Endurance riding and "scoring" endurance rides.
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Previous studies have shown that endurance athletes are endowed with low ventilatory responses to chemical stimuli. The implications of this association have never been clear. Although recent evidence shows that exercise ventilation (VE) correlates with ventilatory chemoresponsiveness in a group of athletes, the extent to which non-athletes may differ from athletes in this regard is unknown. We have examined the relationship between ventilatory chemoresponsiveness and exercise VE in a group of 7 non-athletes, and contrasted these findings with those obtained previously from 8 endurance and 8 non-endurance athletes. Correlation lines of exercise VE with chemical responses were similar in slope and intercept for both athletes and non-athletes. However, we found that non-athletes had greater exercise VE per unit metabolic rate (VO2 or VCO2), and greater ventilatory responses to O2 and CO2, when compared with endurance athletes at equal relative work loads (P less than 0.05). The lower exercise VE/VCO2 of endurance athletes as compared with non-athletes persisted in hyperoxia, indicating that factors other than differences in hypoxic sensitivity explain the lower exercise VE of endurance athletes. Low exercise VE may be the link between low ventilatory chemosensitivity and outstanding endurance athletic performance.
To evaluate possible differences in the cardiac effects of different types of running training, 22 competing male runners--10 sprinters and 12 endurance runners--were studied with a physical examination, electrocardiography, chest X-ray film and echocardiography. Thirteen sedentary men served as control subjects. There were no differences between the athletic groups in physical findings. However, left ventricular hypertrophy in the electrocardiogram was more apparent in the endurance runners (P less than 0.05), whose relative heart size on chest X-ray examination was also greater than in the sprinters (P less than 0.02). On echocardiography the left ventricular end-diastolic volume was equally greater than normal in both groups of athletes (P less than 0.005), but in the endurance runners the percent chance of the minor axis diameter in systole was greater than in the sprinters or control subjects (P less than 0.02). Values for left ventricular wall thickness and mass were greater than normal in both groups of athletes but were higher in the endurance runners than in the sprinters (P less than 0.001). The left atrial diameter was apparently greater in the endurance runners than in the sprinters or control subjects (P less than 0.001), whereas that of the sprinters did not differ from normal. Thus, intensive sprinter training seems to dilate the left ventricle but causes less increase in wall thickness and mass than training for endurance running and no change in left ventricular function or left atrial size. Endurance running causes left ventricular dilatation equal to that of sprinter training, greater wall hypertrophy and improved systolic emptying of the left ventricle, and it also dilates the left atrium perhaps because of decreased left ventricular compliance.
By use of a method of sequential stimulation described previously, the ability to sustain tensions of 3--100% of the initial strength (maximum isometric tension that could be developed in the fresh muscle) to fatigue (endurance) was assessed in the soleus (slow-twitch), medial gastrocnemius (mixed, fast-twitch), and plantaris (mainly fast-twitch) muscles. For all fractions of the initial strength the endurance was longest in soleus and shortest in plantaris. However, although plantaris fatigued at any tension examined, soleus could maintain a tension of up to 30% of its initial strength indefinitely with no sign of fatigue. Part of the difference in endurance between these two muscles could be accounted for in terms of blood flow because arterial occlusion sharply reduced the endurance of soleus but had only a small effect on endurance in plantaris. However, even with an occluded circulation, soleus still had substantially longer endurance than either medial gastrocnemius or plantaris. The origin of fatigue in any of the three muscles examined appeared to be in the muscle; there was no evidence of failure of transmission at the neuromuscular junction.
The aim of the study was to investigate the influence of age on endurance of human skeletal muscle. An attempt was made to correlate muscular performance at various ages with some morphological and enzymatic characteristics of the muscle. Fifty healthy men, 22-65 years of age, with low daily physical activity (clerks) volunteered for the study. Isometric and dynamic endurance were determined under standardized conditions and measured in relation to maximum strength, thereby correcting for individual as well as age differences in maximum strength. Biopsies taken from the quadriceps muscle were used for muscle fibre classification, fibre area determinations, and measurements of some enzyme activities (Mg2+ stimulated ATPase, myokinase (MK), lactate dehydrogenase (LDH),LDH isozymes). Maximum isometric and dynamic strength decreased in the older groups while no significant change was seen in isometric or dynamic endurance. Significant correlations were observed between endurance and fibre type distribution, fibre areas, and LDH isozyme activities.
Studies have been conducted on 13 young healthy adults of average fitness on endurance work of varying durations lasting for 2-31 minutes using bicycle ergometer. Aerobic-anaerobic fractions of oxygen supply during each effort was determined. The data from Astrand and Rodahl on aerobic O2--supply and duration in maximal efforts from 1-120 minutes on a highly trained subject have also been considered. The plot of log endurance time against log (aerobic/anaerobic ratio) exhibits a slight departure from linearity, indicating independent contributions from aerobic and anaerobic fractions of oxygen supply. An equation was derived of the form: T - Au1k1u2--k2 where u1 end u2 are the aerobic and anaerobic fractions respectively which has been found to yield highly significant correlation coefficient between log-estimated and log-observed endurance time (0.9996 for Astrand and Rodahl's data on a single subject and 0.9640 for the present data on 13 subjects). This index is, therefore, quite suitable for the assessment of endurance capacity in terms of a single physiological parameter, and is likely to be superior to indices in current use.
BACKGROUND: Although endurance exercise benefits liver health, sex-specific adaptive trajectories remain unclear. This study mapped dynamic liver adaptation in males and females during prolonged training and identified underlying molecular programs. METHODS: Using publicly available time-resolved liver multi-omics data generated by the Molecular Transducers of Physical Activity Consortium (MoTrPAC), we established a computational pipeline for differential analysis of transcriptomic, proteomic, phosphoproteomic, and metabolomic data with FDR correction, followed by FGSEA pathway enrichment. Kinase activities were inferred through ortholog mapping and PhosphoSitePlus. Cross-omics co-expression networks were constructed using WGCNA and topological overlap to link omics features with physiological phenotypes. For experimental validation, liver tissues were collected from endurance-trained Sprague-Dawley rats, and key nodes were confirmed by Western blotting, qRT-PCR, and immunofluorescence/immunohistochemical staining. Public scRNA-seq data were further integrated to map multi-omics signals to single-cell resolution and assess functional changes in specific cell types. RESULTS: The hepatic response to exercise stress was stage-specific, shifting from early transcriptional activation to later proteomic and metabolic remodeling. Multi-omics integration revealed distinct sex-associated adaptive trajectories: males were more strongly associated with energy metabolism, redox-related programs, and amino acid/organic acid catabolism, whereas females showed prominent membrane lipid remodeling, proteostasis -related programs, and mitochondrial/ribosomal translational features. Single-cell analysis showed that tissue remodeling occurred without major lineage turnover, instead involving altered communication among pre-existing cell communities. Validation of PPP1R3G identified a protein-dominant exercise-responsive marker, supporting the contribution of post-transcriptional or protein-level regulation. CONCLUSIONS: Hepatic adaptation to endurance stress follows a cross-omics evolutionary pattern with sex-specific reprogramming of energy supply and homeostatic maintenance. This time-resolved framework clarifies how exercise improves liver function and supports sex-oriented metabolic interventions and therapeutic target discovery.
Endurance exercise training has been found to enhance the functional capacity of the myocardium in several animal models. The sub-cellular phenomena accompanying the augmented function are yet to be explained. The present study sought to determine if the myosin ATPase activity of cardiac muscle increased as a result of endurance conditioning. Five beagles trained by running on a motor driven treadmill (T) and five control (NT) animals were studied. Follwoing 10 weeks of training the T group had a significantly (P less than .05) lower heart rate than the NT while performing the same submaximal exercise and the gastrocnemius cytochrome oxidase activity was significantly greater (P less than .005) in the T than in the NT. These two measurements established that the exercised animals were physically trained. Myosin was isolated from the left ventricular myocardium and activated in a medium containing K-EDTA. No significant (P less than .05) difference in maximum myosin ATPase activity was observed between the NT and T groups in cardiac muscle. It was concluded that cardiac muscle myosin ATPase activity was not affected by 10 weeks of endurance conditioning induced by treadmill running in dogs.
BACKGROUND: This study investigated whether whole-body cold-water immersion (CWI) following rugby-specific training influences endurance exercise performance 24 h later. METHODS: Eleven healthy male collegiate rugby players completed an incremental cycling test to determine peak oxygen uptake (V̇O 2peak ) and time to exhaustion at baseline (Pre). One week later, participants performed a standardized rugby-specific training session consisting of warm-up, skill-based passing, contact drills, individual training (i.e., conversion kicking and scrummaging), and a bronco endurance test (total duration: 180 min), followed by one of two recovery interventions in a randomized order: 1) whole-body CWI for 8 min at 15 °C (CWI) or 2) seated rest for 8 min (Control). Participants then performed the incremental cycling test 24 h after each intervention. RESULTS: Training load during the rugby-specific training, assessed using heart rate-based training load and blood lactate concentrations, did not differ between the trials. Time to exhaustion (485±72 vs. 518±77 s, P=0.107, d=0.45) and V̇O 2peak did not differ between the Control and CWI trials, whereas the relative changes in these variables from Pre were greater in the CWI than in the Control trials (both P<0.05). Oxygen uptake, minute ventilation, and rating of perceived exertion during submaximal exercise were similar across the Pre, Control, and CWI trials. CONCLUSIONS: These results suggest that whole-body CWI following rugby-specific training may be associated with favorable changes in endurance exercise performance 24 h post-intervention compared with the control condition. However, the expectancy/placebo effect of water immersion on exercise performance could not be excluded.
Eight male and female students were studied during exercise to exhaustion on a bicycle ergometer at 80 and 100% of Vo2max following the ingestion of water (W), 75 g of glucose (G) or a liquid meal (M) (10 g protein, 12.5 g fat, 15 g CHO). When compared to the endurance ride (80% Vo2max) in the W treatment, endurance performance time was reduced by 19%, (p less than .05) (53.2 to 43.2 min) as a result of the preexercise glucose feeding (Trial G). No difference in performance at 80% Vo2max was found between the W and M trials. The preexercise feedings had no effect on exercise time to exhaustion at 100% Vo2max. During the G and M trials at 80% Vo2max, most of the subjects demonstrated a transient decline in serum glucose (less than 3.5 mM). After 30-40 min. of exercise, however, serum glucose returned to normal and was seldom low at the time of exhaustion. Serum free fatty acids (FFA) were depressed throughout the G trial. The results of these experiments indicate impaired lipid mobilization following CHO ingestion. The present data support our earlier findings (11) which demonstrate that glucose feedings 30-45 minutes before endurance exercise increase the rate of CHO oxidation and impede the mobilization of FFA, thereby reducing exercise time to exhaustion.
INTRODUCTION: This study examined the effects of various cycling endurance training modalities, matched for total workload, on muscle mechanical and architectural characteristics in older adults. METHODS: Fifty healthy participants (25 females, 59-79 yrs) were randomly assigned to five age and sex matched groups: one control and four workload-matched training groups (moderate-intensity continuous, heavy-intensity continuous, high-intensity interval, and heavy-intensity continuous in eccentric cycling). Training consisted of three weekly sessions over 8 weeks, with evaluations conducted at the beginning and end of the intervention with maximal voluntary isometric contractions at five different knee angles (90, 75, 60, 45, 30°) and maximal concentric and eccentric isokinetic contractions at five different knee angular velocities (45, 90, 150, 210, 250°/s). Maximum voluntary isometric torque (Tmax) and optimal knee angle (KAopt) were obtained from the isometric contractions; eccentric torque (Tecc) and maximum concentric knee angular velocity (Vmax) were obtained from the isokinetic contractions. The muscle architecture of vastus lateralis (VL) at rest (muscle thickness, pennation angle, and fascicle length) was investigated as well. RESULTS: No statistical differences were detected between groups or time points in VL architecture, in KAopt and in Vmax. A main effect of time was observed for Tmax (p < 0.001, η2p = 0.458) and Tecc (p = 0.002, η2p = 0.191) in all the investigated training groups. The within-group comparisons indicate significant increases in Tmax in the training groups, but not in the control group. CONCLUSIONS: Commonly applied endurance exercises improve muscle mechanical capacity (Tmax and Tecc) in older adults, with no structural (architectural) muscle remodelling, when matched for workload.
Some mitochondrial enzymatic activities (succinate dehydrogenase, NADH cytochrome reductase, cytochrome oxidase) were studied in the gastrocnemius and soleus muscle of the rat. The modifications of the enzyme activity, induced by endurance training, were found to be functions of 1) daily work load and 2) total training time. The treatment with an effective dose of vasodilating substances (papaverine, nicergoline, dipyridamole, and bamethan) showed that 1) nicergoline, bamethan, and dipyridamole were differently able to shorten the time of appearance of the increase in the enzymatic activities; 2) however, long-term treatments with these drugs did not prove able to modify the plateau level of the enzymatic activity increase, for a given amount of endurance training; 3) the pharmacodynamic effect on enzymatic activities was in no way related to the vasodilating effect of these drugs, since the effect was not observed with papaverine. The transition from a given level of endurance training to a lower one led to a proportional decrease of the mitochondrial enzymatic activities, thus pointing out the relation between amount of training and enzymatic activity. The drugs studied were unable to modify the decrease of enzymatic activity induced by lower work load.
Circulating monocytes contribute to atherogenesis and vascular dysfunction. Although clinical cardiovascular disease presents in adulthood, its biological origins often begin in youth and differ substantially between females and males. Twelve males and nine females (13-17 yr) completed an acute exercise protocol consisting of 10, 2-min cycling bouts at 70% of maximal work rate interspersed with 1-min rest intervals, performed before and after an 8-wk supervised endurance training intervention with brief supplementary strength work (60 min/session, 3 sessions/wk). Blood was collected before and immediately after each exercise challenge. Peripheral blood monocytes were isolated, and whole transcriptome RNA sequencing (RNA-seq) was performed. Before training, acute exercise induced a markedly greater monocyte transcriptomic response in females compared with males [5,135 vs. 567 differentially expressed transcripts, false discovery rate (FDR) < 0.1]. Pathway analyses identified vascular function-related pathways in males, whereas females showed enrichment of pathways related to adipose tissue cross talk and oxidative metabolism. Following training, the acute transcriptomic response was markedly attenuated in both sexes (165 transcripts in males and 94 in females, FDR < 0.1), representing an ∼98% reduction in females and a ∼70% reduction in males relative to pre-training responses. These findings reveal sex-specific monocyte responses to acute exercise in youth and suggest that endurance exercise alters immune transcriptional responsiveness in pathways relevant to vascular and cardiovascular health.NEW & NOTEWORTHY Acute exercise induced a markedly greater monocyte transcriptomic response in female adolescents than in males. Females showed activation of pathways related to adipose tissue signaling and oxidative metabolism, whereas males exhibited vascular-function pathways. Following exercise training, the monocyte transcriptomic response to acute exercise was substantially attenuated in both sexes. These findings identify sex-specific immune transcriptional responses to exercise during adolescence with potential implications for cardiovascular health.
Seven young females were subjected to 24 weeks of intensive endurance training. Adaptive changes in myofibrillary ATP-ase activity, capillary supply and mitochondrial content were investigated with light- and electron microscopy in needle biopsies from the quadriceps femoris. 1. The average value for the maximal oxygen uptake increased from 45.7 to 57.2 (ml . kg-1 min-1) (25.2%, P less than 0.005). 2. The average number of capillaries per muscle fibre increased from 1.39 to 1.79 (28.8%, P less than 0.005). Since no significant change in fibre area was found, this suggests that a considerable number of new capillaries have been formed during the training period. 3. An increased capillary supply of all fibre types was found, being greatest for type I and smallest for type IIB. 4. The relative amount of type I fibres before and after the training period was 57.9 and 56.5% respectively (n.s.), for type IIA fibres 26.4 and 31.5% (P less than 0.005), for type IIB fibres 9.2 and 3.4% (P less than 0.005) and for type IIC fibres 0.4 and 2.2% (P less than 0.005). Thus, in the type II group, significant changes in subtypes take place during the endurance training. The data suggest that type IIAB may represent a transitional state between type IIA and IIB. 5. Correlation of capillary supply, myofibrillar ATP-ase activity and mitochondrial content (determined semiquantitatively of individual muscle fibres indicators that the capillary supply to a given fibre is more closely related to its mitochondrial content than to the fibre type as determined on the basis of myofibrillar ATP-ase activity.
Sweating sensitivity has been evaluated at rest in 10 competitive athletes (cross-country skiers and swimmers). Three sedentary men underwent a 3-mo period of endurance training in a temperate climate, (dry bulb temperature (Tdb): 18 degrees C) and had their sweating sensitivity measured before and after the training period. Mean maximum oxygen uptake (Vo2max, ml.min(-1).kg(-1)) was: skiers: 66.5; swimmers 65.8; sedentary men, pretraining 40.9; posttraining: 48.3 (+18%). Sweat output of athletes under a given stress (passive heating) was markedly higher than that of sedentary men. Skiers exhibited a high level of heat tolerance and were better acclimatized than swimmers, although they had never experienced exposure to heat. The increase in Vo2max of sedentary men was accompanied by 1) an increase in sweating sensitivity with a decrease of body heat storage at steady state (pretraining: 5.4 kJ.kg(-1); posttraining: 3.5 kJ.kg(-1); P less than 0.05); 2) significant shift down the temperature scale with reduced rectal temperature (Tre) for sweat onset; 3) an increase of gain constants of sweating (W.m-2 degrees C(-1) (pretraining: 168; posttraining: 269; gain constant of swimmers: 222). It was suggested that endurance training in cold or temperate conditions with significant increase of Vo2max could act on the thermoregulatory function in a way similar to body heating procedures, such as work in heat, and could contribute to heat acclimatization.
The purpose of this study was to test the hypothesis that increased availability of fatty acids could increase endurance by slowing the rate of glycogen depletion. Rats were given corn oil by stomach tube, and 3 h later an injection of heparin was given to raise their plasma free fatty acids (FFA). The rats with raised FFA were able to run approximately 1 h longer than otherwise comparable control animals before becoming exhausted (181 +/- 8 vs. 118 +/- 8 min, P less than 0.001). At the point of exhaustion, both groups were hypoglycemic and had low muscle glycogen concentrations. The fall in blood glucose occurred less rapidly in the animals with raised FFA; these rats also had significantly higher blood glycerol and beta-hydroxybutyrate concentrations than the controls. Glycogen concencentration decreased less rapidly in all three types of skeletal muscle and in liver in the animals with raised FFA than in the controls. We conclude that increased availability of fatty acids delays the development of exhaustion in rats subjected to prolonged running. It appears likely that the carbohydrate-sparing effect of fatty acids is largely responsible for the increase in endurance.
The purpose of this study was to assess cardiac adaptation to endurance training in rats. After 11 wk of progressive treadmill exercise (1 h/day), gastrocnemius cytochrome c oxidase activity was 38% higher (P less than 0.01) in the trained (n = 20) as compared to control (n = 20) rats. Cardiac Mg2+-stimulated myofibril ATPase activity (0.308 +/- 0.012 vs. 0.324 +/- 0.006 micrometer.mg-1.min-1) did not change nor was there any change in myofibril protein concentration (60.0 +/- 1.12 vs. 59.9 +/- 0.85 mg.g-1). The isolated left ventricular papillary muscle showed no significant change in time-to-peak tension (TPT) or half-relaxation time. Tension output, however, was significantly increased with training, 2.2 +/- 0.3 vs. 1.5 +/- 0.1 g.mm-2 (P less than 0.025). Furthermore, when the papillary preparations were perfused with 0.5 mM lanthanum (La3+) to displace membrane-bound Ca2+, the time course for tension decay was significantly prolonged in the trained muscles (P less than 0.001). We conclude that endurance running of this type does not necessarily increase myofibril ATPase activity or the time course of the isometric twitch of rat papillary muscle. However, tension output per unit area does increase and this appears to be due to a greater amount of Ca2+ being made available to the contractile apparatus.
Incretin-based pharmacotherapies, particularly glucagon-like peptide-1 (GLP-1) receptor agonists, have transformed the treatment of type 2 diabetes, with demonstrated benefits across multiple organ systems. Their success has driven the investigation of related gut-derived hormones, most prominently dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP) receptor agonists, but extend to other targets with similar metabolic functions. For this class of drugs, the extent to which organ health improvements are secondary to improved systemic glycemic control versus direct tissue signaling remains unclear, partly because receptor availability across tissues is poorly annotated. We leveraged data from the Molecular Transducers of Physical Activity Consortium to annotate incretin receptor expression across 17 tissues in Fischer 344 rats and the Genotype-Tissue Expression Portal for human-level receptor expression. Furthermore, given the role of exercise in the preservation of muscle mass during weight loss, we analyzed the effects of 1, 2, 4, or 8 wk of treadmill exercise training on incretin-related signaling at the epigenetic, transcript, and protein levels. Endurance training elicited sex- and tissue-specific changes in incretin receptor expression, including downregulation of Gcgr across brown adipose, adrenal glands, and white adipose tissue (WAT). Training-induced Gipr regulation occurred in the adrenal glands, brain cortex, and hippocampus. Collectively, these findings contribute to the map of incretin receptor biology and identify exercise-responsive regulatory axes that may underlie synergistic effects of exercise and incretin-based therapies on weight management and metabolic health.NEW & NOTEWORTHY This study provides the first multiomic, multitissue description of incretin signaling receptor expression and regulation in response to endurance exercise training. We identify time point and sex-specific changes in incretin signaling across tissues, highlighting training effects on Gcgr, Gipr, and Sctr regulation in the adrenals, WAT, and brain. These findings help establish an exercise-responsive incretin signaling axis that may identify interactions from incretin-based therapies and exercise-based lifestyle interventions.