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.

Enjoyment and Affective Responses to Moderate and High-Intensity Exercise: A Randomized Controlled Trial in Individuals with Subsyndromal PTSD.

This crossover randomized controlled trial examined the acute psychological effects of a bout of moderate-intensity continuous aerobic exercise (MICE) and a bout of high-intensity functional exercise (HIFE), relative to a no-exercise sedentary control (SED), in participants (N = 21; 15 f; 24.7 ± 9.3 years) with subsyndromal post-traumatic stress disorder (PTSD). Affective state (Energy, Tiredness, Tension, Calmness) was assessed before (Pre), immediately after (Post 0), 20-min after (Post 20), and 40-min after (Post 40) each condition. Affective valence was assessed during each condition, and exercise enjoyment was assessed at Post 0. Enjoyment was significantly greater following HIFE and MICE relative to SED. Energy was significantly increased Post 0 HIFE and MICE but decreased Post 0 SED. Tension was reduced following all conditions and was significantly lower at Post 40 relative to Pre for HIFE, MICE, and SED. Tiredness was significantly reduced at Post 40 relative to Pre following MICE only, while Calmness was significantly lower at Post 40 relative to Pre following MICE and SED. Overall, both exercise conditions were enjoyed to a greater extent than the control, but MICE may provide greater psychological benefits with respect to Calmness and Tiredness. This study is among the first to assess acute changes in affective states relative to various exercise modes in individuals living with subsyndromal PTSD.

The Impact of High-Intensity Interval Exercise Including Acceleration/Deceleration Patterns on Redox Status of Healthy Male Adults

High-intensity interval exercise (HIIE) is a type of structured physical training characterized by repeated bouts of high-intensity exercise interspersed with recovery periods. Although HIIE was found to improve physical performance in a relatively short period of time, there is emerging evidence suggesting that acute HIIE may induce oxidative stress. The purpose, therefore, of the present study was to examine the effect of intermittency and/or acceleration during HIIE on oxidative stress in male participants. Nine healthy males [(age: 21.0 ± 3.0 years; height: 180.0 ± 4.0 cm; body mass: 79.4 ± 7.9 kg; maximal oxygen uptake (V˙O2max) 52.0 ± 6.0 mL·kg−1·min−1)] were recruited to perform six distinct exercise protocols of various intermittency (high, medium, and low) and acceleration (high, medium, and low) while a control session was also included. Blood samples were obtained to determine oxidative stress indices (lipid hydroperoxides, superoxide dismutase, and total glutathione) at rest, 1 h, 2 h, and 24 h following exercise on a non-motorized treadmill. The intra-individual variability of participants was observed in lipid hydroperoxides at baseline, ranging from 1.80 to 20.69 μmol·L−1. No significant differences among the six different exercise protocols in any of the oxidative stress indices evaluated were observed (p > 0.05). These results suggest that the influence of various intermittency levels and acceleration patterns upon exercise-induced oxidative stress is negligible.

Micro-consolidation occurs when learning an implicit motor sequence, but is not influenced by HIIT exercise

We investigated if micro-consolidation, a phenomenon recently discovered during the brief rest periods between practice when learning an explicit motor sequence, generalises to learning an implicit motor sequence task. We demonstrate micro-consolidation occurs in the absence of explicit sequence awareness. We also investigated the effect of a preceding bout of high-intensity exercise, as exercise is known to augment the consolidation of new motor skills. Micro-consolidation was not modified by exercise.

Exercise-Dependent Modulation of Immunological Response Pathways in Endurance Athletes With and Without Atrial Fibrillation.

Atrial fibrillation (AF) is a common arrhythmia characterized by uncoordinated atrial electrical activity. Lone AF occurs in the absence of traditional risk factors and is frequently observed in male endurance athletes, who face a 2- to 5-fold higher risk of AF compared with healthy, moderately active males. Our understanding of how endurance exercise contributes to the pathophysiology of lone AF remains limited. This study aimed to characterize the circulating protein fluctuations during high-intensity exercise as well as explore potential biomarkers of exercise-associated AF. A prospective cohort of 12 male endurance cyclists between the ages of 40 and 65 years, 6 of whom had a history of exercise-associated AF, were recruited to participate using a convenience sampling method. The circulating proteome was subsequently analyzed using multiplex immunoassays and aptamer-based proteomics before, during, and after an acute high-intensity endurance exercise bout to assess temporality and identify potential markers of AF. The endurance exercise bout resulted in significant alterations to proteins involved in immune modulation (eg, growth/differentiation factor 15), skeletal muscle metabolism (eg, α-actinin-2), cell death (eg, histones), and inflammation (eg, interleukin-6). Subjects with AF differed from those without, displaying modulation of proteins previously known to have associations with incident AF (eg, C-reactive protein, insulin-like growth factor-1, and angiopoietin-2), and also with proteins having no previous association (eg, tapasin-related protein and α2-Heremans-Schmid glycoprotein). These findings provide insights into the proteomic response to acute intense exercise, provide mechanistic insights into the pathophysiology behind AF in athletes, and identify targets for future study and validation.

Fractional amplitude of low-frequency fluctuations associated with μ-opioid and dopamine receptor distributions in the central nervous system after high-intensity exercise bouts.

Dopaminergic, opiod and endocannabinoid neurotransmission are thought to play an important role in the neurobiology of acute exercise and, in particular, in mediating positive affective responses and reward processes. Recent evidence indicates that changes in fractional amplitude of low-frequency fluctuations (zfALFF) in resting-state functional MRI (rs-fMRI) may reflect changes in specific neurotransmitter systems as tested by means of spatial correlation analyses. Here, we investigated this relationship at different exercise intensities in twenty young healthy trained athletes performing low-intensity (LIIE), high-intensity (HIIE) interval exercises, and a control condition on three separate days. Positive And Negative Affect Schedule (PANAS) scores and rs-fMRI were acquired before and after each of the three experimental conditions. Respective zfALFF changes were analyzed using repeated measures ANOVAs. We examined the spatial correspondence of changes in zfALFF before and after training with the available neurotransmitter maps across all voxels and additionally, hypothesis-driven, for neurotransmitter maps implicated in the neurobiology of exercise (dopaminergic, opiodic and endocannabinoid) in specific brain networks associated with "reward" and "emotion." Elevated PANAS Positive Affect was observed after LIIE and HIIE but not after the control condition. HIIE compared to the control condition resulted in differential zfALFF decreases in precuneus, temporo-occipital, midcingulate and frontal regions, thalamus, and cerebellum, whereas differential zfALFF increases were identified in hypothalamus, pituitary, and periaqueductal gray. The spatial alteration patterns in zfALFF during HIIE were positively associated with dopaminergic and μ-opioidergic receptor distributions within the 'reward' network. These findings provide new insight into the neurobiology of exercise supporting the importance of reward-related neurotransmission at least during high-intensity physical activity.

Lower dynamic cerebral autoregulation following acute bout of low-volume high-intensity interval exercise in chronic stroke compared to healthy adults.

Fluctuating arterial blood pressure during high-intensity interval exercise (HIIE) may challenge dynamic cerebral autoregulation (dCA), specifically after stroke after an injury to the cerebrovasculature. We hypothesized that dCA would be attenuated at rest and during a sit-to-stand transition immediately after and 30 min after HIIE in individuals poststroke compared with age- and sex-matched control subjects (CON). HIIE switched every minute between 70% and 10% estimated maximal watts for 10 min. Mean arterial pressure (MAP) and middle cerebral artery blood velocity (MCAv) were recorded. dCA was quantified during spontaneous fluctuations in MAP and MCAv via transfer function analysis. For sit-to-stand, time delay before an increase in cerebrovascular conductance index (CVCi = MCAv/MAP), rate of regulation, and % change in MCAv and MAP were measured. Twenty-two individuals poststroke (age 60 ± 12 yr, 31 ± 16 mo) and twenty-four CON (age 60 ± 13 yr) completed the study. Very low frequency (VLF) gain (P = 0.02, η2 = 0.18) and normalized gain (P = 0.01, η2 = 0.43) had a group × time interaction, with CON improving after HIIE whereas individuals poststroke did not. Individuals poststroke had lower VLF phase (P = 0.03, η2 = 0.22) after HIIE compared with CON. We found no differences in the sit-to-stand measurement of dCA. Our study showed lower dCA during spontaneous fluctuations in MCAv and MAP following HIIE in individuals poststroke compared with CON, whereas the sit-to-stand response was maintained.NEW & NOTEWORTHY This study provides novel insights into poststroke dynamic cerebral autoregulation (dCA) following an acute bout of high-intensity interval exercise (HIIE). In people after stroke, dCA appears attenuated during spontaneous fluctuations in mean arterial pressure (MAP) and middle cerebral artery blood velocity (MCAv) following HIIE. However, the dCA response during a single sit-to-stand transition after HIIE showed no significant difference from controls. These findings suggest that HIIE may temporarily challenge dCA after exercise in individuals with stroke.

Exercise induced plasma volume expansion lowers cardiovascular strain during 15-km cycling time-trial in acute normobaric hypoxia.

The purpose of our study was to assess the influence of a single high-intensity interval exercise (HIIE) bout in normoxia on plasma volume (PV) and consequent cycling performance in normobaric hypoxia (0.15 FiO2, simulating ~2,500 m). Eight males (VO2peak: 48.8 ± 3.4 mL/kg/min, 24.0 ± 1.6 years) completed a hypoxic 15 km cycling time trial (TT), followed by a crossover intervention of either HIIE (8x4 min cycling bouts at 85% of VO2peak) or CON (matched kJ production from HIIE at 50% of VO2peak). 48 hours post intervention, an identical TT was performed. Cardiovascular parameters were measured via impedance cardiography during each TT. Changes in PV was measured 24 and 48 hours post HIIE and CON. HIIE increased PV at 24 (4.1 ± 3.9%, P = 0.031) and 48 (6.7 ± 1.7, P = 0.006) hours post, while no difference was observed following the CON (1.3 ± 1.1% and 0.3 ± 2.8%). The higher PV led to an increased stroke volume (P = 0.03) and cardiac output (P = 0.02) during the hypoxic TT, while heart rate was not changed (P = 0.49). We observed no changes in time to completion (-0.63 ± 0.57 min, P = 0.054) and power output (7.37 ± 7.98 W, P = 0.078) between TTs. In the absence of environmental stress, a single bout of HIIE was an effective strategy to increase PV and reduce the cardiovascular strain during a cycling TT at moderate simulated altitude but did not impact hypoxic exercise performance. Trial registration: Clinical Trials ID: NCT05800808.

Amino acid distribution in blood following high-intensity interval exercise: a preliminary study.

This study investigated the effect of high-intensity interval exercise on total and individual amino acid concentrations in red blood cells (RBCs) and plasma. Seven males (31 ± 13yr) provided venous blood samples at rest, immediately and 15min and 30min following an 8-min high-intensity exercise bout. The exercise bout was 16 × 15s cycle efforts at 0.4N/kg of body mass and 90rpm, interspersed with 15s passive recovery. Total and individual amino acid concentrations of RBC and plasma and blood cell parameters were analysed. No significant differences for total amino acid concentrations between RBC and plasma were found. Individual amino acid analyses showed significant interaction effects for alanine and α-aminoadipic acid (P < 0.05), with plasma alanine significantly increased from baseline across the recovery period (P < 0.001). Blood fraction (group) effects showed greater concentrations of glycine, serine, asparagine, aspartic acid, glutamic acid, α-aminoadipic acid and ornithine in RBC, while greater concentrations of alanine, α-aminobutyric acid, valine, leucine, isoleucine, threonine, proline, phenylalanine, glutamine, tryptophan and cystine were found in plasma (P < 0.05). Comparable levels of histidine, lysine and tyrosine were observed between blood fractions. Significant differences in the variation of total amino acids in RBC were reported with higher variance at rest compared to following exercise (P = 0.01). Haemoglobin, pack cell volume and white blood cell count significantly increased immediately following exercise (P < 0.05) but returned to baseline after 15min recovery. These results support the notion of individualised amino acid transportation roles for RBC and plasma during exercise.

Ammonia Inhalants: Use, Misuse, and Role in Sports Performance.

Ammonia inhalants, also known as smelling salts, are preparations of ammonia designed to treat fainting but more commonly used by athletes to boost awareness and arousal during competition. Despite their widespread use, the physiological and performance-enhancing effects of ammonia inhalants remain poorly understood. The aim of the present study was to review the current literature surrounding the benefits, risks, and physiological effects of ammonia inhalants. An extensive literature review of articles pertaining to ammonia inhalants was performed through MEDLINE and Google Scholar. The search terms "smelling salts," "ammonia inhalants," "strength," "performance," "head injury," and "concussion" were used. Clinical review. Level 4. The physiological response to acute ammonia inhalation includes cerebral vasodilation and heart rate elevation without change in blood pressure. The existing evidence demonstrates an ergogenic benefit to ammonia inhalant use only during repeated bouts of high-intensity exercise; in these subjects, ammonia inhalation was associated with increased power as measured by the Wingate anaerobic test. In contrast, there is no performance benefit to ammonia inhalants in a short burst of maximal effort despite elevated arousal and an associated perception of performance enhancement. Importantly, ammonia inhalants have no role in medical management of head injuries, as they have the potential to exacerbate an underlying brain injury due to the involuntary withdrawal reflex associated with ammonia inhalation. Furthermore, the signs and symptoms of a concussion or more threatening head injury may be masked by ammonia inhalation and lead to continued participation in competition, causing additional harm. Ammonia inhalants have no role in medical management of head injuries and have limited benefit with regards to sports performance. B.

Ghrelin-responsive mediobasal hypothalamic neurons mediate exercise-associated food intake and exercise endurance.

Previous studies have implicated the orexigenic hormone ghrelin as a mediator of exercise endurance and the feeding response postexercise. Specifically, plasma ghrelin levels nearly double in mice when they are subjected to an hour-long bout of high-intensity interval exercise (HIIE) using treadmills. Also, growth hormone secretagogue receptor-null (GHSR-null) mice exhibit decreased food intake following HIIE and diminished running distance (time until exhaustion) during a longer, stepwise exercise endurance protocol. To investigate whether ghrelin-responsive mediobasal hypothalamus (MBH) neurons mediate these effects, we stereotaxically delivered the inhibitory designer receptor exclusively activated by designer drugs virus AAV2-hSyn-DIO-hM4(Gi)-mCherry to the MBH of Ghsr-IRES-Cre mice, which express Cre recombinase directed by the Ghsr promoter. We found that chemogenetic inhibition of GHSR-expressing MBH neurons (upon delivery of clozapine-N-oxide) 1) suppressed food intake following HIIE, 2) reduced maximum running distance and raised blood glucose and blood lactate levels during an exercise endurance protocol, 3) reduced food intake following ghrelin administration, and 4) did not affect glucose tolerance. Further, HIIE increased MBH Ghsr expression. These results indicate that activation of ghrelin-responsive MBH neurons is required for the normal feeding response to HIIE and the usual amount of running exhibited during an exercise endurance protocol.

Regarding the paradox of increased coronary atherosclerosis among highly trained athletes: Might hepcidin be the culprit?

Recent studies have shown that participants of lifelong high-intensity exercise, such as ultramarathon running, compared to individuals engaging in less intense exercise forms, have exhibited more prevalent and severe coronary atherosclerosis. This is counterintuitive to the purported benefits of exercise and this paradox eludes explanation. Interestingly, prolonged bouts of high-intensity exercise have been shown to increase hepcidin concentrations for several hours after exercise. Hepcidin, a hepatic peptide hormone and a central regulator of iron homeostasis, downregulates the expression of the only cellular iron exporter, ferroportin. As such, we posit that the repeated elevations of hepcidin over time among elite athletes lead to increases in arterial wall macrophage iron content, resulting in a proatherogenic macrophage phenotype and subsequent atherosclerosis. Mechanisms and clinical implications are discussed, and more research is suggested.

An acute bout of high-intensity exercise affects nocturnal sleep and sleep-dependent memory consolidation.

Acute exercise has been shown to affect long-term memory and sleep. However, it is unclear whether exercise-induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep-dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross-over design. In two evening sessions, participants either exercised (high-intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired-associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High-intensity interval training lead to an increased declarative memory retention (p = 0.047, d = 0.40) along with a decrease in REM sleep (p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise-induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise-induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise-induced sleep modifications and memory formation which requires further investigation in larger scaled studies.

Muscle miRNAs are influenced by sex at baseline and in response to exercise

BackgroundSex differences in microRNA (miRNA) expression profiles have been found across multiple tissues. Skeletal muscle is one of the most sex-biased tissues of the body. MiRNAs are necessary for development and have regulatory roles in determining skeletal muscle phenotype and have important roles in the response to exercise in muscle. Yet there is limited research into the role and regulation of miRNAs in the skeletal muscle at baseline and in response to exercise, a well-known modulator of miRNA expression. The aim of this study was to investigate the effect of sex on miRNA expression in the skeletal muscle at baseline and after an acute bout of high-intensity interval exercise. A total of 758 miRNAs were measured using Taqman®miRNA arrays in the skeletal muscle of 42 healthy participants from the Gene SMART study (23 males and 19 females of comparable fitness levels and aged 18–45 years), of which 308 were detected. MiRNAs that differed by sex at baseline and whose change in expression following high-intensity interval exercise differed between the sexes were identified using mixed linear models adjusted for BMI and Wpeak. We performed in silico analyses to identify the putative gene targets of the exercise-induced, sex-specific miRNAs and overrepresentation analyses to identify enriched biological pathways. We performed functional assays by overexpressing two sex-biased miRNAs in human primary muscle cells derived from male and female donors to understand their downstream effects on the transcriptome.ResultsAt baseline, 148 miRNAs were differentially expressed in the skeletal muscle between the sexes. Interaction analysis identified 111 miRNAs whose response to an acute bout of high-intensity interval exercise differed between the sexes. Sex-biased miRNA gene targets were enriched for muscle-related processes including proliferation and differentiation of muscle cells and numerous metabolic pathways, suggesting that miRNAs participate in programming sex differences in skeletal muscle function. Overexpression of sex-biased miRNA-30a and miRNA-30c resulted in profound changes in gene expression profiles that were specific to the sex of the cell donor in human primary skeletal muscle cells.ConclusionsWe uncovered sex differences in the expression levels of muscle miRNAs at baseline and in response to acute high-intensity interval exercise. These miRNAs target regulatory pathways essential to skeletal muscle development and metabolism. Our findings highlight that miRNAs play an important role in programming sex differences in the skeletal muscle phenotype.

Acute effects of exercise intensity on butyrylcholinesterase and ghrelin in young men: A randomized controlled study

Background/objectivesButyrylcholinesterase (BChE), a liver-derived enzyme that hydrolyzes acylated ghrelin to des-acylated ghrelin, may trigger a potential mechanism responsible for the acute exercise-induced suppression of acylated ghrelin. However, studies examining the effects of an acute bout of high-intensity exercise on BChE and acylated ghrelin have yielded inconsistent findings. This study aimed to examine the acute effects of exercise intensity on BChE, acylated ghrelin and des-acylated ghrelin concentrations in humans. MethodsFifteen young men (aged 22.7 ± 1.8 years, mean ± standard deviation) completed three, half-day laboratory-based trials (i.e., high-intensity exercise, low-intensity exercise and control), in a random order. In the exercise trials, the participants ran for 60 min (from 09:30 to 10:30) at a speed eliciting 70 % (high-intensity) or 40 % (low-intensity) of their maximum oxygen uptake and then rested for 90 min. In the control trial, participants sat on a chair for the entire trial (from 09:30 to 12:00). Venous blood samples were collected at 09:30, 10:00, 10:30, 11:00, 11:30 and 12:00. ResultsThe BChE concentration was not altered over time among the three trials. Total acylated and des-acylated ghrelin area under the curve during the first 60 min (i.e., from 0 min to 60 min) of the main trial were lower in the high-intensity exercise trial than in the control (acylated ghrelin, mean difference: 62.6 pg/mL, p < 0.001; des-acylated ghrelin, mean difference: 31.4 pg/mL, p = 0.035) and the low-intensity exercise trial (acylated ghrelin, mean difference: 87.7 pg/mL, p < 0.001; des-acylated ghrelin, mean difference: 43.0 pg/mL, p = 0.042). ConclusionThe findings suggest that BChE may not be involved in the modulation of ghrelin even though lowered acylated ghrelin concentration was observed after high-intensity exercise.

Ageing attenuates exercise-enhanced motor cortical plasticity.

Cardiorespiratory exercise is known to modulate motor cortical plasticity in young adults, but the influence of ageing on this relationship is unknown. Here, we compared the effects of a single session of cardiorespiratory exercise on motor cortical plasticity in young and older adults. We acquired measures of cortical excitatory and inhibitory activity of the primary motor cortex using transcranial magnetic stimulation (TMS) from 20 young (mean±SD = 25.30 ± 4.00 years, 14 females) and 20 older (mean±SD = 64.10 ± 6.50 years, 11 females) healthy adults. Single- and paired-pulse TMS measurements were collected before and after a 20min bout of high-intensity interval cycling exercise or an equivalent period of rest, and again after intermittent theta burst stimulation (iTBS). In both young (P = 0.027, Cohen's d = 0.87) and older adults (P = 0.006, Cohen's d = 0.85), there was an increase in glutamatergic excitation and a reduction in GABAergic inhibition from pre- to postexercise. However, in contrast to younger adults, older adults showed an attenuated plasticity response to iTBS following exercise (P = 0.011, Cohen's d = 0.85). These results demonstrate an age-dependent decline in cortical plasticity and indicate that a preceding bout of high-intensity interval exercise might be less effective for enhancing primary motor cortex plasticity in older adults. Our findings align with the hypothesis that the capacity for cortical plasticity is altered in older age. KEY POINTS: Exercise enhances motor cortical plasticity in young adults, but how ageing influences this effect is unknown. Here, we compared primary motor cortical plasticity responses in young and older adults before and after a bout of high-intensity interval exercise and again after a plasticity-inducing protocol, intermittent theta burst stimulation. In both young and older adults, exercise led to an increase in glutamatergic excitation and a reduction in GABAergic inhibition. Our key result was that older adults showed an attenuated plasticity response to theta burst stimulation following exercise, relative to younger adults. Our findings demonstrate an age-dependent decline in exercise-enhanced cortical plasticity and indicate that a preceding bout of high-intensity interval exercise might be less effective for enhancing primary motor cortex plasticity in older adults.

The Effects of Acute Bouts of Aerobic Exercise on Adipokine Concentrations in Individuals with Moderate Stages of Chronic Kidney Disease

This study examined the effects of two different acute bouts of treadmill running (e.g., steady-state moderate-intensity exercise (SSE) and high-intensity interval exercise (HIIE)) on adipokine (e.g., adiponectin, leptin, and omentin) concentrations in individuals with moderate stages of chronic kidney disease (CKD). Fourteen participants (8 females and 6 males) (age 58.7 ± 9.7, height (cm) 168.5 ± 9.7, weight (kg) 83.5 ± 18.2) were classified as having moderate stages of CKD (stages G3a and G3b; estimated glomerular filtration rate (eGFR) between 59 and 30 mL/min/1.73 m2). Participants completed 30 min of either SSE at 65% oxygen consumption reserve (VO2R) or HIIE for 3 min at a 90% VO2R separated by 2 min of slow walking (20% VO2R) in a randomized, crossover design on a treadmill. Venous blood samples were obtained at baseline, 1 h, and 24 h post exercise. Data were analyzed using a two by three repeated measures ANOVA (p &lt; 0.05). There were no significant differences in adiponectin (p &lt; 0.353), leptin (p &lt; 0.084), and omentin (p &lt; 0.235) concentrations between SSE and HIIE. Similarly, no significant differences were seen between the sampled time points for either aerobic exercise condition. In conclusion, this study demonstrated there were no changes in adiponectin, leptin, or omentin concentrations when performing an acute bout of HIIE or SSE for 30 min, at 1 or 24 h post exercise. Future studies should seek to either increase the duration of the exercise bout or identify different adipokines to examine for patients experiencing moderate stages of CKD.

Benefits beyond cardiometabolic health: the potential of frequent high intensity 'exercise snacks' to improve outcomes for those living with and beyond cancer.

High intensity interval training (HIIT) has been shown to consistently elicit rapid and significant adaptations in a number of physiological systems, across many different healthy and clinical populations. In addition, there is increasing interest in how some acute, yet transient responses to high intensity exercise potentially reduce the risks of particular diseases. Recent work has shown that discrete, brief bouts of high intensity exercise (termed 'exercise snacks') can improve glucose control and vascular health and thus counter the negative cardiometabolic consequences of prolonged, uninterrupted periods of inactivity. In this brief review, we advance the case, using evidence available from pre-clinical studies in the exercise oncology literature, that brief, frequently completed bouts of high intensity exercise embedded within an individual's overall daily and weekly physical activity schedule, may transiently impact the tumour microenvironment and improve the health outcomes for those who have been diagnosed and treated for cancer.

Effects of an Acute High Intensity Exercise Bout on Retention of Explicit, Strategic Locomotor Learning in Individuals With Chronic Stroke

Background Exercise priming, pairing high intensity exercise with a motor learning task, improves retention of upper extremity tasks in individuals after stroke, but has shown no benefit to locomotor learning. This difference may relate to the type of learning studied. Upper extremity studies used explicit, strategic tasks; locomotor studies used implicit sensorimotor adaptation (split-belt treadmill). Since walking is an important rehabilitation goal, it is crucial to understand under which circumstances exercise priming may improve retention of a newly learned walking pattern. Objective Determine the impact of exercise priming on explicit, strategic locomotor learning task retention in chronic stroke survivors. Methods Chronic stroke survivors (>6 months) performed 2 treadmill walking sessions. Visual feedback was used to train increased step length. Participants were assigned to control group (no exercise), continuous exercise (5 minutes high intensity), or long-interval exercise (15 minutes high/moderate intervals). After day 1 learning, participants either rested or performed exercise. On day 2, retention of the learned walking pattern was tested. Results All groups learned on day 1 (P < .001). The 2 priming groups showed significant changes in blood lactate and heart rate after exercise priming, the resting control group did not (P < .001). On day 2, there was no significant between-group difference in cued or un-cued task retention (P = .963 and .287, respectively). Conclusions Exercise priming did not affect retention of an explicit locomotor task in chronic stroke survivors. Further work should explore subgroups of individuals for whom priming may have selective clinical benefit to locomotor learning. ClinicalTrials.gov Identifier: NCT03726047

The Effect of High-Intensity Interval Exercise on Short-Term Glycaemic Control, Serum Level of Key Mediator in Hypoxia and Pro-Inflammatory Cytokines in Patients with Type 1 Diabetes-An Exploratory Case Study.

Type 1 diabetes (T1D) is associated with hyperglycaemia-induced hypoxia and inflammation. This study assessed the effects of a single bout of high-intensity interval exercise (HIIE) on glycaemia (BG) and serum level of pro-inflammatory cytokines, and an essential mediator of adaptive response to hypoxia in T1D patients. The macronutrient intake was also evaluated. Nine patients suffering from T1D for about 12 years and nine healthy individuals (CG) were enrolled and completed one session of HIIE at the intensity of 120% lactate threshold with a duration of 4 × 5 min intermittent with 5 min rests after each bout of exercise. Capillary and venous blood were withdrawn at rest, immediately after and at 24 h post-HIIE for analysis of BG, hypoxia-inducible factor alpha (HIF-1α), tumour necrosis factor alpha (TNF-α) and vascular-endothelial growth factor (VEGF). Pre-exercise BG was significantly higher in the T1D patients compared to the CG (p = 0.043). HIIE led to a significant decline in T1D patients' BG (p = 0.027) and a tendency for a lower BG at 24 h post-HIIE vs. pre-HIIE. HIF-1α was significantly elevated in the T1D patients compared to CG and there was a trend for HIF-1α to decline, and for VEGF and TNF-α to increase in response to HIIE in the T1D group. Both groups consumed more and less than the recommended amounts of protein and fat, respectively. In the T1D group, a tendency for a higher digestible carbohydrate intake and more frequent hyperglycaemic episodes on the day after HIIE were observed. HIIE was effective in reducing T1D patients' glycaemia and improving short-term glycaemic control. HIIE has the potential to improve adaptive response to hypoxia by elevating the serum level of VEGF. Patients' diet and level of physical activity should be screened on a regular basis, and they should be educated on the glycaemic effects of digestible carbohydrates.