High-fat diets may induce β-cell dysfunction. This study compared how young and older adults responded to a high-fat meal with regard to β-cell function and whether exercise comparably impacted glucose regulation. Older adults secreted more insulin during the high-fat meal than younger adults. Although exercise increased β-cell function adjusted for skeletal muscle insulin sensitivity in relation to glucose tolerance, it raised adipose insulin resistance and reduced pancreatic β-cell function relative to adipose tissue in older adults. Additional work is needed to discern nutrient-exercise interactions across age to mitigate chronic disease risk.

The purpose of the present study was to determine fasting and high-fat meal (HFM)-induced post-prandial systemic inflammation and airway inflammation (exhaled nitric oxide (eNO)) in older adults (OAs) compared to younger adults (YAs) before and after acute exercise. Twelve YAs (23.3 ± 3.9 y n = 5 M/7 F) and 12 OAs (67.7 ± 6 y, n = 8 M/4 F) completed two HFM challenges. After an overnight fast, participants underwent an HFM session or pre-prandial exercise (EX, 65% VO2Peak to expend 75% of the caloric content of the HFM) plus HFM (EX + HFM) in a randomized order. Systemic inflammatory cytokines were collected at 0, 3, and 6 h, while eNO was determined at 0, 2, and 4 h after the HFM (12 kcal/kg body weight: 61% fat, 35% CHO, 4% PRO). TNF-α was higher in OAs compared to YAs (p = 0.005) and decreased across time from baseline to 6 h post-HFM (p = 0.007). In response to the HFM, IL-6 decreased from 0 to 3 h but increased at 6 h regardless of age or exercise (p = 0.018). IL-8 or IL-1β did not change over the HFM by age or exercise (p > 0.05). eNO was also elevated in OAs compared to YAs (p = 0.003) but was not altered by exercise (p = 0.108). There was a trend, however, towards significance post-prandially in OAs and YAs from 0 to 2 h (p = 0.072). TNF-α and eNO are higher in OAs compared to YAs but are not elevated more in OAs post-prandially compared to YAs. Primary systemic inflammatory cytokines and eNO were not modified by acute exercise prior to an HFM.

AbstractA single high-fat, high-carbohydrate meal (HFHC) results in elevated postprandial glucose (GLU), triglycerides (TAG) and metabolic load index (MLI; TAG (mg/dl) + GLU (mg/dl)) that contributes to chronic disease risk. While disease risk is higher in older adults (OA) compared to younger adults (YA), the acute effects of exercise on these outcomes in OA is understudied. Twelve YA (age 23.3 ± 3.9 yrs, n = 5 M/7 F) and 12 OA (age 67·7 ± 6.0 yrs, n = 8 M/4 F) visited the laboratory in random order to complete a HFHC with no exercise (NE) or acute exercise (EX) condition. EX was performed 12 hours prior to HFHC at an intensity of 65 % of maximal heart rate to expend 75 % of the kcals consumed in HFHC (Marie Callender’s Chocolate Satin Pie; 12 kcal/kgbw; 57 % fat, 37 % CHO). Blood samples were taken at 0, 30, 60, 90 minutes, and then every hour until 6 hours post-meal. TAG levels increased to a larger magnitude in OA (Δ∼61 ± 31 %) compared to YA (Δ∼37 ± 34 %, P < 0·001), which were attenuated in EX compared to NE (P < 0·05) independent of age. There was no difference in GLU between OA and YA after the HFM, however, EX had attenuated GLU independent of age (NE: Δ∼21 ± 26 %; EX: Δ∼12 ± 18 %, P = 0·027). MLI was significantly lower after EX compared to NE in OA and YA (P < 0·001). Pre-prandial EX reduced TAG, GLU and MLI post-HFHC independent of age.

Movement DisordersVolume 35, Issue 7 p. 1286-1286 Letters: Published Articles Reply to: Exercise for “Sleep Rehabilitation” in Parkinson's Disease Amy W. Amara MD, PhD, Corresponding Author amyamara@uab.edu Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USACorrespondence to: Dr. Amy W. Amara, SC360A, 1720 2nd Ave. S, Birmingham, AL 35294-0017, USA; E-mail: amyamara@uab.eduSearch for more papers by this authorKimberly H. Wood PhD, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Psychology, Samford University, Birmingham, Alabama, USASearch for more papers by this authorAllen Joop MS, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorRaima A. Memon MD, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorJennifer Pilkington, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorS. Craig Tuggle MA, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorJohn Reams MA, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorMatthew J. Barrett MD, Department of Neurology, University of Virginia, Charlottesville, Virginia, USASearch for more papers by this authorDavid A. Edwards PhD, Department of Kinesiology, University of Virginia, Charlottesville, Virginia, USASearch for more papers by this authorArthur L. Weltman PhD, Department of Kinesiology, University of Virginia, Charlottesville, Virginia, USASearch for more papers by this authorChristopher P. Hurt PhD, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorGary Cutter PhD, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorMarcas M. Bamman PhD, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA Geriatric Research, Education, and Clinical Center, Birmingham VA Medical Center, Birmingham, Alabama, USASearch for more papers by this author Amy W. Amara MD, PhD, Corresponding Author amyamara@uab.edu Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USACorrespondence to: Dr. Amy W. Amara, SC360A, 1720 2nd Ave. S, Birmingham, AL 35294-0017, USA; E-mail: amyamara@uab.eduSearch for more papers by this authorKimberly H. Wood PhD, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Psychology, Samford University, Birmingham, Alabama, USASearch for more papers by this authorAllen Joop MS, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorRaima A. Memon MD, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorJennifer Pilkington, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorS. Craig Tuggle MA, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorJohn Reams MA, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorMatthew J. Barrett MD, Department of Neurology, University of Virginia, Charlottesville, Virginia, USASearch for more papers by this authorDavid A. Edwards PhD, Department of Kinesiology, University of Virginia, Charlottesville, Virginia, USASearch for more papers by this authorArthur L. Weltman PhD, Department of Kinesiology, University of Virginia, Charlottesville, Virginia, USASearch for more papers by this authorChristopher P. Hurt PhD, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorGary Cutter PhD, University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USASearch for more papers by this authorMarcas M. Bamman PhD, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA University of Alabama, Center for Exercise Medicine, Birmingham, Alabama, USA Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA Geriatric Research, Education, and Clinical Center, Birmingham VA Medical Center, Birmingham, Alabama, USASearch for more papers by this author First published: 21 July 2020 https://doi.org/10.1002/mds.28132 Relevant conflicts of interests/financial disclosures:: Nothing to report. Funding agencies:: This study was funded by the National Institutes of Health (K23NS080912, T32 HD071866), Parkinson's Disease Foundation, The Manning Foundation, The Curry Foundation at the University of Virginia, UAB Center for Exercise Medicine, and the National Institutes of Health National Rehabilitation Research Resource to Enhance Clinical Trials (REACT, P2CHD086851). Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume35, Issue7July 2020Pages 1286-1286 RelatedInformation

Background Sleep dysfunction is common and disabling in persons with Parkinson's Disease (PD). Exercise improves motor symptoms and subjective sleep quality in PD, but there are no published studies evaluating the impact of exercise on objective sleep outcomes. The goal of this study was to to determine if high-intensity exercise rehabilitation combining resistance training and body-weight interval training, compared with a sleep hygiene control improved objective sleep outcomes in PD. Methods Persons with PD (Hoehn & Yahr stages 2-3; aged >= 45 years, not in a regular exercise program) were randomized to exercise (supervised 3 times a week for 16 weeks; n = 27) or a sleep hygiene, no-exercise control (in-person discussion and monthly phone calls; n = 28). Participants underwent polysomnography at baseline and post-intervention. Change in sleep efficiency was the primary outcome, measured from baseline to post-intervention. Intervention effects were evaluated with general linear models with measurement of group x time interaction. As secondary outcomes, we evaluated changes in other aspects of sleep architecture and compared the effects of acute and chronic training on objective sleep outcomes. Results The exercise group showed significant improvement in sleep efficiency compared with the sleep hygiene group (group x time interaction:F= 16.0,P < 0.001,d= 1.08). Other parameters of sleep architecture also improved in exercise compared with sleep hygiene, including total sleep time, wake after sleep onset, and slow-wave sleep. Chronic but not acute exercise improved sleep efficiency compared with baseline. Conclusions High-intensity exercise rehabilitation improves objective sleep outcomes in PD. Exercise is an effective nonpharmacological intervention to improve this disabling nonmotor symptom in PD. (c) 2020 International Parkinson and Movement Disorder Society