Jeremiah Peiffer

Background
Multiple sessions of walking with blood flow restriction (BFR) of the legs can improve cardiovascular fitness, muscle strength and hypertrophy in older adults. However, it is unclear whether BFR impairs walking balance acutely, potentially increasing falls risk during BFR training for this at-risk population.

Research Question
Does bilateral BFR of the legs acutely worsen walking balance of older adults?

Methods
Ten older adults (mean age: 73, SD: 3 y) walked for 10 min on a treadmill at 50 %, 60 % and 70 % of their fast walking speed, with 10 cm-wide cuffs on the proximal thigh of both legs inflated to 0 % (no cuff), 40 % or 60 % of arterial occlusion pressure. We measured four characteristics of walking balance which were selected a priori and combined into a gait quality index predictive of future falls in older adults: autocorrelation of vertical accelerations; magnitude and harmonicity of sideways accelerations; and magnitude of the dominant period of forwards accelerations.

Results
Walking balance worsened with BFR, independent of walking speed, for all outcomes except the magnitude of the dominant period of forwards accelerations, with worse balance observed with increasing cuff pressure. Compared to no BFR, gait quality declined 12 % when walking with 50 % occlusion and declined 20 % with 60 % occlusion (p < 0.001).

Significance
Our findings suggest that BFR results in poorer acute walking balance, with a dose-response relationship for cuff pressure. Supervised walking trials are warranted to further assess the safety of BFR training in community settings and whether these balance-related changes may stimulate beneficial chronic balance adaptations.

Background Physical activity and sleep are both related to brain health, and these lifestyle factors also share a bi‐directional relationship. However, in the context of cognitive function, sleep and physical activity are seldom considered together in cross‐sectional studies, and the influence of each lifestyle factor in the context of interventions (e.g., exercise) remains unclear. The purpose of this research is to investigate whether sleep and physical activity may interact to influence brain health in older adults. Method This will present data from two studies. The first is a previously unpublished cross‐sectional study in healthy older adults (n = 589; 69.8 ±3.7 years). Sleep was measured via the Pittsburgh Sleep Quality Index (PSQI) and both sleep and physical activity were measured via 24‐hour actigraphy for 7 days. We investigated the moderating influence of physical activity on associations between sleep and cognitive function in five domains. Secondly, we will present published data from a randomized controlled trial which was a 6‐month, supervised exercise intervention in 89 cognitively unimpaired older adults (68.76±5.32 years). We investigated the influence of baseline sleep, measured by PSQI, on exercise‐induced cognitive improvement across the course of the intervention. Result Cross‐sectionally, moderate‐to‐vigorous physical activity (MVPA) moderated the association between self‐reported sleep efficiency and episodic memory, processing speed, EF/attentional control, and working memory (β[range] = ‐0.10 – ‐0.17, all p < .05). Light physical activity moderated the association of actigraphy‐measured WASO with EF/attentional control and processing speed (βs = 0.10, all p < .05). The direction of these results was such that the association between lower sleep efficiency and greater WASO with poorer cognitive performance was stronger in those with low physical activity levels. From our exercise intervention study, we found that that those with poorer sleep efficiency at baseline showed the greatest exercise‐induced improvements in episodic memory from pre‐ to post‐intervention (β=−0.024, p = 0.004). Conclusion Our results suggest that physical activity and sleep interact to influence cognitive function, and the efficacy of exercise interventions to improve cognition may be influenced by sleep. Taken together, our data suggest that physical activity may compensate for some negative influences of poor sleep on cognition.

To compare the physiological and perceptual responses during fixed‐power and perceptually regulated cycling, both without and with blood flow restriction (CONPWR, BFRPWR, CONRPE and BFRRPE). Twelve recreationally active men cycled for 10 min at the power corresponding to the first ventilatory threshold or, for CONRPE and BFRRPE, the perceived exertion level reported during CONPWR. Blood flow restriction was set at 60% of estimated arterial occlusion pressure. Ventilatory measures and heart rate were averaged into 2‐min blocks. Perceived exertion, effort, muscular discomfort and cuff pain were recorded every 2 min (0–10 scale). Blood lactate was measured pre‐exercise, post‐exercise, and 2 min post‐exercise. The BFRPWR trial elicited greater physiological and perceptual responses compared to all other conditions. Oxygen consumption during BFRRPE was lower than CONPWR (−19.2 ± 20.6%, p < 0.001) and CONRPE (−6.7 ± 9.3%, p = 0.007). Heart rate during CONPWR was greater than BFRRPE (8.2 ± 9.8%, p < 0.001) and CONRPE (9.4 ± 6.5%, p < 0.001). Blood lactate concentration was not different between CONPWR, CONRPE and BFRRPE; yet was greater during fixed‐power compared to fixed‐RPE trials (31.5 ± 25.6%, p < 0.001). Muscular discomfort was not different between BFRRPE and CONPWR (2.4 ± 1.1 au), yet both were greater compared to CONRPE (1.8 ± 1.5 au, p < 0.001). Cuff pain was greater during BFRPWR (3.3 ± 1.7 au) compared to BFRRPE (2.2 ± 1.1 au, p < 0.001). Prescribing aerobic BFR cycling at a fixed power output increases physiological strain, yet discomfort and pain are also heightened, which may limit its use in healthy adults. The fixed‐RPE method appears to balance the physiological and perceptual demands and thus could be a viable alternative if a fixed power output approach is intolerable.

Introduction
This study examined longitudinal associations between self-reported exercise and cognition, with moderation by sex, in individuals with autosomal dominant Alzheimer's disease (ADAD) mutations. We also examined whether changes in exercise over time differed in ADAD mutation carriers versus non-carriers in the years preceding first cognitive symptom onset.

Methods
Participants (n = 491) were ADAD mutation carriers (63%) and non-carriers (37%) from the Dominantly Inherited Alzheimer Network aged 37.6 ± 11.1 years. Participants reported their average time partaking in various leisure-time exercise activities over the past 12 months.

Results
Greater baseline exercise predicted better longitudinal cognitive performance. Sex did not moderate these associations. In the years preceding first cognitive symptoms or last follow-up visit, mutation carriers showed a decline in their exercise engagement compared to mutation non-carriers.

Discussion
Self-reported exercise is associated with preserved cognitive function in those with ADAD mutations; however, AD-related pathways may influence the level of engagement in exercise prior to cognitive symptom onset.

Highlights
• Greater weekly exercise predicts slower cognitive decline in ADAD mutation carriers.
• These associations varied dependent on closeness to estimated symptom onset.
• These associations were not moderated by sex.
• Weekly exercise declined in ADAD mutation carriers compared to non-carriers.
• Results may suggest a bidirectional relationship between exercise and AD risk.

Type 2 diabetes mellitus (T2DM) is a common metabolic disorder characterized by chronic hyperglycaemia, with physical inactivity and excessive adiposity as predisposing factors. This clinical trial aimed to investigate the effects of an exercise intervention on the metabolome of T2DM participants, fasting and in response to an oral glucose tolerance test (OGTT) and an acute exercise stimulus. Thirteen people with T2DM (age 51 ± 7 years; body mass index 32.7 ± 4.9 kg/m2) completed 45 min of moderate-intensity treadmill exercise on 12 days consecutively. Blood samples were collected before and after the first and last training sessions and during a pre- and postintervention OGTT. Fasted blood samples were collected from 198 healthy control subjects and 208 people with T2DM from an independent cohort for comparison. Samples were analysed using high-resolution 1H nuclear magnetic resonance spectroscopy and liquid chromatography–mass spectrometry. The exercise intervention did not induce a shift towards a healthier fasted metabolome in people living with T2DM. In response to consumption of a glucose bolus (OGTT), glycolysis-related metabolites increased and free fatty acids decreased, with no effect of the exercise intervention. In response to acute exercise, glucose and amino acids decreased and free fatty acids increased, with similar responses on the last day of training as on the first day, indicating no effect of the intervention. The clinical trial was registered prospectively in the Australian New Zealand Clinical Trials Registry ACTRN12617000286347 on 24 February 2017.

Purpose : To explore how graded hypoxia affects perceptual sensations during heart-rate (HR) -clamped cycling using qualitative methods.

Methods : Sixteen trained males cycled for 60 minutes on separate visits, with their HR clamped at 80% of their first ventilatory threshold across simulated altitudes of 2500 m, 3000 m, 3500 m, and 4000 m and in normoxia. After each session, an ∼10-minute structured interview was conducted to gather insights into participants’ perceptions of the exercise under each condition. Interview transcripts were analyzed for key themes, which were presented in a pen profile.

Results : At 4000 m, 5 participants perceived light-headedness and 2 had difficulty focusing, which were not experienced at lower altitudes. Difficulty breathing increased progressively with hypoxic severity, from 1 report in normoxia to 9 at 4000 m. Limb discomfort was consistently reported across all conditions.

Conclusion : Despite comparable physiological responses during HR-clamped cycling, hypoxia severity influenced selected perceived sensations (ie, difficulty focusing, difficulty breathing, and light-headedness). These effects should be considered when selecting the desired hypoxic severity for HR-clamped cycling.

Boynton, JR, Peiffer, JJ, and Abbiss, CR. Effects of HIIT in cool and hot on temperate performance and physiological response in trained cyclists. J Strength Cond Res 39(3): e485-e495, 2025-This study investigated cardiopulmonary responses in hot and cool high-intensity interval training (HIIT) and the subsequent effects on time-trial (TT) performance and physiological responses in temperate conditions. Twenty trained cyclists were separated into 2 groups and completed a 4-week HIIT intervention (8 sessions, 5 × 4 minute) at an environmental temperature (TA) of either 13° C (HIIT13) or 35° C (HIIT35). Cardiorespiratory data (e.g., heart rate [HR] and time above 90% V̇o2max [T > 90% V̇o2max]) were assessed for the first and last interval sessions. Subjects completed 20 km TTs in temperate conditions (22° C) before (TT1) and after (TT2) HIIT training, during which power output, HR, and thermoregulatory measures were recorded. T > 90% V̇o2max was greater in HIIT13 (875 ± 295 seconds; p = 0.007), compared with HIIT35 (420 ± 395 seconds). Average power output during the TT increased from TT1 to TT2 in both groups (HIIT13p = 0.023, 3.3 ± 3.4%; HIIT35p = 0.003, 7.3 ± 6.3%) but with no significant interactions or differences between groups (p = 0.115; p = 0.421, respectively). Within-subject increases for HR and core temperature were observed during TT2 for HIIT13 (2.7 ± 2.1%, 0.5 ± 0.6%) but not HIIT35 (1.5 ± 4.9%, 0.0 ± 0.7%). After 4 weeks of HIIT, the improvement in temperate 20-km TT performance was not greater for HIIT13 than HIIT35, despite greater T > 90% V̇o2max during 13° C HIIT vs. 35° C HIIT. Physiological responses (e.g., HR and thermoregulation) during the TT differed between HIIT13 and HIIT35, indicating varying adaptive responses.

Background
Accumulating evidence indicates exercise may delay or prevent the onset of Alzheimer’s disease (AD). To our knowledge, no study has investigated the longitudinal impact of exercise on AD-related biomarkers in individuals with Autosomal dominant Alzheimer’s disease (ADAD) mutations who are destined to develop AD. This study examined longitudinal associations between self-reported exercise levels and AD-related biomarkers in a cohort of ADAD mutation carriers and investigated whether observed associations depended upon disease stage.

Method
This prospective cohort study included participants from the Dominantly Inherited Alzheimer’s Network (DIAN). Participants were n = 308 ADAD mutation carriers aged 39.7 ± 10.8 years (56.5% female) with data available for self-reported exercise participation and either brain imaging (hippocampal volume, total volume, gray matter volume, white matter hyperintensities, brain Aβ), or biomarkers quantified from cerebrospinal fluid (Aβ40, Aβ42, p-tau, t-tau, p-tau/Aβ42, and Aβ42/40). Associations between exercise and AD biomarkers (i.e., from brain imaging and CSF) were examined using linear mixed models.

Result
Greater weekly baseline exercise was associated with slower accumulation of brain Aβ at preclinical disease stages (β = -0.16, 95% CI -0.23 – -0.08), and slower decline of right and left hippocampal volume (β = 0.06, 95% CI 0.03–0.08; β = 0.06, 95% CI 0.02–0.09, respectively), total cortical volume (β = 0.03, 95% CI 0.01–0.05), total subcortical gray matter volume (β = 0.03, 95% CI 0.01–0.05), and total gray matter volume (β = 0.03, 95% CI 0.01–0.05), effects which became significant approximately 5 years before predicted cognitive symptom onset.

Conclusion
These findings demonstrate that exercise is associated with more favourable profiles of AD-related biomarkers in those with ADAD mutations. The causal direction of this research is difficult to ascertain, thus future study designs investigating the therapeutic potential of exercise in both ADAD and late-onset AD should be considered before clinical recommendation of exercise is implemented.

This study examined internal, external training loads, internal:external ratios, and aerobic adaptations for acute and short-term chronic repeated-sprint training (RST) with blood flow restriction (BFR). Using randomised crossover (Experiment A) and between-subject (Experiment B) designs, 15 and 24 semi-professional Australian footballers completed two and nine RST sessions, respectively. Sessions comprised three sets of 5-7 × 5-second sprints and 25 seconds recovery, with continuous BFR (45% arterial occlusion pressure) or without (Non-BFR). Banister's, Edwards', Lucia's training impulse, and session rating of perceived exertion training load (sRPE
) were calculated. External training loads were determined by total work done (TWD). Ventilatory threshold power outputs were assessed during a graded exercise test post-RST. Internal training loads were comparable between conditions, though BFR reduced (
 < 0.02) TWD during acute (-4.9%) and short-term chronic (-10.0%) RST compared to Non-BFR. Furthermore, BFR increased (
 = 0.049) the sRPE
:TWD ratio during short-term chronic (+14.8%), but not acute RST. First and second ventilatory threshold power outputs improved (+8.3% and + 4.2%, respectively) similarly for both groups following RST. Repeated exposure to progressively overloaded RST with BFR increases internal demands for a given workload, which may promote beneficial physiological adaptations compared to Non-BFR, though aerobic performance was not further enhanced.

Objectives
There are currently 29 genome regions that demonstrate associations with Alzheimer's disease (AD) risk. Regular physical exercise can promote systemic change in gene expression and may modify the risk of cognitive decline and AD. This study is a secondary analysis of a randomised controlled trial and examines the effect of a six-month exercise intervention versus control on AD-related gene expression.

Design
Single-site parallel pilot randomised controlled trial.

Methods
91 cognitively unimpaired older adults were enrolled in the Intense Physical Activity and Cognition (IPAC) study. Participants were randomised into one of three groups: high-intensity exercise, moderate-intensity exercise, or inactive control for six months. Blood samples were collected prior to, and within two weeks of intervention completion, for later expression analysis of 96 genes. To explore the relationship between changes in gene expression and the intervention groups, an interaction term (“timepoint × intervention group”) was subsequently used.

Results
There were no significant differences in gene expression between the three intervention groups at baseline, nor after the intervention. Within groups, five genes were upregulated, seven were downregulated and the remainder remained unchanged. None of the examined genes showed significant change from pre- to post-intervention in the exercise groups compared to the control.

Conclusions
Exercise does not change AD-related gene expression in cognitively unimpaired older adults. Several gene expression targets have been identified for further study.