Recommendations for endurance exercise prescription are often based on percentages of heart rate (HR) or the volume of oxygen consumption ( V ˙ O2) maximum or reserve that is extrapolated to a power ...output (P) or velocity. Previous work has demonstrated dissociations of the expected responses to exercise anchored to the critical heart rate (CHR) compared with the P associated with CHR. However, it is unclear if similar dissociations due to reductions in P to maintain the designated intensity would be present during exercise anchored to the V ˙ O2 associated with CHR ( V ˙ O2CHR). The purpose of this study was to examine the patterns in physiological ( V ˙ O2, HR, P, respiration rate RR, muscle oxygen saturation %SmO2), neuromuscular (electromyographic and mechanomyographic amplitude EMG AMP, MMG AMP, mean power frequency EMG MPF, MMG MPF), and perceptual (rating of perceived exertion RPE) responses during exercise at V ˙ O2CHR ( V ˙ O2-clamp). On separate days, ten participants (age: 25 ± 4 yr) performed a graded exercise test and four constant P trials at 85–100% of peak P (PP) to derive CHR and V ˙ O2CHR. Responses were recorded during a trial to exhaustion at V ˙ O2CHR (32.86 ± 7.12 mL·kg−1·min−1; TLim = 31.31 ± 21.37 min) and normalized in 10% intervals of TLim to their respective values at PP. The one-way repeated-measures ANOVA with post hoc, Bonferroni-corrected, pairwise comparisons indicated differences (p < 0.001) from baseline for HR (mean ± SD %change = 8 ± 3%), RR (43 ± 38%), P (−15 ± 5%), EMG MPF (10 ± 8%), and RPE (65 ± 38%), but no differences (p = 0.077–0.955) for %SmO2 (−17 ± 53%), EMG AMP (−3 ± 16%), MMG AMP (40 ± 61%), and MMG MPF (1 ± 7%). The loss in performance observed during V ˙ O2-Clamp exercise may provide a quantification of the inefficiency associated with the V ˙ O2 slow component phenomenon. The neuromuscular responses suggested constant muscle excitation despite the reductions in P, but the metabolic and perceptual responses suggested a combination of feedforward and feedback mechanisms regulating TLim. Future studies should further examine responses to the V ˙ O2-Clamp exercise at a uniform threshold.
Bradyarrhythmias including sinus bradycardia and atrioventricular (AV) block are frequently encountered in endurance athletes especially at night. While these are well tolerated by the young athlete, ...there is evidence that generally from the fifth decade of life onward, such arrhythmias can degenerate into pathological symptomatic bradycardia requiring pacemaker therapy. For many years, athletic bradycardia and AV block have been attributed to high vagal tone, but work from our group has questioned this widely held assumption and demonstrated a role for intrinsic electrophysiological remodeling of the sinus node and the AV node. In this article, we argue that bradyarrhythmias in the veteran athlete arise from the cumulative effects of exercise training, the circadian rhythm and aging on the electrical activity of the nodes. We consider contemporary strategies for the treatment of symptomatic bradyarrhythmias in athletes and highlight potential therapies resulting from our evolving mechanistic understanding of this phenomenon.
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The mechanisms by which exercise benefits human health remain incompletely understood. With the emergence of omics techniques, mapping of the molecular response to exercise is increasingly ...accessible. Here, we perform an untargeted metabolomics profiling of plasma from a randomized, within-subjects, crossover study of either endurance exercise or resistance exercise, two types of skeletal muscle activity that have differential effects on human physiology. A high-resolution time-series analyses reveal shared as well as exercise-mode-specific perturbations in a multitude of metabolic pathways. Moreover, the analyses reveal exercise-induced changes in metabolites that are recognized to act as signaling molecules. Thus, we provide a metabolomic signature of how dissimilar modes of exercise affect the organism in a time-resolved fashion.
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•Exercise-mode-specific metabolomes enabled by a randomized crossover design•Temporal information on plasma metabolome dynamics•Cluster and pathway analyses reveal mode-linked changes in plasma metabolites•Metabolites with hormone-like signaling properties are regulated by exercise
Using untargeted metabolomics, Morville et al. provide a time-resolved map of circulating metabolites that are regulated in response to an acute bout of endurance exercise or resistance exercise in healthy male subjects. The authors deliver a comprehensive comparative overview of exercise-mode-dependent and mode-independent changes to the plasma metabolome.
Abstract
Cardiovascular (CV) disease (CVD) remains the leading cause of major morbidity and CVD- and all-cause mortality in most of the world. It is now clear that regular physical activity (PA) and ...exercise training (ET) induces a wide range of direct and indirect physiologic adaptations and pleiotropic benefits for human general and CV health. Generally, higher levels of PA, ET, and cardiorespiratory fitness (CRF) are correlated with reduced risk of CVD, including myocardial infarction, CVD-related death, and all-cause mortality. Although exact details regarding the ideal doses of ET, including resistance and, especially, aerobic ET, as well as the potential adverse effects of extreme levels of ET, continue to be investigated, there is no question that most of the world’s population have insufficient levels of PA/ET, and many also have lower than ideal levels of CRF. Therefore, assessment and promotion of PA, ET, and efforts to improve levels of CRF should be integrated into all health professionals’ practices worldwide. In this state-of-the-art review, we discuss the exercise effects on many areas related to CVD, from basic aspects to clinical practice.
The aim of this study was to develop an animal model to investigate whether prolonged intensive endurance exercise induces RV remodeling, taking into account the involvement of Wnt/β-catenin ...signaling.
Four-week-old male Wistar rats (100 to 125 g) were assigned to four groups (n = 8/group): 1) sixteen weeks of intensive (36 m/min) exercise (INT), 2) twelve weeks of the intensive exercise followed by four weeks of moderate intensity (18 m/min) exercise (INT + MOD), 3) twelve weeks of the intensive exercise followed by four weeks of detraining (INT + DT), and 4) sedentary rats (SED). The exercise protocols were performed five days a week for one h/day. Echocardiography, real-time PCR, western blotting, and histological staining were performed at the end of week sixteen.
INT rats developed concentric hypertrophy without diastolic dysfunction compared to SED (p = 0.006) and INT + DT (p = 0.035). Wnt1, β-catenin and CyclinD1 proteins in the training groups were significantly higher than SED rats (p < 0.001). Interestingly, INT rats had higher protein levels than INT + DT and INT + MOD (p < 0.001), with higher gene expression compared to SED rats (p < 0.05). There was also a significant increase in collagen deposition in INT rats compared to SED (p = 0.046) and INT + DT (p = 0.034). Furthermore, INT + MOD and INT + DT rats did not show any adverse structural, functional, or histological changes.
Long-term intensive endurance training seems to be associated with increased collagen deposition and wall thickness in the RV through Wnt/β-catenin signaling (which is concentration dependent), without changes in diastolic function.
Over the past decades, there has been an ongoing debate about whether the structural and functional adaptations of the cardiovascular system in trained endurance athletes are benign physiological responses to training or potentially pathological changes related to disease. While the adaptations of the left heart are well-documented, the remodeling of the right heart remains a subject of discussion. To gain insights into the ability of sustained high-intensity exercise to cause adverse right ventricular (RV) remodeling, we conducted an experimental study in which male rats were trained to run vigorously for 1 h daily over a 16-week period and compared them to a parallel group of sedentary control rats. Our findings revealed that intense long-term exercise induced morphological changes along with fibrosis affecting the RV. These fibrotic changes were a result of the 16-week vigorous exercise training regimen. If these results are confirmed in humans, they suggest that prolonged high-intensity endurance exercise training may lead to adverse cardiac remodeling. Our findings have important potential implications for the assessment of cardiac remodeling in individuals engaged in high-level exercise training.
•Long-term vigorous endurance exercise may induce fibrosis and concentric hypertrophy in the right ventricle•Wnt/β-catenin signaling pathway plays a role in right ventricular remodeling induced by long-term intensive endurance exercise•Increases in RV wall thickness maintain cardiac function
Endurance is an important capacity to sustain healthy lifestyles. Aged garlic extract (AGE) has been reported to exert endurance-enhancing effect in the clinical and animal studies, though little is ...known of its active ingredients and mechanism of action.
The current study investigated the potential effect of S-1-propenylcysteine (S1PC), a characteristic sulfur amino acid in AGE, on the swimming endurance of mice and examined its mechanism of action by a metabolomics-based approach.
Male ICR mice (6 weeks old) were orally administered water (control) or S1PC (6.5 mg/kg/day) for 2 weeks and swimming duration to exhaustion was measured at 24 hours after the last administration. Non-targeted metabolomic analysis was conducted on the plasma samples obtained from mice following 40-minute submaximal swimming bouts. Subsequently, the enzyme activity of carnitine acyltransferase-1 (CPT-1) and the content of malonyl-coenzyme A (CoA), acetyl-CoA and adenosine triphosphate (ATP) were quantified in heart, skeletal muscles and liver of mice.
The duration time of swimming was substantially increased in the S1PC-treated mice as compared to the control group. Metabolomic analysis revealed significant alterations in the plasma level of the metabolites involved in the fatty acid metabolism, in particular medium- or long-chain acylcarnitines in the mice treated with S1PC. Moreover, administration of S1PC significantly enhanced the CPT-1 activity with the concomitant decrease in the malonyl-CoA content in the heart and skeletal muscles. These effects of S1PC were accompanied by the elevation of the acetyl-CoA and ATP levels to enhance the energy production in those tissues.
S1PC is a key constituent responsible for the endurance-enhancing effect of AGE. The present study suggests that S1PC helps provide the energy during the endurance exercise by increasing fatty acid metabolism via CPT-1 activation in the heart and skeletal muscles.
Studies in middle-age and older (masters) athletes with atherosclerotic risk factors for coronary artery disease report higher coronary artery calcium (CAC) scores compared with sedentary ...individuals. Few studies have assessed the prevalence of coronary artery disease in masters athletes with a low atherosclerotic risk profile.
We assessed 152 masters athletes 54.4±8.5 years of age (70% male) and 92 controls of similar age, sex, and low Framingham 10-year coronary artery disease risk scores with an echocardiogram, exercise stress test, computerized tomographic coronary angiogram, and cardiovascular magnetic resonance imaging with late gadolinium enhancement and a 24-hour Holter. Athletes had participated in endurance exercise for an average of 31±12.6 years. The majority (77%) were runners, with a median of 13 marathon runs per athlete.
Most athletes (60%) and controls (63%) had a normal CAC score. Male athletes had a higher prevalence of atherosclerotic plaques of any luminal irregularity (44.3% versus 22.2%;
=0.009) compared with sedentary males, and only male athletes showed a CAC ≥300 Agatston units (11.3%) and a luminal stenosis ≥50% (7.5%). Male athletes demonstrated predominantly calcific plaques (72.7%), whereas sedentary males showed predominantly mixed morphology plaques (61.5%). The number of years of training was the only independent variable associated with increased risk of CAC >70th percentile for age or luminal stenosis ≥50% in male athletes (odds ratio, 1.08; 95% confidence interval, 1.01-1.15;
=0.016); 15 (14%) male athletes but none of the controls revealed late gadolinium enhancement on cardiovascular magnetic resonance imaging. Of these athletes, 7 had a pattern consistent with previous myocardial infarction, including 3(42%) with a luminal stenosis ≥50% in the corresponding artery.
Most lifelong masters endurance athletes with a low atherosclerotic risk profile have normal CAC scores. Male athletes are more likely to have a CAC score >300 Agatston units or coronary plaques compared with sedentary males with a similar risk profile. The significance of these observations is uncertain, but the predominantly calcific morphology of the plaques in athletes indicates potentially different pathophysiological mechanisms for plaque formation in athletic versus sedentary men. Coronary plaques are more abundant in athletes, whereas their stable nature could mitigate the risk of plaque rupture and acute myocardial infarction.
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