but does not decrease intramuscular expression of IL‐ 6 mRNA.
Abstract: To examine whether glucose ingestion during exercise affects the release of interleukin-6 (IL-6) from the contracting limb, seven men performed 120 min of semi-recumbent cycling on two occasions while ingesting either 250 ml of a 6.4 % carbohydrate (GLU trial) or sweet placebo (CON trial) beverage at the onset of, and at 15 min intervals throughout, exercise. Muscle biopsies obtained before and immediately after exercise were analysed for glycogen and IL-6 mRNA expression. Blood samples were simultaneously obtained from a brachial artery and a femoral vein prior to and during exercise and leg blood flow was measured by thermodilution in the femoral vein. Net leg IL-6 release, and net leg glucose and free fatty acid (FFA) uptake, were calculated from these measurements. The arterial IL-6 concentration was lower (P < 0.05) after 120 min of exercise in GLU, but neither intramuscular glycogen nor IL-6 mRNA were different when comparing GLU with CON. However, net leg IL-6 release was attenuated (P < 0.05) in GLU compared with CON. This corresponded with an enhanced (P < 0.05) glucose uptake and a reduced (P < 0.05) FFA uptake in GLU. These results demonstrate that glucose ingestion during exercise attenuates leg IL-6 release but does not decrease intramuscular expression of IL-6 mRNA.
TL;DR: It is indicated that IL‐6 release from human muscle is positively related to exercise intensity, arterial adrenaline concentration and muscle glucose uptake, and this supports the hypothesis thatIL‐6 may be linked to the regulation of glucose homeostasis during exercise.
Abstract: In this study, the hypothesis that the release of interleukin (IL)-6 from human muscle is linked to exercise intensity and muscle glucose uptake was investigated. In the overnight fasted state, seven healthy males performed knee extension exercise, kicking with both legs, each at 25 % of maximal power (Wmax) for 45 min (eliciting 23 ± 1 % of pulmonary maximal oxygen uptake, VO2,max) and then simultaneously with one leg at 65 % and the other leg at 85 % Wmax for 35 min (40 ± 1 % of pulmonary VO2,max). Blood was sampled from a femoral artery and both femoral veins, and blood flow was determined by thermodilution. Thigh plasma flow (0.15 ± 0.01, 1.4 ± 0.2, 2.0 ± 0.1 and 2.3 ± 0.2 l min−1 thigh−1 at rest and 25 %, 65 % and 85 % Wmax, respectively) and thigh oxygen uptake (0.02 ± 0.01, 0.27 ± 0.03, 0.48 ± 0.04 and 0.55 ± 0.05 l min−1 thigh−1 at rest and 25 %, 65 % and 85 % Wmax, respectively) increased with increasing exercise intensity (P < 0.05). Also, thigh IL-6 release (0.4 ± 0.1, 1.3 ± 0.5, 1.5 ± 0.6 and 2.5 ± 0.7 ng min−1 thigh−1 at rest and 25 %, 65 % and 85 % Wmax, respectively) and thigh glucose uptake (0.05 ± 0.01, 0.3 ± 0.05, 0.75 ± 0.16, 1.07 ± 0.15 mmol min−1 thigh−1 at rest and 25 %, 65 % and 85 % Wmax, respectively) increased with increasing exercise intensity (P < 0.05). During the last 35 min of exercise, arterial catecholamine concentrations were higher (P < 0.05) than at rest and during low-intensity exercise. During exercise, thigh IL-6 release was positively related to both thigh glucose uptake (P < 0.001) and thigh glucose delivery (P < 0.005), but not to thigh glucose extraction. Thigh IL-6 release was also positively related to arterial plasma adrenaline concentration. The pre-exercise muscle glycogen concentration tended to correlate with the arteriovenous IL-6 concentration difference at rest, and the postexercise glycogen concentration was inversely correlated with IL-6 release during the final 35 min of exercise. In conclusion, the study indicates that IL-6 release from human muscle is positively related to exercise intensity, arterial adrenaline concentration and muscle glucose uptake. This supports the hypothesis that IL-6 may be linked to the regulation of glucose homeostasis during exercise. The observation of a relationship between IL-6 release and muscle glycogen store both at rest and after exercise suggests that IL-6 may act as a carbohydrate sensor.
TL;DR: The acute anabolic response of muscle to EAA intake and exercise is additive to the response at rest and thus reflects the 24-h response.
Abstract: The purpose of this study was to determine if the acute anabolic muscle response to resistance exercise and essential amino acids (EAA) reflects the response over 24 h. Seven subjects participated ...