David Hood (physiologist)

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David Albert Hood
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BornOctober 8
Alma materQueen's University,

Dalhousie University,

State University of New York
OccupationProfessor and Canada Research Chair, School of Kinesiology and Health Science
OrganizationYork University
Spouse(s)Cindy
ChildrenAndrew, Ryan, Erin and Michelle
Websitehttp://dhood.lab.yorku.ca/

David Hood is a Canadian physiologist.

Biography

David Hood completed his PhD in physiology with Dr. Ronald Terjung at the State University of New York, Health Science Center, in Syracuse, New York in 1986.[1][2] He then spent two years as a Post-Doctoral Fellow with Dr. Dirk Pette at the University of Konstanz in Germany.[3] He joined York University's School of Kinesiology and Health Science, and Department of Biology (Faculty of Graduate Studies) as an Assistant Professor in 1988. He became an Associate Professor in 1992, and Full Professor in 1999.

Awards

He was the recipient of the American College of Sports Medicine's New Investigator Award in 1989. He has been awarded several research prizes in his career, including the Canadian Society of Exercise Physiology (CSEP) Honour Award, their highest distinction, in 2010.[4]

Leadership, teaching and training

Hood is the founding director, since 2009, of York University's Muscle Health Research Centre (MHRC), designed with a vision to be Canada's leading centre for muscle health research, education and training.[5] In 2020, the MHRC was comprised of 24 active faculty members and more than 120 trainees at all levels of education and has hosted > 175 invited Seminar speakers since 2009.  In his career at York, Hood has supervised 53 Master's students, 18 PhD students, and 17 Postdoctoral Fellows, along with 95 undergraduate thesis and Summer scholarship trainees.

He has been an undergraduate and graduate course director since 1991, having taught courses from years one through four in physiology, exercise physiology, muscle biochemistry and mitochondrial function over the years. Hood has attracted more than $5 million in research funds since receiving his Canada Research Chair in 2003, with $2.3 million obtained in the last five years. Many of the >180 students and post-doctoral fellows that have trained in his lab have graduated to successful careers in academia, medicine, and industry. Hood has received Teaching Awards from each of three faculties: 1) Faculty of Science Teaching Award (1999), 2) Faculty of Graduate Studies Teaching Award (2007), 3) Faculty of Health Teaching Award (Established Career) in 2013. In addition, he was a top 5 finalist nationally for the Canadian Association of Graduate Studies Mentorship Award (2019).[6]

Research

Hood's NSERC- and CIHR-funded research programs are devoted to the study of "Mitochondrial Turnover in Health and Disease", with a particular focus on mammalian skeletal muscle and the role of exercise and/or disuse and aging (Reviewed in [7]). A number of in vivo and cell culture experimental models are used to interrogate the mechanisms of both mitochondrial synthesis (biogenesis), as well as degradation (mitophagy) in muscle. Multi-disciplinary approaches involving physiological, biochemical and molecular biology techniques are employed. Hood has published over 180 full-paper academic publications in peer-reviewed journals and book chapters as well as greater than 260 abstracts with his trainees (h-index 57; total citations 16,588).

Some noteworthy research findings and discoveries by Hood and co-workers include:

  • Description of the energy cost of muscle contractions[1]
  • Mitochondrial and nuclear gene products are coordinately regulated during adaptations to contractile activity [3]
  • Leucine is metabolized by muscle but is not a major contributor to the energy cost of muscle contractions[2]
  • First demonstration of insulin binding to receptors in human muscle.[8]
  • Extensive description of mitochondrial and performance decrements during chronic muscle disuse.[9]
  • Lipids are synthesized before proteins during muscle mitochondrial biogenesis.[10]
  • Thorough description of mitochondrial biochemical characteristics in muscle.[11]       
  • Dystrophic muscle is not deficient in mitochondrial content during early development.[12]
  • Pressure overload stimulates mitochondrial biogenesis in the heart.[13]
  • Thyroid hormone modifies mitochondria in heart and muscle during growth and development, in part via increases in protein import.[14][15]
  • First demonstration of the regulation of protein import into skeletal muscle mitochondria, and the effect of contractile activity.[16][17]
  • Calcium is an important signal for transcription and mitochondrial gene expression in muscle.[18][19]
  • Contractile activity activates cytochrome c transcription in muscle.[20]
  • Exercise attenuates mitochondrially-mediated apoptotic susceptibility in muscle.[21]
  • AMP kinase regulates PGC-1alpha transcription in muscle cells.[22]
  • Mitochondrial from aging muscle are pro-apoptotic with a loss of function. Aged skeletal muscle adapts to exercise, but with a reduced response compared to muscle from young individuals.[23][24]
  • Both thyroid hormone and exercise training can improve mitochondria in cells from patients with mtDNA mutations.[25][26]
  • First descriptions of how p53 controls mitochondrial content and function in muscle via exercise, in part via signaling and interaction with mtDNA.[27][28][29]
  • Mitochondrial content determines the degree of gene expression signaling in muscle.[30]
  • PGC-1 alpha is not required to restore mitochondrial respiratory function as a result of exercise.[31]
  • Both age and exercise affect multi-subunit mitochondrial complex assembly in muscle.[32][33]
  • Chronic muscle disuse alters mitochondrial function and import of proteins.[34]
  • Exercise and resveratrol synergistically increase mitochondria in muscle.[35]
  • Exercise rescues a mitochondrial protein import defect in muscle.[36]
  • Exercise modifies mitochondrial morphology by controlling regulatory proteins. Morphology is regulated by organelle dynamics and movements in the cell.[37][38]
  • One bout of exercise simultaneously activates mitochondrial biogenesis and mitophagy.[39]
  • Nrf2 is involved in determining muscle and mitochondrial function.[40]
  • Unfolded protein response activation during chronic exercise.[41]
  • Exercise-induced lysosomal biogenesis in skeletal muscle.[42]
  • Retrograde signaling from mitochondria to nucleus in muscle.[43][44]
  • Defining the roles of parkin, exercise and aging on mitophagy in skeletal muscle.[45][46]
  • Exercise reverses mitochondrial defects in muscle cells.[47]
  • Exercise serves as "Mitochondrial Medicine" for muscle.[48]

In the media

  

References

  1. ↑ 1.0 1.1 Hood, D. A.; Gorski, J.; Terjung, R. L. (April 1986). "Oxygen cost of twitch and tetanic isometric contractions of rat skeletal muscle". The American Journal of Physiology. 250 (4 Pt 1): E449–456. doi:10.1152/ajpendo.1986.250.4.E449. ISSN 0002-9513. PMID 3963186.
  2. ↑ 2.0 2.1 Hood, D. A.; Terjung, R. L. (1987-12-01). "Effect of endurance training on leucine metabolism in perfused rat skeletal muscle". American Journal of Physiology-Endocrinology and Metabolism. 253 (6): E648–E656. doi:10.1152/ajpendo.1987.253.6.E648. ISSN 0193-1849. PMID 3425711.
  3. ↑ 3.0 3.1 Hood, David A.; Zak, Radovan; Pette, Dirk (1989). "Chronic stimulation of rat skeletal muscle induces coordinate increases in mitochondrial and nuclear mRNAs of cytochrome-c-oxidase subunits". European Journal of Biochemistry. 179 (2): 275–280. doi:10.1111/j.1432-1033.1989.tb14551.x. ISSN 1432-1033. PMID 2537205.
  4. ↑ "CSEP Honour Award". www.csep.ca. Retrieved 2020-10-05.
  5. ↑ "Faculty | Muscle Health Research Centre (MHRC)". Retrieved 2020-10-05.
  6. ↑ Sep 9; Outst, 2019 |; Finalists, ing Graduate Mentorship; Prizes. "Finalist – 2019 Award for Outstanding Graduate Mentorship – David Hood | CAGS". Retrieved 2020-10-05.{{cite web}}: CS1 maint: numeric names: authors list (link)
  7. ↑ Hood, David A.; Memme, Jonathan M.; Oliveira, Ashley N.; Triolo, Matthew (2019-02-10). "Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging". Annual Review of Physiology. 81: 19–41. doi:10.1146/annurev-physiol-020518-114310. ISSN 1545-1585. PMID 30216742.
  8. ↑ Bonen, A.; Hood, D. A.; Tan, M. H.; Sopper, M. M.; Bégin-Heick, N. (1984-09-28). "Insulin binding in human skeletal muscle". Biochimica et Biophysica Acta (BBA) - General Subjects. 801 (2): 171–176. doi:10.1016/0304-4165(84)90064-3. ISSN 0006-3002. PMID 6383482.
  9. ↑ Wicks, K. L.; Hood, D. A. (April 1991). "Mitochondrial adaptations in denervated muscle: relationship to muscle performance". The American Journal of Physiology. 260 (4 Pt 1): C841–850. doi:10.1152/ajpcell.1991.260.4.C841. ISSN 0002-9513. PMID 1850197.
  10. ↑ Takahashi, M.; Hood, D. A. (1993-02-01). "Chronic stimulation-induced changes in mitochondria and performance in rat skeletal muscle". Journal of Applied Physiology. 74 (2): 934–941. doi:10.1152/jappl.1993.74.2.934. ISSN 8750-7587. PMID 8458817.
  11. ↑ Cogswell, A. M.; Stevens, R. J.; Hood, D. A. (February 1993). "Properties of skeletal muscle mitochondria isolated from subsarcolemmal and intermyofibrillar regions". The American Journal of Physiology. 264 (2 Pt 1): C383–389. doi:10.1152/ajpcell.1993.264.2.C383. ISSN 0002-9513. PMID 8383431.
  12. ↑ Rezvani, M.; Cafarelli, E.; Hood, D. A. (1995-03-01). "Performance and excitability of mdx mouse muscle at 2, 5, and 13 wk of age". Journal of Applied Physiology. 78 (3): 961–967. doi:10.1152/jappl.1995.78.3.961. ISSN 8750-7587.
  13. ↑ Nishio, M. L.; Ornatsky, O. I.; Craig, E. E.; Hood, D. A. (May 1995). "Mitochondrial biogenesis during pressure overload induced cardiac hypertrophy in adult rats". Canadian Journal of Physiology and Pharmacology. 73 (5): 630–637. doi:10.1139/y95-080. ISSN 0008-4212. PMID 7585330.
  14. ↑ Stevens, Rebecca J.; Nishio, Mary L.; Hood, David A. (1995-02-01). "Effect of hypothyroidism on the expression of cytochrome c and cytochrome c oxidase in heart and muscle during development". Molecular and Cellular Biochemistry. 143 (2): 119–127. doi:10.1007/BF01816945. ISSN 1573-4919. PMID 7541108.
  15. ↑ Craig, Elaine E.; Chesley, Alan; Hood, David A. (1998-12-01). "Thyroid hormone modifies mitochondrial phenotype by increasing protein import without altering degradation". American Journal of Physiology-Cell Physiology. 275 (6): C1508–C1515. doi:10.1152/ajpcell.1998.275.6.C1508. ISSN 0363-6143. PMID 9843712.
  16. ↑ Takahashi, M.; Hood, D. A. (1996-11-01). "Protein import into subsarcolemmal and intermyofibrillar skeletal muscle mitochondria. Differential import regulation in distinct subcellular regions". The Journal of Biological Chemistry. 271 (44): 27285–27291. doi:10.1074/jbc.271.44.27285. ISSN 0021-9258. PMID 8910303.
  17. ↑ Takahashi, Mark; Chesley, Alan; Freyssenet, Damien; Hood, David A. (1998-05-01). "Contractile activity-induced adaptations in the mitochondrial protein import system". American Journal of Physiology-Cell Physiology. 274 (5): C1380–C1387. doi:10.1152/ajpcell.1998.274.5.C1380. ISSN 0363-6143. PMID 9612226.
  18. ↑ Freyssenet, Damien; Di Carlo, Martino; Hood, David A. (1999-04-02). "Calcium-dependent Regulation of CytochromecGene Expression in Skeletal Muscle Cells". Journal of Biological Chemistry. 274 (14): 9305–9311. doi:10.1074/jbc.274.14.9305. ISSN 0021-9258.
  19. ↑ Freyssenet, Damien; Irrcher, Isabella; Connor, Michael K.; Di Carlo, Martino; Hood, David A. (May 2004). "Calcium-regulated changes in mitochondrial phenotype in skeletal muscle cells". American Journal of Physiology-Cell Physiology. 286 (5): C1053–C1061. doi:10.1152/ajpcell.00418.2003. ISSN 0363-6143.
  20. ↑ Connor, Michael K.; Irrcher, Isabella; Hood, David A. (2001-02-20). "Contractile Activity-induced Transcriptional Activation of CytochromecInvolves Sp1 and Is Proportional to Mitochondrial ATP Synthesis in C2C12 Muscle Cells". Journal of Biological Chemistry. 276 (19): 15898–15904. doi:10.1074/jbc.m100272200. ISSN 0021-9258. PMID 11279044.
  21. ↑ Adhihetty, Peter J.; Ljubicic, Vladimir; Hood, David A. (March 2007). "Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle". American Journal of Physiology-Endocrinology and Metabolism. 292 (3): E748–E755. doi:10.1152/ajpendo.00311.2006. ISSN 0193-1849. PMID 17106065.
  22. ↑ Irrcher, Isabella; Ljubicic, Vladimir; Kirwan, Angie F.; Hood, David A. (2008-10-31). Lucia, Alejandro (ed.). "AMP-Activated Protein Kinase-Regulated Activation of the PGC-1α Promoter in Skeletal Muscle Cells". PLOS ONE. 3 (10): e3614. doi:10.1371/journal.pone.0003614. ISSN 1932-6203. PMC 2570798. PMID 18974883.
  23. ↑ Chabi, Béatrice; Ljubicic, Vladimir; Menzies, Keir J.; Huang, Julianna H.; Saleem, Ayesha; Hood, David A. (January 2008). "Mitochondrial function and apoptotic susceptibility in aging skeletal muscle". Aging Cell. 7 (1): 2–12. doi:10.1111/j.1474-9726.2007.00347.x. ISSN 1474-9726. PMID 18028258.
  24. ↑ Ljubicic, Vladimir; Joseph, Anna-Maria; Adhihetty, Peter J.; Huang, Julianna H.; Saleem, Ayesha; Uguccioni, Giulia; Hood, David A. (2009-09-12). "Molecular basis for an attenuated mitochondrial adaptive plasticity in aged skeletal muscle". Aging (Albany NY). 1 (9): 818–830. doi:10.18632/aging.100083. ISSN 1945-4589. PMC 2815739. PMID 20157569.
  25. ↑ Menzies, Keir J.; Robinson, Brian H.; Hood, David A. (2009-02-01). "Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects". American Journal of Physiology-Cell Physiology. 296 (2): C355–C362. doi:10.1152/ajpcell.00415.2007. ISSN 0363-6143. PMID 19036942.
  26. ↑ Adhihetty, Peter J.; Taivassalo, Tanja; Haller, Ronald G.; Walkinshaw, Donald R.; Hood, David A. (2007-09-01). "The effect of training on the expression of mitochondrial biogenesis- and apoptosis-related proteins in skeletal muscle of patients with mtDNA defects". American Journal of Physiology-Endocrinology and Metabolism. 293 (3): E672–E680. doi:10.1152/ajpendo.00043.2007. ISSN 0193-1849. PMID 17551003.
  27. ↑ Saleem, Ayesha; Adhihetty, Peter J.; Hood, David A. (2009-03-01). "Role of p53 in mitochondrial biogenesis and apoptosis in skeletal muscle". Physiological Genomics. 37 (1): 58–66. doi:10.1152/physiolgenomics.90346.2008. ISSN 1094-8341. PMID 19106183.
  28. ↑ Saleem, Ayesha; Hood, David A. (2013). "Acute exercise induces tumour suppressor protein p53 translocation to the mitochondria and promotes a p53–Tfam–mitochondrial DNA complex in skeletal muscle". The Journal of Physiology. 591 (14): 3625–3636. doi:10.1113/jphysiol.2013.252791. ISSN 1469-7793. PMC 3731618. PMID 23690562.
  29. ↑ Saleem, Ayesha; Carter, Heather N.; Hood, David A. (2014-02-01). "p53 is necessary for the adaptive changes in cellular milieu subsequent to an acute bout of endurance exercise". American Journal of Physiology – Cell Physiology. 306 (3): C241–C249. doi:10.1152/ajpcell.00270.2013. ISSN 0363-6143. PMC 3919998. PMID 24284795.
  30. ↑ Ljubicic, Vladimir; Hood, David A. (2009-09-01). "Specific attenuation of protein kinase phosphorylation in muscle with a high mitochondrial content". American Journal of Physiology-Endocrinology and Metabolism. 297 (3): E749–E758. doi:10.1152/ajpendo.00130.2009. ISSN 0193-1849. PMID 19549794.
  31. ↑ Adhihetty, Peter J.; Uguccioni, Giulia; Leick, Lotte; Hidalgo, Juan; Pilegaard, Henriette; Hood, David A. (2009-07-01). "The role of PGC-1α on mitochondrial function and apoptotic susceptibility in muscle". American Journal of Physiology-Cell Physiology. 297 (1): C217–C225. doi:10.1152/ajpcell.00070.2009. ISSN 0363-6143. PMID 19439529.
  32. ↑ Joseph, Anna-Maria; Ljubicic, Vladimir; Adhihetty, Peter J.; Hood, David A. (June 2010). "Biogenesis of the mitochondrial Tom40 channel in skeletal muscle from aged animals and its adaptability to chronic contractile activity". American Journal of Physiology-Cell Physiology. 298 (6): C1308–C1314. doi:10.1152/ajpcell.00644.2008. ISSN 0363-6143. PMC 6189513. PMID 20107041.
  33. ↑ Joseph, Anna-Maria; Hood, David A. (March 2012). "Plasticity of TOM complex assembly in skeletal muscle mitochondria in response to chronic contractile activity". Mitochondrion. 12 (2): 305–312. doi:10.1016/j.mito.2011.11.005. ISSN 1872-8278. PMID 22142511.
  34. ↑ Singh, Kaustabh; Hood, David A. (2010-10-13). "Effect of denervation-induced muscle disuse on mitochondrial protein import". American Journal of Physiology-Cell Physiology. 300 (1): C138–C145. doi:10.1152/ajpcell.00181.2010. ISSN 0363-6143. PMID 20943961.
  35. ↑ Menzies, Keir J.; Singh, Kaustabh; Saleem, Ayesha; Hood, David A. (2013-03-08). "Sirtuin 1-mediated Effects of Exercise and Resveratrol on Mitochondrial Biogenesis". Journal of Biological Chemistry. 288 (10): 6968–6979. doi:10.1074/jbc.M112.431155. ISSN 0021-9258. PMID 23329826.
  36. ↑ Zhang, Yuan; Iqbal, Sobia; O'Leary, Michael F. N.; Menzies, Keir J.; Saleem, Ayesha; Ding, Shuzhe; Hood, David A. (2013-06-19). "Altered mitochondrial morphology and defective protein import reveal novel roles for Bax and/or Bak in skeletal muscle". American Journal of Physiology-Cell Physiology. 305 (5): C502–C511. doi:10.1152/ajpcell.00058.2013. ISSN 0363-6143. PMID 23784543.
  37. ↑ Iqbal, Sobia; Ostojic, Olga; Singh, Kaustabh; Joseph, Anna-Maria; Hood, David A. (2013). "Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse". Muscle & Nerve. 48 (6): 963–970. doi:10.1002/mus.23838. ISSN 1097-4598.
  38. ↑ Iqbal, Sobia; Hood, David A. (2014). "Cytoskeletal regulation of mitochondrial movements in myoblasts". Cytoskeleton. 71 (10): 564–572. doi:10.1002/cm.21188. ISSN 1949-3592. PMID 25147078.
  39. ↑ Vainshtein, Anna; Tryon, Liam D.; Pauly, Marion; Hood, David A. (2015-02-11). "Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle". American Journal of Physiology-Cell Physiology. 308 (9): C710–C719. doi:10.1152/ajpcell.00380.2014. ISSN 0363-6143. PMC 4420796. PMID 25673772.
  40. ↑ Crilly, Matthew J.; Tryon, Liam D.; Erlich, Avigail T.; Hood, David A. (2016-07-28). "The role of Nrf2 in skeletal muscle contractile and mitochondrial function". Journal of Applied Physiology. 121 (3): 730–740. doi:10.1152/japplphysiol.00042.2016. ISSN 8750-7587. PMC 5142253. PMID 27471236.
  41. ↑ Memme, Jonathan M.; Oliveira, Ashley N.; Hood, David A. (2016-04-27). "Chronology of UPR activation in skeletal muscle adaptations to chronic contractile activity". American Journal of Physiology-Cell Physiology. 310 (11): C1024–C1036. doi:10.1152/ajpcell.00009.2016. ISSN 0363-6143. PMC 4935206. PMID 27122157.
  42. ↑ Kim, Yuho; Hood, David A. (2017). "Regulation of the autophagy system during chronic contractile activity-induced muscle adaptations". Physiological Reports. 5 (14): e13307. doi:10.14814/phy2.13307. ISSN 2051-817X. PMC 5532476. PMID 28720712.
  43. ↑ Oliveira, Ashley N.; Hood, David A. (2018-06-27). "Effect of Tim23 knockdown in vivo on mitochondrial protein import and retrograde signaling to the UPRmt in muscle". American Journal of Physiology-Cell Physiology. 315 (4): C516–C526. doi:10.1152/ajpcell.00275.2017. ISSN 0363-6143. PMC 6230686. PMID 29949403.
  44. ↑ Joseph, Anna-Maria; Rungi, Arne A.; Robinson, Brian H.; Hood, David A. (April 2004). "Compensatory responses of protein import and transcription factor expression in mitochondrial DNA defects". American Journal of Physiology-Cell Physiology. 286 (4): C867–C875. doi:10.1152/ajpcell.00191.2003. ISSN 0363-6143. PMID 14656719.
  45. ↑ Carter, Heather N.; Kim, Yuho; Erlich, Avigail T.; Zarrin-khat, Dorrin; Hood, David A. (2018-07-03). "Autophagy and mitophagy flux in young and aged skeletal muscle following chronic contractile activity". The Journal of Physiology. 596 (16): 3567–3584. doi:10.1113/jp275998. ISSN 0022-3751. PMID 29781176.
  46. ↑ Chen, Chris Chin Wah; Erlich, Avigail T.; Crilly, Matthew J.; Hood, David A. (2018-05-29). "Parkin is required for exercise-induced mitophagy in muscle: impact of aging". American Journal of Physiology-Endocrinology and Metabolism. 315 (3): E404–E415. doi:10.1152/ajpendo.00391.2017. ISSN 0193-1849. PMID 29812989.
  47. ↑ Parousis, Alexa; Carter, Heather N.; Tran, Claudia; Erlich, Avigail T.; Moosavi, Zahra S. Mesbah; Pauly, Marion; Hood, David A. (2018-11-02). "Contractile activity attenuates autophagy suppression and reverses mitochondrial defects in skeletal muscle cells". Autophagy. 14 (11): 1886–1897. doi:10.1080/15548627.2018.1491488. ISSN 1554-8627. PMC 6152519. PMID 30078345.
  48. ↑ Oliveira, Ashley N.; Hood, David A. (December 2019). "Exercise is mitochondrial medicine for muscle". Sports Medicine and Health Science. 1 (1): 11–18. doi:10.1016/j.smhs.2019.08.008. ISSN 2666-3376.

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