Publications by authors named "Derick A Anglin"

Previous research indicates that gastrointestinal discomfort from milk consumption may be attributable to A1 β-casein, rather than lactose intolerance alone. A2 milk (free of A1 β-casein) consumption may result in fewer symptoms compared to conventional milk containing both A1/A2 β-casein. In this five-week, double-blind, double-crossover study, we assessed the physiological responses to doses escalating in volume of lactose-free conventional milk (Lactaid), A2 milk, and lactose-free A2 milk in fluid milk-avoiding participants.

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We recently reported that resistance-trained (T, = 10) and untrained (UT, = 11) young adults experience vastus lateralis (VL) muscle atrophy following 2 wk of disuse, and 8 wk of recovery resistance training (RT) promotes VL hypertrophy in both participant cohorts. Skeletal muscle angiogenesis is appreciated for supporting skeletal muscle hypertrophy, but its activity following disuse-induced atrophy in humans is largely unexplored in the context of RT. Thus, we sought to determine whether these outcomes were affected.

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We sought to examine how resistance training (RT) status in young healthy individuals, either well resistance trained (T, = 10) or untrained (UT, = 11), affected molecular markers with leg immobilization followed by recovery RT. All participants underwent 2 wk of left leg immobilization via a locking leg brace. Afterward, all participants underwent 8 wk (3 days/wk) of knee extensor-focused progressive RT.

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We recently reported that resistance trained (T, n=10) and untrained (UT, n=11) young adults experience vastus lateralis (VL) muscle atrophy following two weeks of disuse, and 8 weeks of recovery resistance training (RT) promotes VL hypertrophy in both participant cohorts. However, angiogenesis targets and muscle capillary number were not examined and currently no human studies that have sought to determine if disuse followed by recovery RT affects these outcomes. Thus, we examined whether disuse and/or recovery RT affected these outcomes.

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Article Synopsis
  • The study analyzed how resistance exercise and endurance cycling affect protein lactylation and acetylation in skeletal muscles using biopsies from college-aged participants.
  • Results showed that while acute and chronic resistance training reduced cytoplasmic protein acetylation, they did not significantly impact protein lactylation.
  • In vitro tests with sodium lactate treatments also found no significant changes in protein lactylation or acetylation, suggesting that exercise primarily influences protein acetylation rather than lactylation.
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We examined how resistance exercise (RE), cycling exercise and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation. The 1boutRE study involved younger men (n = 8; 5 ± 2 years of RE experience) performing a lower body RE bout with vastus lateralis (VL) biopsies being obtained prior to and acutely following exercise. With the 10weekRT study, VL biopsies were obtained in 36 younger adults before and 24 h after their first/naïve RE bout.

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We sought to examine how resistance exercise (RE), cycling exercise, and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation in humans. In the first study (1boutRE), younger adult men (n=8; 5±2 years of RE experience) performed a lower body RE bout with vastus lateralis (VL) biopsies obtained immediately before, 3-, and 6-hours post-exercise. In the second study (10weekRT), VL biopsies were obtained in untrained younger adults (n=36, 18 men and 18 women) before and 24 hours (24h) after their first/naïve RE bout.

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Through decades of empirical data, it has become evident that resistance training (RT) can improve strength/power and skeletal muscle hypertrophy. Yet, until recently, vascular outcomes have historically been underemphasized in RT studies, which is underscored by several exercise-related reviews supporting the benefits of endurance training on vascular measures. Several lines of evidence suggest large artery diameter and blood flow velocity increase after a single bout of resistance exercise, and these events are mediated by vasoactive substances released from endothelial cells and myofibers (e.

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Although several reports have hypothesized that exercise may increase skeletal muscle protein lactylation, empirical evidence in humans is lacking. Thus, we adopted a multi-faceted approach to examine if acute and subchronic resistance training (RT) altered skeletal muscle protein lactylation levels. In mice, we also sought to examine if surgical ablation-induced plantaris hypertrophy coincided with increases in muscle protein lactylation.

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