Single Bout Of High-intensity Exercise Research Articles

Ascorbic Acid Supplementation and Immune Response in Healthy Women during High-intensity Exercise

Introduction the benefits of consuming extra Ascorbic Acid (AA) while exercising are not well understood. Aim This study aims to explore the effects of AA supplementation on oxidative stress, the immunological response, and inflammation in healthy women after a single bout of high-intensity exercise. Materials and Methods In a crossover design, 20 sedentary women (aged 18-22) underwent 30 minutes of vigorous cycling. They were divided into two groups: one receiving daily 1,000 mg ascorbic acid supplementation (1,000AA) and the other without supplementation (0AA). This regimen was maintained for one week. Blood samples obtained pre-exercise, immediately post-exercise, and 24 hours post-exercise underwent analysis for oxidative stress, inflammatory markers, CD4+ and CD8+ lymphocytes, and neutrophil phagocytic activity. Results An AA supplement significantly increased plasma concentrations of AA (p<0.05) and reduced post-exercise plasma MDA levels (p<0.05) but did not affect creatine kinase activity. White blood cells, CD8+ T cells, and IL-6 increased significantly after exercise but remained unchanged in the 1,000AA group compared to the 0AA group, while the neutrophil count increased (p<0.05) after exercise with no change in phagocytic function. A slight drop in phagocytic function was observed 24 hours after exercise in the 1,000AA group. Exercise and AA supplements had no effect on CD4+ T cells. Conclusion a single session of high-intensity exercise caused oxidative stress, muscle injury, and inflammation, as well as a transient increase in CD8+ T cells. A short administration of AA attenuated the exercise-induced oxidative stress and reduced inflammation by limiting the increase in IL-6 and CD8+ T cells.

Exercised blood plasma promotes hippocampal neurogenesis in the Alzheimer's disease rat brain

BackgroundExercise training promotes brain plasticity and is associated with protection against cognitive impairment and Alzheimer's disease (AD). These beneficial effects may be partly mediated by blood-borne factors. Here we used an in vitro model of AD to investigate effects of blood plasma from exercise-trained donors on neuronal viability, and an in vivo rat model of AD to test whether such plasma impacts cognitive function, amyloid pathology, and neurogenesis. MethodsMouse hippocampal neuronal cells were exposed to AD-like stress using amyloid-β and treated with plasma collected from human male donors 3 h after a single bout of high-intensity exercise. For in vivo studies, blood was collected from exercise-trained young male Wistar rats (high-intensity intervals 5 days/week for 6 weeks). Transgenic AD rats (McGill-R-Thy1-APP) were injected 5 times/fortnight for 6 weeks at 2 months or 5 months of age with either (a) plasma from the exercise-trained rats, (b) plasma from sedentary rats, or (c) saline. Cognitive function, amyloid plaque pathology, and neurogenesis were assessed. The plasma used for the treatment was analyzed for 23 cytokines. ResultsPlasma from exercised donors enhanced cell viability by 44.1% (p = 0.032) and reduced atrophy by 50.0% (p < 0.001) in amyloid-β-treated cells. In vivo exercised plasma treatment did not alter cognitive function or amyloid plaque pathology but did increase hippocampal neurogenesis by ∼3 fold, regardless of pathological stage, when compared to saline-treated rats. Concentrations of 7 cytokines were significantly reduced in exercised plasma compared to sedentary plasma. ConclusionOur proof-of-concept study demonstrates that plasma from exercise-trained donors can protect neuronal cells in culture and promote adult hippocampal neurogenesis in the AD rat brain. This effect may be partly due to reduced pro-inflammatory signaling molecules in exercised plasma.

Temporal Skin Temperature as an Indicator of Cardiorespiratory Fitness Assessed with Selected Methods.

Simple SummaryThe aim of this study was to investigate whether it is possible to use infrared thermography to assess cardiovascular fitness and aerobic capacity. Changes in temporal temperature during and after a single bout of high-intensity exercise were measured from subjects with varying levels of physical activity. Significant correlation between the temporal temperature measured during recovery time with cardiovascular fitness parameters (HRR and HRV) and maximum oxygen consumption confirm the usefulness of thermal imagining in aerobic capacity evaluation. These results could foster the employment of infrared thermography to monitor athletic/athletes’ performance.The aim of this study was to determine whether there are associations between cardiovascular fitness (and aerobic capacity) and changes in temporal skin temperature during and after a single bout of high-intensity exercise. Twenty-three men with varying levels of physical activity (VO2max: 59.03 ± 11.19 (mL/kg/min), body mass 71.5 ± 10.4 (kg), body height 179 ± 8 (cm)) participated in the study. Each subject performed an incremental test and, after a 48-h interval, a 110%Pmax power test combined with an analysis of the thermal parameters, heart rate recovery and heart rate variability. Thermal radiation density from the body surface (temple) was measured using a Sonel KT384 thermal imaging camera immediately after warm-up (Tb), immediately after exercise (Te) and 120 sec after the end of exercise (Tr). The differences between measurements were then calculated. The correlation analysis between the thermal and cardiovascular function parameters during the recovery period showed strong positive associations between the Tr-Te difference and measures of cardiovascular fitness (50 < r < 69, p < 0.05). For example, the correlation coefficient between Tr-Te and VO2max reached 0.55 and between Tr-Te and Pmax reached 0.68. The results obtained indicate that the measurement of temporal temperature during and after an intense 3-min bout of exercise can be used to assess aerobic physical capacity and cardiovascular fitness.

The relationship between neurotransmission-related amino acid blood concentrations and neuropsychological performance following acute exercise

Amino acid neurotransmitters, including glutamate, phenylalanine, tyrosine, alanine, and glycine, underlie the majority of the excitatory and inhibitory neurotransmission in the nervous system, and acute exercise has been shown to modulate their concentrations. We aimed to determine whether any correlation exists between the above-mentioned amino acid blood concentrations and the neuropsychological performance after an acute exercise intervention. Sixty basketball players were randomly assigned to one of two experimental conditions: exercise or inactive resting. All participants underwent a comprehensive neuropsychological assessment and blood samples were taken on a Guthrie card before and after the end of the experimental conditions. Amino acid blood concentrations were significantly elevated and cognitive performance significantly improved post-exercise on specific neuropsychological assessments. Significant intervention × group interaction effects were apparent for Trail Making Test part-B [F(1,58) = 20.46, p < .0001, η 2 = .26] and Digit Span Backwards [F(1,58) = 15.47, p < .0001, η 2 = .21] neuropsychological assessments. Additionally, regression analysis indicated that tyrosine accounted for 38.0% of the variance in the Trail Making Test part-A test. These results suggest that elevated blood concentrations of neurotransmission-related amino acids are associated with improved neuropsychological performance after a single bout of high-intensity exercise.

Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington\u2019s disease

Huntington’s disease (HD) mouse models suggest that cardiovascular exercise may enhance neuroplasticity and delay disease signs, however, the effects of exercise on neuroplasticity in people with HD are unknown. Using a repeated-measures experimental design, we compared the effects of a single bout of high-intensity exercise, moderate-intensity exercise, or rest, on motor cortex synaptic plasticity in 14 HD CAG-expanded participants (9 premanifest and 5 early manifest) and 20 CAG-healthy control participants, using transcranial magnetic stimulation. Measures of cortico-motor excitability, short-interval intracortical inhibition and intracortical facilitation were obtained before and after a 20-min bout of either high-intensity interval exercise, moderate-intensity continuous exercise, or rest, and again after intermittent theta burst stimulation (iTBS). HD participants showed less inhibition at baseline compared to controls. Whereas the control group showed increased excitability and facilitation following high-intensity exercise and iTBS, the HD group showed no differences in neuroplasticity responses following either exercise intensity or rest, with follow-up Bayesian analyses providing consistent evidence that these effects were absent in the HD group. These findings indicate that exercise-induced synaptic plasticity mechanisms in response to acute exercise may be attenuated in HD, and demonstrate the need for future research to further investigate exercise and plasticity mechanisms in people with HD.

Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters.

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

A single bout of high-intensity exercise modulates the expression of vitamin D receptor and vitamin D-metabolising enzymes in horse skeletal muscle.

The expressions of vitamin D receptor (VDR) and vitamin D-metabolising enzymes (CYP27B1 and CYP24A1) in skeletal muscle have been reported. However, the regulation of this vitamin D system in horse skeletal muscle after high-intensity exercise has not yet been elucidated. To investigate the effect of high-intensity exercise on the expression of vitamin D system-related proteins in horse skeletal muscle and its associations with skeletal muscle stem cell (SMSC) activity and serum 25(OH)D level. Longitudinal study. Six healthy ponies (5 geldings, 1 mare; age 6.3±2.2years) were studied. Serum and muscle samples were taken from the jugular vein and gluteus medius respectively. Samples were collected at pre-exercise, post-exercise, 1 and 3weeks after a single bout of high-intensity exercise. Protein expression levels of VDR, CYP27B1, CYP24A1, OxPhos and Pax7 (SMSC marker) were determined using immunohistochemical analysis. Oxidative capacity and intramuscular glycogen content were evaluated using histochemical analysis. Blood biochemistry was analysed for lactate concentration and creatine kinase (CK), and 25(OH)D activity. High-intensity exercise significantly upregulated Pax7 and VDR protein expression, which correlated with significantly increased blood lactate and serum CK levels immediately post-exercise. Serum 25(OH)D2 level correlated with CYP27B1 protein expression in skeletal muscle, and it reduced significantly immediately post-exercise and at 1 and 3weeks post-exercise. However, CYP24A1 protein expression was unchanged throughout study periods. The healthy ponies could not represent a fit population of racehorses and eventers. The rapid increase in Pax7 and VDR protein expression along with serum CK level after high-intensity exercise demonstrated an association between SMSC activity and activation of the vitamin D system in response to muscle injury in horses. Moreover, a decrease in CYP27B1 protein expression, correlated with a reduction in serum 25(OH)D2 , may indicate a compromised vitamin D metabolism after high-intensity exercise.

Quantification of exercise-regulated ubiquitin signaling in human skeletal muscle identifies protein modification cross talk via NEDDylation.

The maintenance of muscle function is extremely important for whole body health and exercise is essential to this process. The ubiquitin-proteasome system (UPS) is required for muscle adaptation following exercise but little is known about acute posttranslational regulation and proteome remodeling during and after high-intensity exercise. Here, we used quantitative proteomics to study ubiquitin signaling dynamics in human skeletal muscle biopsies from healthy males before, during, and after a single bout of high-intensity exercise. Exercise resulted in a marked depletion of protein ubiquitylation in the vastus lateralis muscle consistent with proteasome activation. This was also associated with acute posttranslational modification of protein abundance. Integration of these data with phosphoproteomics identified co-regulated proximal modifications suggesting a cross talk between phosphorylation and ubiquitylation. We also identified additional protein modification cross talk and showed acute activation of protein NEDDylation. In vitro experiments revealed that cAMP-dependent activation of the proteasome requires NEDD8, an ubiquitin-like protein involved in protein NEDDylation, to maintain cellular protein ubiquitylation levels. Our data reveal the complexity of ubiquitin signaling and proteome remodeling in muscle during and after high-intensity exercise. We propose a model whereby exercise and the resulting cAMP signaling activate both the proteasome and ubiquitylation via NEDDylation to rapidly remove potentially damaged proteins.

Effects of daily ingestion of sodium bicarbonate on acid-base status and anaerobic performance during an altitude sojourn at high altitude: a randomized controlled trial

BackgroundThe present study investigated the effects of chronic sodium bicarbonate (NaHCO3) ingestion on a single bout of high-intensity exercise and on acid-base balance during 7-day high-altitude exposure.MethodsTen recreationally active subjects participated in a pre-test at sea level and a 7-day hiking tour in the Swiss Alps up to 4554 m above sea level. Subjects received either a daily dose of 0.3 g/kg NaHCO3 solution (n = 5) or water as a placebo (n = 5) for 7 days. Anaerobic high-intensity exercise performance was assessed using the portable tethered sprint running (PTSR) test under normoxic and hypoxic conditions (3585 m). PTSR tests assessed overall peak force, mean force, and fatigue index. Blood lactate levels and blood gas parameters were assessed pre- and post-PTSR. Urinary pH and blood gas parameters were further analyzed daily at rest in early morning samples under normoxic and hypoxic conditions.ResultsThere were no significant differences between the bicarbonate and control group in any of the PTSR-related parameters. However, urinary pH (p = 0.003, ηp2 = 0.458), early morning blood bicarbonate concentration (p < 0.001, ηp2 = 0.457) and base excess (p = 0.002, ηp2 = 0.436) were significantly higher in the bicarbonate group compared with the control group under hypoxic conditions.ConclusionsThese results indicate that oral NaHCO3 ingestion does not ameliorate the hypoxia-induced impairment in anaerobic, high-intensity exercise performance, represented by PTSR-related test parameters, under hypobaric, hypoxic conditions, but the maximal performance measurements may have been negatively affected by other factors, such as poor implementation of PTSR test instructions, pre-acclimatization, the time course of hypoxia-induced renal [HCO3−] compensation, changes in the concentrations of intra- and extracellular ions others than [H+] and [HCO3−], or gastrointestinal disturbances caused by NaHCO3 ingestion. However, chronic NaHCO3 ingestion improves blood bicarbonate concentration and base excess at altitude, which partially represent the blood buffering capacity.

Caffeine Augments the Prothrombotic but Not the Fibrinolytic Response to Exercise.

The purpose of this study was to assess the effect of a single dose of caffeine on measures of coagulation and fibrinolysis before and after a single bout of high-intensity exercise. Forty-eight men (age, 23 ± 3 yr; body mass index, 24 ± 3 kg·m) completed two trials, with 6 mg·kg of caffeine (CAFF) or placebo (PLAC), in random order, followed by a maximal cycle ergometer test. Plasma concentrations of fibrinogen, factor VIII antigen, active tissue plasminogen activator (tPA:c), tissue plasminogen activator antigen (tPA:g), and active plasminogen activator inhibitor-1 (PAI-1:c) were assessed at baseline and immediately after exercise. Exercise led to significant changes in tPA:c (Δ 8.5 ± 4.36 IU·mL for CAFF, 6.6 ± 3.7 for PLAC), tPA:g (Δ 2.4 ± 3.2 ng·mL for CAFF, 1.9 ± 3.1 for PLAC), fibrinogen (Δ 30.6 ± 61.4 mg·dL for CAFF, 28.1 ± 66.4 for PLAC), and PAI-1:c (Δ -3.4 ± 7.9 IU·mL for CAFF, -4.0 ± 12.0 for PLAC) (all P < 0.05), but no effect of condition or time-condition interactions were observed. Main effects of time, condition, and a significant time-condition interaction were observed for factor VIII, which increased from 1.0 ± 0.4 IU·mL to 3.3 ± 1.3 IU·mL with CAFF and 1.0 ± 0.4 IU·mL to 2.4 ± 0.9 IU·mL with PLAC. Coagulation potential during exercise is augmented after caffeine intake, without a similar increase in fibrinolysis. These results suggest caffeine intake may increase risk of a thrombotic event during exercise.

OR-029 Effects of BCAA Plus Glucose Supplement Timing on Inflammatory Response Indicators after a Resistant Exercise

OR-029 Effects of BCAA Plus Glucose Supplement Timing on Inflammatory Response Indicators after a Resistant Exercise

Effect of pre-exercise carbohydrate availability on fat oxidation and energy expenditure after a high-intensity exercise

The aim of this study was to test the hypothesis that reduced pre-exercise carbohydrate (CHO) availability potentiates fat oxidation after an exhaustive high-intensity exercise bout. Eight physically active men underwent a high-intensity exercise (∼95% V̇O2max) until exhaustion under low or high pre-exercise CHO availability. The protocol to manipulate pre-exercise CHO availability consisted of a 90-min cycling bout at ∼70% V̇O2max + 6 × 1-min at 125% V̇O2max with 1-min rest, followed by 48 h under a low- (10% CHO, low-CHO availability) or high-CHO diet (80% CHO, high-CHO availability). Time to exhaustion was shorter and energy expenditure (EE) lower during the high-intensity exercise in low- compared to high-CHO availability (8.6±0.8 and 11.4±1.6 min, and 499±209 and 677±343 kJ, respectively, P<0.05). Post-exercise EE was similar between low- and high-CHO availability (425±147 and 348±54 kJ, respectively, P>0.05), but post-exercise fat oxidation was significantly higher (P<0.05) in low- (7,830±1,864 mg) than in high-CHO availability (6,264±1,763 mg). The total EE (i.e., exercise EE plus post-exercise EE) was similar between low- and high-CHO availability (924±264 and 1,026±340 kJ, respectively, P>0.05). These results suggest that a single bout of high-intensity exercise performed under low-CHO availability increased post-exercise fat oxidation, and even with shorter exercise duration, both post-exercise EE and total EE were not impaired.

Perspectives on high-intensity interval exercise for health promotion in children and adolescents.

Physical activity lowers future cardiovascular disease (CVD) risk; however, few children and adolescents achieve the recommended minimum amount of daily activity. Accordingly, there is virtue in identifying the efficacy of small volumes of high-intensity exercise for health benefits in children and adolescents for the primary prevention of CVD risk. The purpose of this narrative review is to provide a novel overview of the available literature concerning high-intensity interval-exercise (HIIE) interventions in children and adolescents. Specifically, the following areas are addressed: 1) outlining the health benefits observed following a single bout of HIIE, 2) reviewing the role of HIIE training in the management of pediatric obesity, and 3) discussing the effectiveness of school-based HIIE training. In total, 39 HIIE intervention studies were included in this review. Based upon the available data, a single bout of high-intensity exercise provides a potent stimulus for favorable, acute changes across a range of cardiometabolic outcomes that are often superior to a comparative bout of moderate-intensity exercise (14 studies reviewed). HIIE also promotes improvements in cardiorespiratory fitness and cardiometabolic health status in overweight and obese children and adolescents (10 studies reviewed) and when delivered in the school setting (15 studies reviewed). We thus conclude that high-intensity exercise is a feasible and potent method of improving a range of cardiometabolic outcomes in children and adolescents. However, further work is needed to optimize the delivery of HIIE interventions in terms of participant enjoyment and acceptability, to include a wider range of health outcomes, and to control for important confounding variables (eg, changes in diet and habitual physical activity). Finally, research into the application of HIIE training interventions to children and adolescents of different ages, sexes, pubertal status, and sociocultural backgrounds is required.

Equine skeletal muscle adaptations to exercise and training: evidence of differential regulation of autophagosomal and mitochondrial components

BackgroundA single bout of exercise induces changes in gene expression in skeletal muscle. Regular exercise results in an adaptive response involving changes in muscle architecture and biochemistry, and is an effective way to manage and prevent common human diseases such as obesity, cardiovascular disorders and type II diabetes. However, the biomolecular mechanisms underlying such responses still need to be fully elucidated. Here we performed a transcriptome-wide analysis of skeletal muscle tissue in a large cohort of untrained Thoroughbred horses (n = 51) before and after a bout of high-intensity exercise and again after an extended period of training. We hypothesized that regular high-intensity exercise training primes the transcriptome for the demands of high-intensity exercise.ResultsAn extensive set of genes was observed to be significantly differentially regulated in response to a single bout of high-intensity exercise in the untrained cohort (3241 genes) and following multiple bouts of high-intensity exercise training over a six-month period (3405 genes). Approximately one-third of these genes (1025) and several biological processes related to energy metabolism were common to both the exercise and training responses. We then developed a novel network-based computational analysis pipeline to test the hypothesis that these transcriptional changes also influence the contextual molecular interactome and its dynamics in response to exercise and training. The contextual network analysis identified several important hub genes, including the autophagosomal-related gene GABARAPL1, and dynamic functional modules, including those enriched for mitochondrial respiratory chain complexes I and V, that were differentially regulated and had their putative interactions ‘re-wired’ in the exercise and/or training responses.ConclusionHere we have generated for the first time, a comprehensive set of genes that are differentially expressed in Thoroughbred skeletal muscle in response to both exercise and training. These data indicate that consecutive bouts of high-intensity exercise result in a priming of the skeletal muscle transcriptome for the demands of the next exercise bout. Furthermore, this may also lead to an extensive ‘re-wiring’ of the molecular interactome in both exercise and training and include key genes and functional modules related to autophagy and the mitochondrion.

Acute exercise and motor memory consolidation: Does exercise type play a role?

A single bout of high-intensity exercise can augment off-line gains in skills acquired during motor practice. It iscurrently unknown if the type of physical exercise influences the effect on motor skill consolidation. This study investigated the effect of three types of high-intensity exercise following visuomotor skill acquisition on the retention of motor memory in 40 young (25.3±3.6years), able-bodied male participants randomly assigned to one of four groups either performing strength training (STR), circuit training (CT), indoor hockey (HOC) or rest (CON). Retention tests of the motor skill were performed 1 (R1h) and 24h (R1d) post acquisition. For all exercise groups, mean motor performance scores decreased at R1h compared to post acquisition (POST) level; STR (P=0.018), CT (P=0.02), HOC (P=0.014) and performance scores decreased for CT compared to CON (P=0.049). Mean performance scores increased from POST to R1d for all exercise groups; STR (P=0.010), CT (P=0.020), HOC (P=0.007) while performance scores for CON decreased (P=0.043). Changes in motor performance were thus greater for STR (P=0.006), CT (P<0.001) and HOC (P<0.001) compared to CON from POST to R1d. The results demonstrate that high-intensity, acute exercise can lead to a decrease in motor performance assessed shortly after motor skill practice (R1h), but enhances offline effects promoting long-term retention (R1d). Given that different exercise modalities produced similar positive off-line effects on motor memory, we conclude that exercise-induced effects beneficial to consolidation appear to depend primarily on the physiological stimulus rather than type of exercise and movements employed.

Lifelong endurance training attenuates age-related genotoxic stress in human skeletal muscle

BackgroundThe aim of the present study was to determine the influence of age and habitual activity level, at rest and following a single bout of high-intensity exercise, on the levels of three proteins poly(ADP-ribose) polymerase-1 (PARP-1), cleaved-PARP-1 and poly(ADP-ribose) glycohydrolase (PARG), involved in the DNA repair and cell death responses to stress and genotoxic insults. Muscle biopsies were obtained from the vastus lateralis of young trained (22 ± 3 years, n = 6), young untrained (24 ± 4 years, n = 6), old trained (64 ± 3 years, n = 6) and old untrained (65 ± 6 years, n = 6) healthy males before, immediately after and three days following a high-intensity interval exercise bout.ResultsPARP-1, which catalyzes poly(ADP-ribosyl)ation of proteins and DNA in response to a range of intrinsic and extrinsic stresses, was increased at baseline in old trained and old untrained compared with young trained and young untrained participants (P ≤ 0.05). Following exercise, PARP-1 levels remained unchanged in young trained participants, in contrast to old trained and old untrained where levels decreased and young untrained where levels increased (P ≤ 0.05). Interestingly, baseline levels of the cleaved PARP-1, a marker of apoptosis, and PARG, responsible for polymer degradation, were both significantly elevated in old untrained compared with old trained, young trained and young untrained (P ≤ 0.05). Despite this baseline difference in PARG, there was no change in any group following exercise. There was a non-significant statistical trend (P = 0.072) towards increased cleaved-PARP-1 expression post-exercise in younger but not old persons, regardless of training status.ConclusionsCollectively, these results show that exercise slows the progression towards a chronically stressed state but has no impact on the age-related attenuated response to acute exercise. Our findings provide valuable insight into how habitual exercise training could protect skeletal muscle from chronic damage to macromolecules and may reduce sarcopenia in older people.

Endothelial Function in Highly Endurance-Trained Men: Effects of Acute Exercise

Exercise training reverses endothelial dysfunction, but the effect in young, healthy subjects is less clear. We determined the influence of maximal oxygen uptake (VO2max) and a single bout of high-intensity exercise on flow-mediated dilatation (FMD), brachial artery diameter, peak blood flow, nitric oxide (NO) bioavailability, and antioxidant status in highly endurance-trained men and their sedentary counterparts. Ten men athletes (mean +/- SEM age 23.5 +/- 0.9 years, height 182.6 +/- 2.4 cm, weight 72.5 +/- 2.4 kg, VO2max 75.9 +/- 0.8 mL.kg.min) and seven healthy controls (age 25.4 +/- 1.2 years, height 183.9 +/- 3.74 cm, weight 92.8 +/- 3.9 kg, VO2max 47.7 +/- 1.7 mL.kg.min) took part in the study. FMD, brachial artery diameter, and peak blood flow were measured using echo-Doppler before, 1 hour, 24 hours, and 48 hours after a single bout of interval running for 5 x 5 minutes at 90% of maximal heart rate. NO bioavailability and antioxidant status in blood were measured at all time points. Maximal arterial diameter and peak flow were 10-15% (P < 0.02) and 28-35% (P < 0.02) larger, respectively, in athletes vs. controls at all time points, and similar FMD were observed, apart from a transient decay of FMD in athletes 1 hour post exercise. NO bioavailability increased significantly after exercise in both groups and decreased to baseline levels after 24 hours in controls but remained increased 80% and 93% above baseline 24 and 48 hours post exercise in athletes. Antioxidant status was equal in the two groups at baseline and increased by approximately 10% 1 hour post exercise, an effect that lasted for 24 hours. Athletes had larger arterial diameter but similar FMD as untrained subjects, i.e., athletes had larger capacity for blood transport compared with their untrained counterparts. The observed FMD, bioavailability of NO, and antioxidant status in blood were highly dependent on the time elapsed after the exercise session.

Effects of high-intensity training and acute exercise on in vitro function of rat sarcoplasmic reticulum

To evaluate the effects of high-intensity training and/or a single bout of exercise on in vitro function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of interval running program (final training: 2.5-min running x 4 sets per day, 50 m/min at 10% incline). Following training, SR function, i.e., Ca2+-ATPase activity and Ca2+-uptake and release rates, was examined in homogenates of the superficial region of the vastus lateralis muscle from rats subjected to a single bout of treadmill running (50 m/min at 10% incline) for 2.5 min or to exhaustion. Training brought about a 12.4% increase (P < 0.05) in SR Ca2+-uptake rate in rested muscles. This change was not accompanied by alterations in Ca2+-ATPase activity, Ca2+-release rate, Ca2+ dependence of enzyme and protein contents of Ca2+-ATPase and ryanodine receptor. A single bout of high-intensity exercise to exhaustion evoked significant reductions (P < 0.05) in SR function, irrespective of whether or not the animals were trained. For 2.5-min run and exhausted rats, no differences existed between SR functions of untrained and trained muscles. These data suggest that high-intensity training may be capable of enhancing SR Ca2+-sequestering ability, and may not protect against decreasing SR function with high-intensity exercise.

High-intensity exercise acutely decreases the membrane content of MCT1 and MCT4 and buffer capacity in human skeletal muscle

The regulation of intracellular pH during intense muscle contractions occurs via a number of different transport systems [e.g., monocarboxylate transporters (MCTs)] and via intracellular buffering (beta m(in vitro)). The aim of this study was to investigate the effects of an acute bout of high-intensity exercise on both MCT relative abundance and beta m(in vitro) in humans. Six active women volunteered for this study. Biopsies of the vastus lateralis were obtained at rest and immediately after 45 s of exercise at 200% of maximum O2 uptake. Beta m(in vitro) was determined by titration, and MCT relative abundance was determined in membrane preparations by Western blots. High-intensity exercise was associated with a significant decrease in both MCT1 (-24%) and MCT4 (-26%) and a decrease in beta m(in vitro) (-11%; 135 +/- 3 to 120 +/- 2 micromol H+ x g dry muscle(-1) x pH(-1); P < 0.05). These changes were consistently observed in all subjects, and there was a significant correlation between changes in MCT1 and MCT4 relative abundance (R2 = 0.92; P < 0.05). In conclusion, a single bout of high-intensity exercise decreased both MCT relative abundance in membrane preparations and beta m(in vitro). Until the time course of these changes has been established, researchers should consider the possibility that observed training-induced changes in MCT and beta m(in vitro) may be influenced by the acute effects of the last exercise bout, if the biopsy is taken soon after the completion of the training program. The implications that these findings have for lactate (and H+) transport following acute, exhaustive exercise warrant further investigation.