Journal Articles

Permanent URI for this collectionhttps://mro.massey.ac.nz/handle/10179/7915

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Author: search.filters.author.Perry BGSubject: search.filters.subject.Humans

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    Nicotine exacerbates exertional heat strain in trained men: A randomized, placebo-controlled, double-blind study.
    (American Physiological Society, 2024-08-16) Moyen NE; Barnes MJ; Perry BG; Fujii N; Amano T; Kondo N; Mundel T
    To determine whether using nicotine exacerbates exertional heat strain through an increased metabolic heat production (Hprod) or decreased skin blood flow (SkBF), 10 nicotine-naïve trained males [37 ± 12 yr; peak oxygen consumption (V̇o2peak): 66 ± 10 mL·min−1·kg−1] completed four trials at 20°C and 30°C following overnight transdermal nicotine (7 mg·24 h−1) and placebo use in a crossover, double-blind design. They cycled for 60 min (55% V̇o2peak) followed by a time trial (∼75% V̇o2peak) during which measures of gastrointestinal (Tgi) and mean weighted skin (̅Tsk) temperatures, SkBF, Hprod, and mean arterial pressure (MAP) were made. The difference in ΔTgi between nicotine and placebo trials was greater during 30°C (0.4 ± 0.5°C) than 20°C (0.1 ± 0.7°C), with ̅Tsk higher during nicotine than placebo trials (0.5 ± 0.5°C, P = 0.02). SkBF became progressively lower during nicotine than placebo trials (P = 0.01) and progressively higher during 30°C than 20°C trials (P < 0.01); MAP increased from baseline (P < 0.01) and remained elevated in all trials. The difference in Hprod between 30°C and 20°C trials was lower during nicotine than placebo (P = 0.01) and became progressively higher during 30°C than 20°C trials with exercise duration (P = 0.03). Mean power output during the time trial was lower during 30°C than 20°C trials (24 ± 25 W, P = 0.02), and although no effect of nicotine was observed (P > 0.59), two participants (20%) were unable to complete their 30°C nicotine trials as one reached the ethical limit for Tgi (40.0°C), whereas the other withdrew due to “nausea and chills” (Tgi = 39.7°C). These results demonstrate that nicotine use increases thermal strain and risk of exertional heat exhaustion by reducing SkBF. NEW & NOTEWORTHY In naïve participants, acute nicotine use exerts a hyperthermic effect that increases the risk of heat exhaustion during exertional heat strain, which is driven by a blunted skin blood flow response. This has implications for 1) populations that face exertional heat strain and demonstrate high nicotine use (e.g., athletes and military, 25%–50%) and 2) study design whereby screening and exclusion for nicotine use or standardization of prior use (e.g., overnight abstinence) is encouraged.
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    Changes to insulin sensitivity in glucose clearance systems and redox following dietary supplementation with a novel cysteine-rich protein: A pilot randomized controlled trial in humans with type-2 diabetes.
    (Elsevier B.V, 2023-10-07) Peeters WM; Gram M; Dias GJ; Vissers MCM; Hampton MB; Dickerhof N; Bekhit AE; Black MJ; Oxbøll J; Bayer S; Dickens M; Vitzel K; Sheard PW; Danielson KM; Hodges LD; Brønd JC; Bond J; Perry BG; Stoner L; Cornwall J; Rowlands DS
    We recently developed a novel keratin-derived protein (KDP) rich in cysteine, glycine, and arginine, with the potential to alter tissue redox status and insulin sensitivity. The KDP was tested in 35 human adults with type-2 diabetes mellitus (T2DM) in a 14-wk randomised controlled pilot trial comprising three 2×20 g supplemental protein/day arms: KDP-whey (KDPWHE), whey (WHEY), non-protein isocaloric control (CON), with standardised exercise. Outcomes were measured morning fasted and following insulin-stimulation (80 mU/m2/min hyperinsulinaemic-isoglycaemic clamp). With KDPWHE supplementation there was good and very-good evidence for moderate-sized increases in insulin-stimulated glucose clearance rate (GCR; 26%; 90% confidence limits, CL 2%, 49%) and skeletal-muscle microvascular blood flow (46%; 16%, 83%), respectively, and good evidence for increased insulin-stimulated sarcoplasmic GLUT4 translocation (18%; 0%, 39%) vs CON. In contrast, WHEY did not effect GCR (-2%; -25%, 21%) and attenuated HbA1c lowering (14%; 5%, 24%) vs CON. KDPWHE effects on basal glutathione in erythrocytes and skeletal muscle were unclear, but in muscle there was very-good evidence for large increases in oxidised peroxiredoxin isoform 2 (oxiPRX2) (19%; 2.2%, 35%) and good evidence for lower GPx1 concentrations (-40%; -4.3%, -63%) vs CON; insulin stimulation, however, attenuated the basal oxiPRX2 response (4%; -16%, 24%), and increased GPx1 (39%; -5%, 101%) and SOD1 (26%; -3%, 60%) protein expression. Effects of KDPWHE on oxiPRX3 and NRF2 content, phosphorylation of capillary eNOS and insulin-signalling proteins upstream of GLUT4 translocation AktSer437 and AS160Thr642 were inconclusive, but there was good evidence for increased IRSSer312 (41%; 3%, 95%), insulin-stimulated NFκB-DNA binding (46%; 3.4%, 105%), and basal PAK-1Thr423/2Thr402 phosphorylation (143%; 66%, 257%) vs WHEY. Our findings provide good evidence to suggest that dietary supplementation with a novel edible keratin protein in humans with T2DM may increase glucose clearance and modify skeletal-muscle tissue redox and insulin sensitivity within systems involving peroxiredoxins, antioxidant expression, and glucose uptake.
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    Cerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia.
    (John Wiley & Sons Ltd on behalf of Scandinavian Society of Clinical Physiology and Nuclear Medicine, 2023-06-18) Perry BG; Korad S; Mündel T
    BACKGROUND: During hyperthermia, the perturbations in mean arterial blood pressure (MAP) produced by the Valsalva manoeuvre (VM) are more severe. However, whether these more severe VM-induced changes in MAP are translated to the cerebral circulation during hyperthermia is unclear. METHODS: Healthy participants (n = 12, 1 female, mean ± SD: age 24 ± 3 years) completed a 30 mmHg (mouth pressure) VM for 15 s whilst supine during normothermia and mild hyperthermia. Hyperthermia was induced passively using a liquid conditioning garment with core temperature measured via ingested temperature sensor. Middle cerebral artery blood velocity (MCAv) and MAP were recorded continuously during and post-VM. Tieck's autoregulatory index was calculated from the VM responses, with pulsatility index, an index of pulse velocity (pulse time) and mean MCAv (MCAvmean ) also calculated. RESULTS: Passive heating significantly raised core temperature from baseline (37.9 ± 0.2 vs. 37.1 ± 0.1°C at rest, p < 0.01). MAP during phases I through III of the VM was lower during hyperthermia (interaction effect p < 0.01). Although an interaction effect was observed for MCAvmean (p = 0.02), post-hoc differences indicated only phase IIa was lower during hyperthermia (55 ± 12 vs. 49.3 ± 8 cm s- 1 for normothermia and hyperthermia, respectively, p = 0.03). Pulsatility index was increased 1-min post-VM in both conditions (0.71 ± 0.11 vs. 0.76 ± 0.11 for pre- and post-VM during normothermia, respectively, p = 0.02, and 0.86 ± 0.11 vs. 0.99 ± 0.09 for hyperthermia p < 0.01), although for pulse time only main effects of time (p < 0.01), and condition (p < 0.01) were apparent. CONCLUSION: These data indicate that the cerebrovascular response to the VM is largely unchanged by mild hyperthermia.
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    Cerebral autoregulation across the menstrual cycle in eumenorrheic women
    (Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society, 2022-05-06) Korad S; Mündel T; Fan J-L; Perry BG
    There is emerging evidence that ovarian hormones play a significant role in the lower stroke incidence observed in pre-menopausal women compared with men. However, the role of ovarian hormones in cerebrovascular regulation remains to be elucidated. We examined the blood pressure-cerebral blood flow relationship (cerebral autoregulation) across the menstrual cycle in eumenorrheic women (n = 12; mean ± SD: age, 31 ± 7 years). Participants completed sit-to-stand and Valsalva maneuvers (VM, mouth pressure of 40 mmHg for 15 s) during the early follicular (EF), late follicular (LF), and mid-luteal (ML) menstrual cycle phases, confirmed by serum measurement of progesterone and 17β-estradiol. Middle cerebral artery blood velocity (MCAv), arterial blood pressure and partial pressure of end-tidal carbon dioxide were measured. Cerebral autoregulation was assessed by transfer function analysis during spontaneous blood pressure oscillations, rate of regulation (RoR) during sit-to-stand maneuvers, and Tieck's autoregulatory index during VM phases II and IV (AI-II and AI-IV, respectively). Resting mean MCAv (MCAvmean ), blood pressure, and cerebral autoregulation were unchanged across the menstrual cycle (all p > 0.12). RoR tended to be different (EF, 0.25 ± 0.06; LF; 0.19 ± 0.04; ML, 0.18 ± 0.12 sec-1 ; p = 0.07) and demonstrated a negative relationship with 17β-estradiol (R2  = 0.26, p = 0.02). No changes in AI-II (EF, 1.95 ± 1.20; LF, 1.67 ± 0.77 and ML, 1.20 ± 0.55) or AI-IV (EF, 1.35 ± 0.21; LF, 1.27 ± 0.26 and ML, 1.20 ± 0.2) were observed (p = 0.25 and 0.37, respectively). Although, a significant interaction effect (p = 0.02) was observed for the VM MCAvmean response. These data indicate that the menstrual cycle has limited impact on cerebrovascular autoregulation, but individual differences should be considered.