Dynamic responses of O2 uptake at the onset and end of exercise in trained subjects.

Inconsistencies about dynamic asymmetry between the on- and off-transient responses in .VO2 are found in the literature. Therefore the purpose of this study was to examine .VO2on- and off-transients during moderate- and heavy-intensity cycling exercise in trained subjects. Ten men underwent an initial incremental test for the estimation of ventilatory threshold (VT) and, on different days, two bouts of square-wave exercise at moderate (<VT) and heavy (>VT) intensities. .VO2 kinetics in exercise and recovery were better described by a single exponential model (<VT) or by a double exponential with two time delays (>VT). For moderate exercise, we found a symmetry of .VO2 kinetics between the on- and off-transients (i.e., fundamental component), consistent with a system manifesting linear control dynamics. For heavy exercise, a slow component superimposed on the fundamental phase was expressed in both the exercise and recovery, with similar parameter estimates. But the on-transient values of the time constant were appreciably faster than the associated off-transient, and independent of the work rate imposed (<VT and >VT). Our results do not support a dynamically linear system model of .VO2 during cycling exercise in the heavy-intensity domain.

Relation of heart rate to percent VO2 peak during submaximal exercise in the heat.

We tested the hypothesis that elevation in heart rate (HR) during submaximal exercise in the heat is related, in part, to increased percentage of maximal O(2) uptake (%Vo(2 max)) utilized due to reduced maximal O(2) uptake (Vo(2 max)) measured after exercise under the same thermal conditions. Peak O(2) uptake (Vo(2 peak)), O(2) uptake, and HR during submaximal exercise were measured in 22 male and female runners under four environmental conditions designed to manipulate HR during submaximal exercise and Vo(2 peak). The conditions involved walking for 20 min at approximately 33% of control Vo(2 max) in 25, 35, 40, and 45 degrees C followed immediately by measurement of Vo(2 peak) in the same thermal environment. Vo(2 peak) decreased progressively (3.77 +/- 0.19, 3.61 +/- 0.18, 3.44 +/- 0.17, and 3.13 +/- 0.16 l/min) and HR at the end of the submaximal exercise increased progressively (107 +/- 2, 112 +/- 2, 120 +/- 2, and 137 +/- 2 beats/min) with increasing ambient temperature (T(a)). HR and %Vo(2 peak) increased in an identical fashion with increasing T(a). We conclude that elevation in HR during submaximal exercise in the heat is related, in part, to the increase in %Vo(2 peak) utilized, which is caused by reduced Vo(2 peak) measured during exercise in the heat. At high T(a), the dissociation of HR from %Vo(2 peak) measured after sustained submaximal exercise is less than if Vo(2 max) is assumed to be unchanged during exercise in the heat.

Does 'altitude training' increase exercise performance in elite athletes?

The general practice of altitude training is widely accepted as a means to enhance sport performance despite a lack of rigorous scientific studies. For example, the scientific gold-standard design of a double-blind, placebo-controlled, cross-over trial has never been conducted on altitude training. Given that few studies have utilised appropriate controls, there should be more scepticism concerning the effects of altitude training methodologies. In this brief review we aim to point out weaknesses in theories and methodologies of the various altitude training paradigms and to highlight the few well-designed studies to give athletes, coaches and sports medicine professionals the current scientific state of knowledge on common forms of altitude training. Another aim is to encourage investigators to design well-controlled studies that will enhance our understanding of the mechanisms and potential benefits of altitude training.

International exercise on 124Sb activity measurements.

An international exercise, registered as EUROMET project no. 907, was launched to measure both the activity of a solution of (124)Sb and the photon emission intensities of its decay. The same solution was sent by LNE-LNHB to eight participating laboratories. In order to identify possible biases, the participants were asked to use all possible activity measurement methods available in their laboratory and then to determine their reference value for comparison. Thus, measurement results from 4pibeta-gamma coincidence/anti-coincidence counting, CIEMAT/NIST liquid-scintillation counting, 4pigamma counting with well-type ionization chambers and well-type crystal detectors were given. The results are compared and show a maximum discrepancy of about 1.6%: possible explanations are proposed.

Enhanced diastolic reflections on arterial pressure pulse during exercise recovery.

During recovery from a maximal or submaximal aerobic exercise, augmentation of central (aortic) systolic pressure by reflected pressure waves is blunted in healthy humans. However, the extent to which reflected pressure waves modify the central pulse in diastole in these conditions remains unknown. We evaluated systolic and diastolic central reflected waves in 11 endurance-trained athletes on recovery from a maximal running test on a treadmill (treadmill-max) and a 4000 m run in field conditions. On both occasions in each subject, the radial pulse was recorded with applanation tonometry in the resting preexercise state and then 5, 15, 25, 35, and 45 min after exercise termination. From the central waveform, as reconstructed by application of a generalized transfer function, we computed a systolic (AIx) and a diastolic index (AId) of pressure augmentation by reflections. At 5 min, both indices were below preexercise. At further time-points, AIx remained low, while AId progressively increased, to overshoot above preexercise at 45 min. The same behavior was observed with both exercise types. Beyond the first few minutes of recovery following either maximal or submaximal aerobic exercise, reflected waves selectively augment the central pressure pulse in diastole, at least in endurance-trained athletes.

The forgotten face of regular physical exercise: a 'natural' anti-atherogenic activity.

Humans are not programmed to be inactive. The combination of both accelerated sedentary lifestyle and constant food availability disturbs ancient metabolic processes leading to excessive storage of energy in tissue, dyslipidaemia and insulin resistance. As a consequence, the prevalence of Type 2 diabetes, obesity and the metabolic syndrome has increased significantly over the last 30 years. A low level of physical activity and decreased daily energy expenditure contribute to the increased risk of cardiovascular morbidity and mortality following atherosclerotic vascular damage. Physical inactivity leads to the accumulation of visceral fat and consequently the activation of the oxidative stress/inflammation cascade, which promotes the development of atherosclerosis. Considering physical activity as a 'natural' programmed state, it is assumed that it possesses atheroprotective properties. Exercise prevents plaque development and induces the regression of coronary stenosis. Furthermore, experimental studies have revealed that exercise prevents the conversion of plaques into a vulnerable phenotype, thus preventing the appearance of fatal lesions. Exercise promotes atheroprotection possibly by reducing or preventing oxidative stress and inflammation through at least two distinct pathways. Exercise, through laminar shear stress activation, down-regulates endothelial AT1R (angiotensin II type 1 receptor) expression, leading to decreases in NADPH oxidase activity and superoxide anion production, which in turn decreases ROS (reactive oxygen species) generation, and preserves endothelial NO bioavailability and its protective anti-atherogenic effects. Contracting skeletal muscle now emerges as a new organ that releases anti-inflammatory cytokines, such as IL-6 (interleukin-6). IL-6 inhibits TNF-α (tumour necrosis factor-α) production in adipose tissue and macrophages. The down-regulation of TNF-α induced by skeletal-muscle-derived IL-6 may also participate in mediating the atheroprotective effect of physical activity.

Effect of high-intensity interval exercise on lipid oxidation during postexercise recovery.

PURPOSE: The aim of this study was to examine whether lipid oxidation predominates during 3 h of postexercise recovery in high-intensity interval exercise as compared with moderate-intensity continuous exercise on a cycle ergometer in fit young men (n = 12; 24.6 +/- 0.6 yr). METHODS: The energy substrate partitioning was evaluated during and after high-intensity submaximal interval exercise (INT, 1-min intervals at 80% of maximal aerobic power output [Wmax] with an intervening 1 min of active recovery at 40% Wmax) and 60-min moderate-intensity continuous exercise at 45% of maximal oxygen uptake (C45%) as well as a time-matched resting control trial (CON). Exercise bouts were matched for mechanical work output. RESULTS: During exercise, a significantly greater contribution of CHO and a lower contribution of lipid to energy expenditure were found in INT (512.7 +/- 26.6 and 41.0 +/- 14.0 kcal, respectively) than in C45% (406.3 +/- 21.2 and 170.3 +/- 24.0 kcal, respectively; P < 0.001) despite similar overall energy expenditure in both exercise trials (P = 0.13). During recovery, there were no significant differences between INT and C45% in substrate turnover and oxidation (P > 0.05). On the other hand, the mean contribution of lipids to energy yield was significantly higher after exercise trials (C45% = 61.3 +/- 4.2 kcal; INT = 66.7 +/- 4.7 kcal) than after CON (51.5 +/- 3.4 kcal; P < 0.05). CONCLUSIONS: These findings show that lipid oxidation during postexercise recovery was increased by a similar amount on two isoenergetic exercise bouts of different forms and intensities compared with the time-matched no-exercise control trial.

Mitofusins 1/2 and ERRalpha expression are increased in human skeletal muscle after physical exercise

Mitochondrial impairment is hypothesized to contribute to the pathogenesis of insulin resistance. Mitofusin (Mfn) proteins regulate the biogenesis and maintenance of the mitochondrial network, and when inactivated, cause a failure in the mitochondrial architecture and decreases in oxidative capacity and glucose oxidation. Exercise increases muscle mitochondrial content, size, oxidative capacity and aerobic glucose oxidation. To address if Mfn proteins are implicated in these exercise-induced responses, we measured Mfn1 and Mfn2 mRNA levels, pre-, post-, 2 and 24 h post-exercise. Additionally, we measured the expression levels of transcriptional regulators that control mitochondrial biogenesis and functions, including PGC-1alpha, NRF-1, NRF-2 and the recently implicated ERRalpha. We show that Mfn1, Mfn2, NRF-2 and COX IV mRNA were increased 24 h post-exercise, while PGC-1alpha and ERRalpha mRNA increased 2 h post-exercise. Finally, using in vitro cellular assays, we demonstrate that Mfn2 gene expression is driven by a PGC-1alpha programme dependent on ERRalpha. The PGC-1alpha/ERRalpha-mediated induction of Mfn2 suggests a role of these two factors in mitochondrial fusion. Our results provide evidence that PGC-1alpha not only mediates the increased expression of oxidative phosphorylation genes but also mediates alterations in mitochondrial architecture in response to aerobic exercise in humans

Effects of smoking and physical exercise on platelet free cytosolic calcium in healthy normotensive volunteers.

Platelet free cytosolic calcium (PFCC) was measured in 21 healthy volunteers before and after cigarette smoking or physical exercise. The aim was to investigate whether acute blood pressure changes and increases in circulating levels of catecholamines and vasopressin modify PFCC. PFCC was determined using the Quin-2 method. Following cigarette smoking, significant increases in blood pressure, heart rate, plasma epinephrine (35 +/- 18 pg/ml before versus 51 +/- 31 pg/ml after smoking, P less than 0.05, mean +/- s.d.) and vasopressin levels (0.8 +/- 0.3 pg/ml before and 4.2 +/- 4.1 pg/ml after smoking, P less than 0.001) were observed. However, despite these acute hormonal and hemodynamic changes, PFCC remained stable at 156 +/- 55 nmol/l prior to the study and 157 +/- 29 nmol/l and 156 +/- 38 nmol/l at 20 and 80 min post-smoking, respectively. Acute physical exercise led to an increase in heart rate and systolic blood pressure but to a decrease in diastolic pressure. Moreover, a marked increase in plasma norepinephrine levels was observed after exercise (213 +/- 71 pg/ml before versus 747 +/- 501 pg/ml after exercise, P +/- 0.001). Again, PFCC was stable at 185 +/- 56 nmol/l at baseline versus 188 +/- 51 nmol/l at 20 min and 155 +/- 26 nmol/l at 80 min after exercise. These results therefore demonstrate that PFCC is not influenced acutely either by blood pressure increases, or by elevations in circulating catecholamine and vasopressin concentrations.

Tree line shifts in the Swiss Alps: Climate change or land abandonment?

Questions: Did the forest area in the Swiss Alps increase between 1985 and 1997? Does the forest expansion near the tree line represent an invasion into abandoned grasslands (ingrowth) or a true upward shift of the local tree line? What land cover / land use classes did primarily regenerate to forest, and what forest structural types did primarily regenerate? And, what are possible drivers of forest regeneration in the tree line ecotone, climate and/or land use change? Location: Swiss Alps. Methods: Forest expansion was quantified using data from the repeated Swiss land use statistics GEOSTAT. A moving window algorithm was developed to distinguish between forest ingrowth and upward shift. To test a possible climate change influence, the resulting upward shifts were compared to a potential regional tree line. Results: A significant increase of forest cover was found between 1650 to and 2450 m. Above 1650 m, 10% of the new forest areas were identified as true upward shifts whereas 90% represented ingrowth, and we identified both land use and climate change as likely drivers. Most upward shift activities were found to occur within a band of 300 m below the potential regional tree line, indicating land use as the most likely driver. Only 4% of the upward shifts were identified to rise above the potential regional tree line, thus indicating climate change. Conclusions: Land abandonment was the most dominant driver for the establishment of new forest areas, even at the tree line ecotone. However, a small fraction of upwards shift can be attributed to the recent climate warming, a fraction that is likely to increase further if climate continues to warm, and with a longer time-span between warming and measurement of forest cover.

Enhanced diastolic reflections on arterial pressure pulse during exercise recovery

RESUMEDurant la phase de récupération d'un exercice de course à pied d'intensité maximale ou submaximale, une augmentation de la pression artérielle systolique centrale (aortique) résultant de la réflexion des ondes de pouls sur l'arbre vasculaire est constatée chez l'individu en bonne santé. En diastole cependant, l'impact de la réflexion de ces ondes de pouls sur la pression centrale demeure inconnu durant la récupération d'un exercice.Nous avons évalué les ondes de pouls centrales systolique et diastolique chez onze athlètes d'endurance durant la phase de récupération d'un exercice de course à pied dans des conditions d'effort maximal (sur tapis de course) et lors d'un effort submaximal lors d'une course à pied de 4000 mètres en plein air sur terrain mixte.Pour chaque sujet et lors des deux exercices, l'onde de pouls a été mesurée au niveau radial par tonométrie d'aplanation durant une phase de repos précédant l'exercice, puis à 5, 15, 25, 35 et 45 minutes après la fin de l'exercice. En utilisant une fonction mathématique de transfert, l'onde de pouls centrale a été extrapolée à partir de l'onde de pouls radiale. En compilant la forme de l'onde de pouls centrale avec une mesure simultanée de la pression artérielle brachiale, un index d'augmentation de l'onde de pouls en systole (Alx) et en diastole (Als) peut être calculé, reflétant l'augmentation des pressions résultant de la réflexion des ondes sur l'arbre vasculaire périphérique.A 5 minutes de la fin de l'exercice, les deux index ont été mesurés moindres que ceux mesurés lors de la phase précédant celui-ci. Lors des mesures suivantes, Alx est resté bas, alors que Aid a progressivement augmenté pour finalement dépasser la valeur de repos après 45 minutes de récupération. Le même phénomène a été constaté pour les deux modalités d'exercice (maximal ou submaximal). Ainsi, au-delà de quelques minutes de récupération après un exercice de course d'intensité maximale ou submaximale, nous avons montré par ces investigations que les ondes de pouls réfléchies en périphérie augmentent de façon sélective la pression centrale en diastole chez l'athlète d'endurance.ABSTRACTDuring recovery from a maximal or submaximal aerobic exercise, augmentation of central (aortic) systolic pressure by reflected pressure waves is blunted in healthy humans. However, the extent to which reflected pressure waves modify the central pulse in diastole in these conditions remains unknown. We evaluated systolic and diastolic central reflected waves in 11 endurance-trained athletes on recovery from a maximal running test on a treadmill (treadmill-max) and a 4000m run in field conditions. On both occasions in each subject, the radial pulse was recorded with applanation tonometry in the resting preexercise state and then 5, 15, 25, 35, and 45 minutes after exercise termination. From the central waveform, as reconstructed by application of a generalized transfer function, we computed a systolic (Alx) and a diastolic index (Aid) of pressure augmentation by reflections. At 5 minutes, both indices were below preexercise. At further time-points, Alx remained low, while Aid progressively increased, to overshoot above preexercise at 45 minutes. The same behavior was observed with both exercise types. Beyond the first few minutes of recovery following either maximal or submaximal aerobic exercise, reflected waves selectively augment the central pressure pulse in diastole, at least in endurance- trained athletes.