Steven K. Malin

Kinesiology departments navigate uncertainty across federal, state, institutional, and disciplinary levels. Fluctuations in research funding, state policy, institutional restructuring, and evolving societal expectations require leaders to interpret complexity while preserving academic excellence. The purpose of this article was to present a practical framework for faculty called the Leadership Survival Toolkit that is built around four metaphors: (a) compass (vision), (b) hammer (roadblock breaker), (c) bridge (organizational architect), and (d) shield (protective stewardship). The framework provides strategies for research-intensive and teaching-focused institutions. The compass emphasizes differentiated and adaptable vision, while the hammer addresses momentum, structural constraints, and power dynamics. The bridge offers insight toward policy alignment and collaborative infrastructure, and the shield emphasizes resilience, buffering external shocks, and sustaining morale among faculty, staff, and students. Together, this Leadership Survival Toolkit provides faculty a framework to navigate institutional complexity as well as make focused, adaptive, and student-centered decisions in academia’s ever-changing environment.

Aim: Low moderate-to-vigorous physical activity (MVPA), high sedentary behavior (SB), and inadequate sleep are individually associated with type 2 diabetes (T2D) risk. However, the aggregate impact of these movement patterns remains unclear. Purpose: Assess whether being aligned with 24-h movement guidelines of MVPA, SB, and sleep relates to cardiometabolic health, and compare this with the American Heart Association’s Life’s Essential 8. Methods: In a cross-sectional study, adults with obesity [ n = 56 (39 F); 55.6 ± 1.1 y; 34.5 ± 0.7 kg/m ² ] with low 24-h movement z -scores [“aligned”; n = 28 (21 F)] were compared to those with high z -scores [“misaligned” n = 28 (18 F)]. MVPA and SB (accelerometer) and sleep (Pittsburgh Sleep Quality Index) were assessed to calculate z scores. LE8 scores were calculated according to AHA guidelines. A 120-min hyperinsulinemic-euglycemic clamp (40 mU/m ² /min, 90 mg/dl) with indirect calorimetry was used to determine metabolic insulin sensitivity [glucose infusion rate (GIR)] and substrate oxidation. Pulse wave velocity and augmentation index (AIx75) were assessed at 0 and 120 min of the clamp to assess arterial stiffness. Fitness ( V O _2max ) and body fat (DXA) were also assessed. Results: Despite no differences in age, body fat, or V O _2max , the misaligned group had higher fasting DBP, MAP, and AIx75 ( P < 0.05), lower GIR ( P = 0.07), and lower FFA suppression ( P = 0.01). While both the z -score and LE8 related to blood pressure, only the z -score correlated with AIx75 and FFA suppression. Conclusion: Aligning with 24-h movement patterns related to better cardiometabolic health in people with obesity. Clinical trials registration: NCT03355469.

Purpose: The clinical implications of metformin attenuating the insulin sensitizing effects of exercise are unclear. We tested the hypothesis that metformin would blunt reductions in post-prandial glucose in an exercise intensity-based manner in adults with metabolic syndrome (MetS) risk. Methods: In a double-blind trial, participants were randomized to low intensity exercise plus placebo (~55%VO ₂ max 5d/wk, LoEx+PL, n=22) or metformin (2000mg/d, LoEx+Met, n=21) and high intensity exercise plus placebo (~85%VO ₂ max 5d/wk, HiEx+PL, n=24) or metformin (HiEx+Met, n=24) for 16 weeks. A 120-min 75g oral glucose tolerance test was conducted pre- and post-treatment to assess early (0-30min), late (60-120min), and total (0-120min) phase glucose tolerance and circulating insulin (total area under the curve; tAUC). Results: HiEx+Met increased 1-hr and 2-hr glucose by ~18-21mg/dl ( P P =0.008). Late phase and total phase glucose tAUC was also higher after HiEx+Met versus HiEx+PL and LoEx+PL (both, P P , P <0.04) after exercise training only. Conclusions: Metformin increased post-prandial glucose after high, but not low, intensity exercise training in adults with MetS risk.

Background: Insulin contributes to blood pressure (BP) regulation through, in part, effects on the brain. Whether exercise impacts brain insulin action in parallel with alterations in BP is unclear. Purpose: Examine if an acute exercise lowers BP after intranasal insulin (INI) and increases cerebral blood flow (CBF) in aging adults with cardiometabolic risk. Methods: In a counter-balanced design, 15 cognitively unimpaired (MoCA: 28.2±1.3 a.u.) adults (56.7±2.1 yr; VO ₂ max: 23.9±0.9 ml/kg/min) with obesity (BMI 31.8±1.3 kg/m ² ) were randomized to a rest or acute treadmill exercise bout (70% VO ₂ max for 60 minutes) in the evening. The next morning, participants arrived fasted and BP, heart rate, glucose and insulin were assessed. Brainstem and hypothalamus CBF were then tested via pseudo-Continuous Arterial Spin Labeling (pCASL) MRI. INI (40 IU) was administered and 30 as well as 90 minutes later, BP, heart rate, glucose, and insulin were measured. Then a 75g oral glucose tolerance test (OGTT) was provided, and outcomes were obtained again every 30 minutes up to 120 minutes. Results: Exercise had no effect on glucose following INI, although insulin was reduced during the OGTT ( P<0.05). Exercise blunted the rise in systolic BP after INI as well as during the entire protocol (both P<0.05), independent of heart rate. Exercise raised CBF in the brainstem ( P<0.05) but not the hypothalamus. However, the increase in fasting hypothalamus CBF correlated with reductions in INI-mediated systolic BP (r=-0.51, P=0.05). Conclusion: In adults with cardiometabolic risk, an acute exercise bout blunted systolic BP rises after INI in parallel with increased fasting brainstem and hypothalamic CBF.

Insulin acts in the brain to promote satiety. Aging individuals may have brain insulin resistance and altered appetite perceptions. However, it is unclear if exercise impacts cerebral reward centers and appetite perception in middle-aged to older individuals. Purpose: To assess whether a single exercise bout alters cerebral blood flow (CBF) in reward centers in relation to appetite perceptions. Methods: Fifteen sedentary adults (12F; ~56 ± 2y; ~31 ± 1 kg/m²) completed a control and acute exercise condition (70% maximal oxygen consumption) in a randomized, counterbalanced order in the evening. Following an overnight fast, CBF in the accumbens, thalamus, and amygdala (pCASL MRI) was evaluated before and after intranasal insulin spray (INI, 40 IU) administration. Plasma glucose and insulin as well as an appetite visual analog scale (VAS) were assessed at fasting, 30, and 90 min post-INI, as well as at 30 min intervals of a 120 min 75 g oral glucose tolerance test (OGTT). Total area under the curve (tAUC) was calculated. Results: Exercise tended to lower blood glucose (p = 0.072) and plasma insulin (p = 0.007) tAUC, compared with rest. Exercise also raised right thalamus (p = 0.029) and left amygdala CBF (p = 0.023). The rise in fasting CBF in these regions, and the accumbens, correlated with reduced insulin tAUC (r = −0.55 to −0.73, p < 0.050). Although there was no difference in hunger, satisfaction, fullness, or prospective food consumption after exercise, changes in INI-stimulated thalamus CBF related to fullness tAUC after exercise (r = −0.57, p = 0.044). Conclusions: A single exercise bout might increase fasting CBF in some brain regions associated with appetite perception through a potential insulin-related mechanism.

Exercise may lower Alzheimer's Disease and Related Dementia (ADRD) risk. While insulin has been proposed to benefit cognition, the effect of exercise on neuronal insulin signaling in humans is unclear. Purpose: We tested the hypothesis that a single bout of aerobic exercise would raise insulin signaling mediators from plasma‐derived neuronal extracellular vesicles (nEVs). Methods: Fifteen sedentary adults with obesity (12F; ~56y; ~31 kg/m ² ) completed an evening rest and acute exercise condition (70% maximal oxygen consumption (VO ₂ max)) in a randomized, counterbalanced order. Following an overnight fast, plasma was collected for analysis of nEV insulin signaling biomarkers before and after intranasal insulin spray (INI, 40 IU) as well as 60 min following a 75 g oral glucose tolerance test (OGTT). Plasma glucose and insulin were also measured at 30 and 60 min during the OGTT, and total area under the curve (tAUC) was calculated. Results: Exercise tended to lower glucose tAUC _0‐150min ( p = 0.08, d = 0.50), independent of insulin tAUC _0‐150min ( p = 0.99, d = 0.00). Exercise increased pIR‐Tyr1162/Tyr1163 ( p = 0.05, η ² = 0.05), pIRS‐1‐Ser636 ( p = 0.02, η ² = 0.07), pAkt‐Ser473 ( p = 0.03, η ² = 0.06), and pTSC2‐Ser939 ( p = 0.01, η ² = 0.08) with medium effect sizes across blood draws, compared with the resting condition. Exercise also raised fasting and decreased pp70S6K‐Thr412 before and after the OGTT, compared with increased levels after rest during the OGTT ( p = 0.02, η ² = 0.10). Exercise had no effect on other insulin signaling proteins (e.g., pmTOR‐Ser2448, pGSK3β‐Ser9, etc.). Conclusions: A single bout of aerobic exercise increases some nEV‐associated insulin signaling phosphoproteins in people with cardiometabolic risk. Additional work is warranted to determine if changes in brain insulin signaling translate to lower ADRD risk. Clinical Trials Registration: NCT05853913.

Context: Bisphenol A (BPA) is a synthetic chemical used in consumer goods that has been linked to type 2 diabetes in observational studies. No human experimental studies have examined whether BPA reduces peripheral insulin sensitivity. Purpose: To determine the effects of oral BPA administration on peripheral insulin sensitivity over 5 days. Methods: Forty sedentary, but otherwise healthy adults (22 F, 18 M; 21.3 ± 2.1 year; 22.1 ± 2.3 kg/m2; 85% non-Hispanic White) completed a 2-day baseline energy-balanced diet low in BPA during which urine, blood, and peripheral insulin sensitivity via 120 minutes euglycemic hyperinsulinemic clamp technique (40 mU/m2/min; 90 mg/dL) were assessed. In a double-blind fashion, participants were randomly assigned to receive 5 days of oral BPA administration at 50 µg/kg body weight (BPA-50) or placebo (PL). All participants were fed the same energy-balanced diet. Outcomes were assessed using a two-way repeated-measures ANOVA adjusted for baseline sex, BMI, physical activity, and ethnicity. Results: After treatment, urine BPA levels were significantly higher in BPA-50 compared to PL (+ 268 700 ± 63 983 vs PL: + 8893 ± 6786 pg/mL, P = .009). After treatment, body weight and fasting glucose were not statistically different between PL and BPA-50 (P > .05). However, BPA significantly decreased peripheral insulin sensitivity by 0.02 ± 0.01 mg/kg/min/uU/mL compared with an increase observed following PL by 0.02 ± 0.01 mg/kg/min/uU/mL (P = .01). Conclusion: BPA administration decreased peripheral insulin sensitivity after 5 days. These data provide the first experimental evidence in humans that BPA administration may reduce insulin sensitivity.

Metformin reduces hyperglycemia and cardiovascular disease risk. However, no study has determined if metformin alters blood pressure and/or aortic waveforms in an exercise intensity dependent manner. We tested if metformin alters blood pressure and aortic waveforms before and during insulin‐stimulation following low and high intensity exercise training. In a double‐blind, placebo controlled trial, participants were randomized to low intensity exercise plus placebo (∼55% VO ₂ max 5 days/week, LoEx+PL, n = 22) or metformin (2000 mg/day, LoEx+Met, n = 21) and high intensity exercise plus placebo (∼85% VO ₂ max 5 days/week, HiEx+PL, n = 24) or metformin (HiEx+Met, n = 24) for 16 weeks. Carotid‐femoral pulse wave velocity (cfPWV) was assessed to determine arterial stiffness. A 120 min euglycemic‐hyperinsulinemic clamp (40mU/m ² /min, 90 mg/dL) was conducted to assess peripheral and central blood pressures as well as aortic waveforms via applanation tonometry. Inflammatory measures (e.g., hs‐CRP, IL‐8, MMP‐1 and MMP‐7) along with fitness (VO ₂ max) and body composition (DXA) were also analyzed. While LoEx+PL tended to decrease cfPWV ( p = 0.051), HiEx+Met reduced fasting peripheral diastolic blood pressure (pDBP; p  < 0.05) and all treatments except HiEx+Met increased fasting central pulse pressure ( p  < 0.05). Upon insulin‐stimulation, pDBP and reflection magnitude increased while pulse pressure amplification (PPA) decreased after LoEx+Met and HiEx+Met compared with LoEx+PL and HiEx+PL independent of exercise intensity (all, p  < 0.05). Interestingly, fasting MMP‐1 ( p  < 0.05) and MMP‐7 ( p = 0.063) tended to be higher after Met compared with PL, independent of exercise intensity. In conclusion, metformin altered blood pressure and aortic waveform adaptations in relation to inflammation following exercise training in adults at risk for metabolic syndrome. Trial Registration : NCT03355469

Aims: Mixed evidence exists on whether metformin adds to or attenuates the insulin‐sensitising effects of exercise. To date, no studies have tested whether metformin differentially impacts exercise training intensity–mediated insulin sensitivity. We tested the hypothesis that metformin would blunt metabolic insulin sensitivity and carbohydrate oxidation in an intensity‐based manner among adults with metabolic syndrome (MetS) risk. Materials and methods: In a double‐blind, placebo‐controlled trial, participants were randomised to low‐intensity exercise plus placebo (~55% VO ₂ max 5 days/week, LoEx + PL, n = 22) or metformin (2000 mg/day, LoEx + Met, n = 21) and high‐intensity exercise plus placebo (~85% VO ₂ max 5 days/week, HiEx + PL, n = 24) or metformin (HiEx + Met, n = 24) for 16 weeks. A 120‐min euglycaemic–hyperinsulinemic clamp (40 mU/m ² /min, 90 mg/dL) was conducted pre‐ and post‐treatment to assess metabolic insulin sensitivity (M‐value/insulin). Fasting and insulin‐stimulated carbohydrate oxidation was also assessed using indirect calorimetry. Adipokines (leptin, high molecular weight (HWM), and total adiponectin) were measured at 0 and 120 min of the clamp. Aerobic fitness (VO ₂ max) and body composition (DXA) were also analysed. Results: HiEx + PL increased metabolic insulin sensitivity ( p = 0.017) while HiEx + Met, LoEx + PL, or LoEx + Met did not. HiEx + PL also raised insulin‐stimulated carbohydrate oxidation and decreased fat oxidation compared with LoEx + Met (both, p = 0.008). Increased metabolic insulin sensitivity related to reductions in fasting glucose ( r = −0.41, p = 0.025), VO ₂ max ( r = 0.55, p = 0.002), fasting leptin ( r = −0.54, p = 0.01), and weight loss ( r = −0.60, p < 0.001) after exercise and placebo, but not exercise and metformin. Conclusions: Metformin attenuated metabolic insulin sensitivity and insulin‐stimulated carbohydrate oxidation after high‐intensity exercise training in adults at risk for MetS.