19 results on '"Scott, Matthew C."'
Search Results
2. Markers of poor sleep quality increase sedentary behavior in college students as derived from accelerometry
- Author
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Hargens, Trent A., Scott, Matthew C., Olijar, Valerie, Bigman, Matthew, and Edwards, Elizabeth S.
- Published
- 2021
- Full Text
- View/download PDF
3. Impact of low‐load resistance exercise with and without blood flow restriction on muscle strength, endurance, and oxidative capacity: A pilot study.
- Author
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Davis, Brett H., Stampley, James E., Granger, Joshua, Scott, Matthew C., Allerton, Timothy D., Johannsen, Neil M., Spielmann, Guillaume, and Irving, Brian A.
- Subjects
BLOOD flow restriction training ,RESISTANCE training ,MUSCLE strength ,MUSCLE mass ,LEAN body mass ,ANAEROBIC capacity - Abstract
Low‐load resistance exercise (LLRE) to failure can increase muscle mass, strength, endurance, and mitochondrial oxidative capacity (OXPHOS). However, the impact of adding blood flow restriction to low‐load resistance exercise (LLBFR) when matched for volume on these outcomes is incompletely understood. This pilot study examined the impact of 6 weeks of single‐legged LLBFR and volume‐matched LLRE on thigh bone‐free lean mass, strength, endurance, and mitochondrial OXPHOS. Twenty (12 males and 8 females) untrained young adults (mean ± SD; 21 ± 2 years, 168 ± 11 cm, 68 ± 12 kg) completed 6 weeks of either single‐legged LLBFR or volume‐matched LLRE. Participants performed four sets of 30, 15, 15, and 15 repetitions at 25% 1‐RM of leg press and knee extension with or without BFR three times per week. LLBFR increased knee extension 1‐RM, knee extension endurance, and thigh bone‐free lean mass relative to control (all p < 0.05). LLRE increased leg press and knee extension 1‐RM relative to control (p = 0.012 and p = 0.054, respectively). LLRE also increased mitochondrial OXPHOS (p = 0.047 (nonparametric)). Our study showed that LLBFR increased muscle strength, muscle endurance, and thigh bone‐free lean mass in the absence of improvements in mitochondrial OXPHOS. LLRE improved muscle strength and mitochondrial OXPHOS in the absence of improvements in thigh bone‐free lean mass or muscle endurance. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
4. The Effects of Intermittent Cold Exposure on Adipose Tissue.
- Author
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Scott, Matthew C. and Fuller, Scott
- Subjects
- *
WEIGHT loss , *WHITE adipose tissue , *TYPE 2 diabetes , *WATER immersion , *ADIPOSE tissues , *BODY weight , *BROWN adipose tissue - Abstract
Intermittent cold exposure (ICE) has garnered increased attention in popular culture, largely for its proposed effects on mood and immune function, but there are also suggestions that the energy-wasting mechanisms associated with thermogenesis may decrease body weight and fat mass. Considering the continued and worsening prevalence of obesity and type II diabetes, any protocol that can reduce body weight and/or improve metabolic health would be a substantial boon. Here, we present a narrative review exploring the research related to ICE and adipose tissue. Any publicly available original research examining the effects of repeated bouts of ICE on adipose-related outcomes was included. While ICE does not consistently lower body weight or fat mass, there does seem to be evidence for ICE as a positive modulator of the metabolic consequences of obesity, such as glucose tolerance and insulin signaling. Further, ICE consistently increases the activity of brown adipose tissue (BAT) and transitions white adipose tissue to a phenotype more in line with BAT. Lastly, the combined effects of ICE and exercise do not seem to provide any additional benefit, at least when exercising during ICE bouts. The majority of the current literature on ICE is based on rodent models where animals are housed in cold rooms, which does not reflect protocols likely to be implemented in humans such as cold water immersion. Future research could specifically characterize ICE via cold water immersion in combination with controlled calorie intake to clearly determine the effects of ICE as it would be implemented in humans looking to lower their body weight via reductions in fat mass. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
5. Trabecular Bone Score And Bone Mineral Density In Older Adults: 313 Board #129 May 27 10:30 AM - 12:00 PM
- Author
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Scott, Matthew C., Stampley, James, Davis, Brett, Quiriarte, Heather, Cho, Eunhan, Theall, Bailey, Granger, Josh, Johannsen, Neil M., Heymsfield, Steve B., Greenway, Frank, and Irving, Brian A.
- Published
- 2020
- Full Text
- View/download PDF
6. Response of Liver Metabolic Pathways to Ketogenic Diet and Exercise Are Not Additive
- Author
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HUANG, TAI-YU, GOLDSMITH, FELICIA R., FULLER, SCOTT E., SIMON, JACOB, BATDORF, HEIDI M., SCOTT, MATTHEW C., ESSAJEE, NABIL M., BROWN, JOHN M., BURK, DAVID H., MORRISON, CHRISTOPHER D., BURKE, SUSAN J., COLLIER, J. JASON, and NOLAND, ROBERT C.
- Published
- 2020
- Full Text
- View/download PDF
7. Extract of Artemisia dracunculus L. Modulates Osteoblast Proliferation and Mineralization.
- Author
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Scott, Matthew C., Bourgeois, Aleah, Yu, Yongmei, Burk, David H., Smith, Brenda J., and Floyd, Z. Elizabeth
- Subjects
- *
BONE morphogenetic proteins , *BONE health , *MINERALIZATION , *ARTEMISIA , *INSULIN sensitivity , *INSULIN , *CELL culture - Abstract
Thiazolidinediones (TZD) significantly improve insulin sensitivity via action on adipocytes. Unfortunately, TZDs also degrade bone by inhibiting osteoblasts. An extract of Artemisia dracunculus L., termed PMI5011, improves blood glucose and insulin sensitivity via skeletal muscle, rather than fat, and may therefore spare bone. Here, we examine the effects of PMI5011 and an identified active compound within PMI5011 (2′,4′-dihydroxy-4-methoxydihydrochalcone, DMC-2) on pre-osteoblasts. We hypothesized that PMI5011 and DMC-2 will not inhibit osteogenesis. To test our hypothesis, MC3T3-E1 cells were induced in osteogenic media with and without PMI5011 or DMC-2. Cell lysates were probed for osteogenic gene expression and protein content and were stained for osteogenic endpoints. Neither compound had an effect on early stain outcomes for alkaline phosphatase or collagen. Contrary to our hypothesis, PMI5011 at 30 µg/mL significantly increases osteogenic gene expression as early as day 1. Further, osteogenic proteins and cell culture mineralization trend higher for PMI5011-treated wells. Treatment with DMC-2 at 1 µg/mL similarly increased osteogenic gene expression and significantly increased mineralization, although protein content did not trend higher. Our data suggest that PMI5011 and DMC-2 have the potential to promote bone health via improved osteoblast maturation and activity. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
8. A Prior High-Intensity Exercise Bout Attenuates the Vascular Dysfunction Resulting From a Prolonged Sedentary Bout.
- Author
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Garten, Ryan S., Scott, Matthew C., Zúñiga, Tiffany M., Hogwood, Austin C., Fralin, R. Carson, and Weggen, Jennifer
- Subjects
EXERCISE ,AEROBIC exercises ,BLOOD sampling ,OXIDATIVE stress ,OXIDANT status - Abstract
Background: This study sought to determine the impact of an acute prior bout of high-intensity interval aerobic exercise on attenuating the vascular dysfunction associated with a prolonged sedentary bout. Methods: Ten young (24 ± 1 y) healthy males completed two 3-hour sessions of prolonged sitting with (SIT-EX) and without (SIT) a high-intensity interval aerobic exercise session performed immediately prior. Prior to and 3 hours into the sitting bout, leg vascular function was assessed with the passive leg movement technique, and blood samples were obtained from the lower limb to evaluate changes in oxidative stress (malondialdehyde and superoxide dismutase) and inflammation (interleukin-6). Results: No presitting differences in leg vascular function (assessed via passive leg movement technique-induced hyperemia) were revealed between conditions. After 3 hours of prolonged sitting, leg vascular function was significantly reduced in the SIT condition, but unchanged in the SIT-EX. Lower limb blood samples revealed no alterations in oxidative stress, antioxidant capacity, or inflammation in either condition. Conclusions: This study revealed that lower limb vascular dysfunction was significantly attenuated by an acute presitting bout of high-intensity interval aerobic exercise. Further analysis of lower limb blood samples revealed no changes in circulating oxidative stress or inflammation in either condition. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
9. Heart Rate Response And Activity Level In Division I Football Players During Pre-Season Scrimmage Play: 1023 Board #339 June 1, 2: 00 PM - 3: 30 PM
- Author
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Early, Kate S., Lemoine, Nathan P., SImoneaux, Annie B., Scott, Matthew C., Mullenix, Shelly, Marucci, Jack, Barker, Andrew, MacLellan, Michael, Castle, Ray R., Church, Tim S., Earnest, Conrad P., and Johannsen, Neil M.
- Published
- 2016
- Full Text
- View/download PDF
10. Rest Interval Effects On Prolonged Epoc: 2395 Board #142 May 29, 9: 30 AM - 11: 00 AM
- Author
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Miskowiec, Ryan W., Scott, Matthew C., and Nelson, Arnold G.
- Published
- 2015
- Full Text
- View/download PDF
11. Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle.
- Author
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Tai-Yu Huang, Linden, Melissa A., Fuller, Scott E., Goldsmith, Felicia R., Simon, Jacob, Batdorf, Heidi M., Scott, Matthew C., Essajee, Nabil M., Brown, John M., and Noland, Robert C.
- Subjects
LOW-fat diet ,SKELETAL muscle ,KETOGENIC diet ,ADIPOSE tissues ,AEROBIC capacity ,MITOCHONDRIA - Abstract
Ketogenic diets (KDs) are reported to improve body weight, fat mass, and exercise performance in humans. Unfortunately, most rodent studies have used a low-protein KD, which does not recapitulate diets used by humans. Since skeletal muscle plays a critical role in responding to macronutrient perturbations induced by diet and exercise, the purpose of this study was to test if a normal-protein KD (NPKD) impacts shifts in skeletal muscle substrate oxidative capacity in response to exercise training (ExTr). A high fat, carbohydrate-deficient NPKD (16.1% protein, 83.9% fat, 0% carbohydrate) was given to C57BL/6J male mice for 6 wk, whereas controls (Con) received a low-fat diet with similar protein (15.9% protein, 11.9% fat, 72.2% carbohydrate). After 3wk on the diet, mice began treadmill training 5 days/wk, 60 min/day for 3 wks. The NPKD increased body weight and fat mass, whereas ExTr negated a continued rise in adiposity. ExTr increased intramuscular glycogen, whereas the NPKD increased intramuscular triglycerides. Neither the NPKD nor ExTr alone altered mitochondrial content; however, in combination, the NPKD-ExTr group showed increases in PGC-1α and markers of mitochondrial fission/fusion. Pyruvate oxidative capacity was unchanged by either intervention, whereas ExTr increased leucine oxidation in NPKD-fed mice. Lipid metabolism pathways had the most notable changes as the NPKD and ExTr interventions both enhanced mitochondrial and peroxisomal lipid oxidation and many adaptations were additive or synergistic. Overall, these results suggest that a combination of a NPKD and ExTr induces additive and/or synergistic adaptations in skeletal muscle oxidative capacity. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
12. Low sleep efficiency does not impact upper or lower limb vascular function in young adults.
- Author
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Scott, Matthew C., Hogwood, Austin C., Fralin, Richard C., Weggen, Jennifer B., Zúñiga, Tiffany M., and Garten, Ryan S.
- Subjects
- *
YOUNG adults , *LEG , *ARM , *HEART beat , *SYMPATHETIC nervous system - Abstract
New Findings: What is the central question of this study?We sought to investigate whether young adults reporting low sleep quality possessed lower vascular function and altered autonomic nervous system modulation when compared with young adults reporting high sleep quality.What is the main finding and its importance?The study revealed that in young adults reporting low sleep quality, neither vascular nor autonomic function was significantly different when compared with young adults reporting high sleep quality. These findings suggest that young adults are either not substantially impacted by or can adequately adapt to the negative consequences commonly associated with poor sleep. The aim of the study was to investigate whether young adults reporting low sleep quality also possessed lower vascular function, potentially stemming from altered autonomic nervous system modulation, when compared with young adults reporting high sleep quality. Thirty‐one healthy young adults (age 24 ± 4 years) underwent a 7 night sleep assessment (Actigraph GT3X accelerometer). After the sleep assessment, subjects meeting specific criteria were separated into high (HSE; ≥85%; n = 11; eight men and three women) and low (LSE; <80%; n = 11; nine men and two women) sleep efficiency groups. Peripheral vascular function was assessed in the upper and lower limb, using the flow‐mediated dilatation technique in the arm (brachial artery) and leg (superficial femoral artery). Heart rate variability was evaluated during 5 min of rest and used frequency parameters reflective of parasympathetic and/or sympathetic nervous system modulation (high‐ and low‐frequency parameters). By experimental design, significant differences in sleep quality between groups were reported, with the LSE group exhibiting a longer time awake after sleep onset, higher number of awakenings and longer average time per awakening when compared with the HSE group. Despite these differences in sleep quality, no significant differences in upper and lower limb vascular function and heart rate variability measures were revealed when comparing the LSE and HSE groups. Additionally, in all subjects (n = 31), no correlations between sleep efficiency and vascular function/autonomic modulation were revealed. This study revealed that low sleep quality does not impact upper or lower limb vascular function or autonomic nervous system modulation in young adults. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
13. Low-intensity exercise induces acute shifts in liver and skeletal muscle substrate metabolism but not chronic adaptations in tissue oxidative capacity.
- Author
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Fuller, Scott E., Tai-Yu Huang, Simon, Jacob, Batdorf, Heidi M., Essajee, Nabil M., Scott, Matthew C., Waskom, Callie M., Brown, John M., Burke, Susan J., Collier, J. Jason, and Noland, Robert C.
- Subjects
MUSCLE metabolism ,SKELETAL muscle ,TREADMILL exercise ,LIVER ,EXERCISE - Abstract
Adaptations in hepatic and skeletal muscle substrate metabolism following acute and chronic (6 wk; 5 days/wk; 1 h/day) low-intensity treadmill exercise were tested in healthy male C57BL/6J mice. Low-intensity exercise maximizes lipid utilization; therefore, we hypothesized pathways involved in lipid metabolism would be most robustly affected. Acute exercise nearly depleted liver glycogen immediately postexercise (0 h), whereas hepatic triglyceride (TAG) stores increased in the early stages after exercise (0-3 h). Also, hepatic peroxisome proliferatoractivated receptor-γ coactivator-1α (PGC-1α) gene expression and fat oxidation (mitochondrial and peroxisomal) increased immediately postexercise (0 h), whereas carbohydrate and amino acid oxidation in liver peaked 24-48 h later. Alternatively, skeletal muscle exhibited a less robust response to acute exercise as stored substrates (glycogen and TAG) remained unchanged, induction of PGC-1α gene expression was delayed (up at 3 h), and mitochondrial substrate oxidation pathways (carbohydrate, amino acid, and lipid) were largely unaltered. Peroxisomal lipid oxidation exhibited the most dynamic changes in skeletal muscle substrate metabolism after acute exercise; however, this response was also delayed (peaked 3-24 h postexercise), and expression of peroxisomal genes remained unaffected. Interestingly, 6 wk of training at a similar intensity limited weight gain, increased muscle glycogen, and reduced TAG accrual in liver and muscle; however, substrate oxidation pathways remained unaltered in both tissues. Collectively, these results suggest changes in substrate metabolism induced by an acute low-intensity exercise bout in healthy mice are more rapid and robust in liver than in skeletal muscle; however, training at a similar intensity for 6 wk is insufficient to induce remodeling of substrate metabolism pathways in either tissue. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
14. Dim Light Exposure or Melatonin Ingestion Lowers a Type 2 Diabetic's Blood Glucose Removal Rate: A Single Case.
- Author
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SCOTT, MATTHEW C., NELSON, ARNOLD G., and HEARON, CHRISTOPHER M.
- Subjects
MELATONIN ,TYPE 2 diabetes ,BLOOD sugar ,METABOLIC disorders ,DIET ,EXERCISE - Abstract
International Journal of Exercise Science 12(2): 1161-1168, 2019. The purpose of this case study is to compare a Type 2 diabetic's postprandial glucoregulatory ability under two different room lighting conditions. The subject was a 56-year-old physically active male with well controlled blood glucose levels (HbA1c ≤ 6% for 5 y) from a combination of diet, exercise, and medication. Two hours post evening meal (380 kcal, 18 g fat, 44 g carbohydrate, 12 g protein), a 45 g carbohydrate challenge was given, and blood glucose was measured every 30 minutes for 2.5 hours under three conditions: dim light (<50 lux) (DL), bright light (>40000 lux) (BL), and bright light plus 6 mg melatonin (BLM). Each condition was repeated 3 times over a period of 6 months with each trial a minimum of seven days apart. The area under the average glucose concentration vs. time plot was different between the three conditions (BL = 909 + 76; DL = 1078 + 106; and BLM = 1130 + 45 mmol·min·l
-1 ). Visual inspection of the average blood glucose vs. time plot suggested that DL and BLM displayed very similar patterns and magnitude, with both DL and BLM having the blood glucose concentrations at each time point that are noticeably greater than BL. Additionally, the average (± standard deviation) blood glucose concentrations for DL (8.8 ± 0.9 mmol·l-1 ) and BLM (9.1 ± 1.1 mmol·l-1 ) were respectively 18% and 22% greater than BL (7.5 ± 0.5 mmol·l-1 ). Melatonin and/or dim light can reduce a Type 2 diabetic's glucoregulatory ability. [ABSTRACT FROM AUTHOR]- Published
- 2019
- Full Text
- View/download PDF
15. Bone Density And Quality After 4-months Of Resistance Exercise In Older Adults: 2299.
- Author
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Scott, Matthew C., Stampley, James E., Davis, Brett, Quiriarte, Heather, Cho, Eunhan, Theall, Bailey M., Granger, Joshua A., Spielmann, Guillaume, Johannsen, Neil M., Greenway, Frank, and Irving, Brian A.
- Subjects
- *
LUMBAR vertebrae physiology , *RESISTANCE training , *AEROBIC exercises , *EXERCISE physiology , *CONFERENCES & conventions , *BONE density , *CANCELLOUS bone - Published
- 2022
- Full Text
- View/download PDF
16. Bone Mineral Density In Older Adults With T2DM After Exercise Training: Results From Hart-D: 3083 Board #8 June 2 9:00 AM - 11:00 AM.
- Author
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Scott, Matthew C., Johannsen, Neil M., Swift, Damon L., Earnest, Conrad P., and Church, Timothy S.
- Subjects
- *
CONFERENCES & conventions , *EXERCISE physiology , *TYPE 2 diabetes , *BONE density - Published
- 2018
- Full Text
- View/download PDF
17. Isolation of Murine Adipose-Derived Stromal/Stem Cells for Adipogenic and Osteogenic Differentiation or Flow Cytometry-Based Analysis.
- Author
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Scott MC, Park CH, Dietrich M, Wu X, Gimble JM, Elks CM, Chang JS, and Floyd ZE
- Subjects
- Mice, Humans, Animals, Flow Cytometry methods, Osteogenesis, Adipocytes, Adipose Tissue, Cell Differentiation, Obesity metabolism, Stem Cells, Adipogenesis, Adiposity
- Abstract
Murine models of obesity or reduced adiposity are a valuable resource for understanding the role of adipocyte dysfunction in metabolic disorders. Adipose tissue stromal vascular cells or primary adipocytes derived from murine adipose tissue and grown in culture are essential tools for studying the mechanisms underlying adipocyte development and function. Herein, we describe methods for the isolation, expansion, and long-term storage of murine adipose-derived stromal/stem cells, along with protocols for inducing adipogenesis to white or beige adipocytes in this cell population and osteogenic differentiation. Isolation of the adipose stromal vascular fraction cells for flow cytometric analysis is also described., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)
- Published
- 2024
- Full Text
- View/download PDF
18. The Effects of Intermittent Cold Exposure on Adipose Tissue.
- Author
-
Scott MC and Fuller S
- Subjects
- Animals, Humans, Adipose Tissue, Brown, Body Weight, Obesity, Water, Diabetes Mellitus, Type 2
- Abstract
Intermittent cold exposure (ICE) has garnered increased attention in popular culture, largely for its proposed effects on mood and immune function, but there are also suggestions that the energy-wasting mechanisms associated with thermogenesis may decrease body weight and fat mass. Considering the continued and worsening prevalence of obesity and type II diabetes, any protocol that can reduce body weight and/or improve metabolic health would be a substantial boon. Here, we present a narrative review exploring the research related to ICE and adipose tissue. Any publicly available original research examining the effects of repeated bouts of ICE on adipose-related outcomes was included. While ICE does not consistently lower body weight or fat mass, there does seem to be evidence for ICE as a positive modulator of the metabolic consequences of obesity, such as glucose tolerance and insulin signaling. Further, ICE consistently increases the activity of brown adipose tissue (BAT) and transitions white adipose tissue to a phenotype more in line with BAT. Lastly, the combined effects of ICE and exercise do not seem to provide any additional benefit, at least when exercising during ICE bouts. The majority of the current literature on ICE is based on rodent models where animals are housed in cold rooms, which does not reflect protocols likely to be implemented in humans such as cold water immersion. Future research could specifically characterize ICE via cold water immersion in combination with controlled calorie intake to clearly determine the effects of ICE as it would be implemented in humans looking to lower their body weight via reductions in fat mass.
- Published
- 2023
- Full Text
- View/download PDF
19. Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle.
- Author
-
Huang TY, Linden MA, Fuller SE, Goldsmith FR, Simon J, Batdorf HM, Scott MC, Essajee NM, Brown JM, and Noland RC
- Subjects
- Animals, Lipid Metabolism physiology, Male, Mice, Mice, Inbred C57BL, Mitochondrial Dynamics physiology, Oxidation-Reduction, Oxidative Stress physiology, Diet, Ketogenic, Mitochondria, Muscle metabolism, Muscle, Skeletal metabolism, Peroxisomes metabolism, Physical Conditioning, Animal physiology
- Abstract
Ketogenic diets (KDs) are reported to improve body weight, fat mass, and exercise performance in humans. Unfortunately, most rodent studies have used a low-protein KD, which does not recapitulate diets used by humans. Since skeletal muscle plays a critical role in responding to macronutrient perturbations induced by diet and exercise, the purpose of this study was to test if a normal-protein KD (NPKD) impacts shifts in skeletal muscle substrate oxidative capacity in response to exercise training (ExTr). A high fat, carbohydrate-deficient NPKD (16.1% protein, 83.9% fat, 0% carbohydrate) was given to C57BL/6J male mice for 6 wk, whereas controls (Con) received a low-fat diet with similar protein (15.9% protein, 11.9% fat, 72.2% carbohydrate). After 3 wk on the diet, mice began treadmill training 5 days/wk, 60 min/day for 3 wks. The NPKD increased body weight and fat mass, whereas ExTr negated a continued rise in adiposity. ExTr increased intramuscular glycogen, whereas the NPKD increased intramuscular triglycerides. Neither the NPKD nor ExTr alone altered mitochondrial content; however, in combination, the NPKD-ExTr group showed increases in PGC-1α and markers of mitochondrial fission/fusion. Pyruvate oxidative capacity was unchanged by either intervention, whereas ExTr increased leucine oxidation in NPKD-fed mice. Lipid metabolism pathways had the most notable changes as the NPKD and ExTr interventions both enhanced mitochondrial and peroxisomal lipid oxidation and many adaptations were additive or synergistic. Overall, these results suggest that a combination of a NPKD and ExTr induces additive and/or synergistic adaptations in skeletal muscle oxidative capacity. NEW & NOTEWORTHY A ketogenic diet with normal protein content (NPKD) increases body weight and fat mass, increases intramuscular triglyceride storage, and upregulates pathways related to protein metabolism. In combination with exercise training, a NPKD induces additive and/or synergistic activation of AMPK, PGC-1α, mitochondrial fission/fusion genes, mitochondrial fatty acid oxidation, and peroxisomal adaptations in skeletal muscle. Collectively, results from this study provide mechanistic insight into adaptations in skeletal muscle relevant to keto-adaptation.
- Published
- 2021
- Full Text
- View/download PDF
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