NEW RESEARCH: INTENSE TRAINING CAUSES MITOCHONDRIAL IMPAIRMENTS IN ELITE ENDURANCE ATHLETES
Posted on July 07 2021
By Steve Blechman
It was reported by MedicalExpress.com on June 24, 2021 that, “New research finds elite athletes have temporary mitochondrial impairment after intense workouts, suggesting that they may need to be mindful about overtraining. The study is published ahead of print in the Journal of Applied Physiology.”
The mitochondria are often referred to as the powerhouses of our muscle cell. They help generate the energy from the food we eat into adenosine triphosphate (ATP), the energy currency of the cell. This process is called oxidative phosphorylation. This new research found that “short-term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes.” And their muscle cells’ ability to generate energy, according to research scientists from Denmark and Sweden.
“In the research team's new study, the researchers worked with a small group of male elite athletes, many of whom held national titles or were internationally recognized for their performance in cycling and triathlon. The athletes participated in a four-week training program in their primary sport that consisted of two to four days of low- to moderate-intensity endurance workouts, followed by three days of more intense training. The intense workouts included high-intensity interval training in the morning, followed by a seven-hour break and then a moderate-intensity cycling session in the afternoon. The total number of activity hours ranged between 12 and 20 per week for each volunteer. Though the men were used to heavy training, they were not accustomed to this specific workout schedule.”
“To the research team's surprise, the highly trained participants' mitochondrial capacity was impaired after the month-long training period. We thought that elite athletes should be more resistant against [these] kind of alterations,” said Filip Larsen, Ph.D., of the Swedish School of Sport and Health Sciences and corresponding author of the study.”
In a study published in the March 18th, 2021 issue of the journal Cell Metabolism, a team of Swedish researchers reported that excessive high-intensity interval training (HIIT) can cause mitochondrial dysfunction and insulin resistance. The researchers found that “excessive exercise training induces substantial respiratory impairment” and that “mitochondrial impairment is associated with impaired glucose tolerance.” HIIT training involves short burst of high-intensity exercise interspersed with a few minutes of rest or lower intensity exercise to enhance recovery. Research has shown that the benefits and advantages of HIIT training is that you can get maximum health effects in the least amount of time. Studies have shown that high-intensity interval training can increase muscle mitochondrial biogenesis, protein synthesis and enhance mitochondrial function and cardiorespiratory fitness. But is more HIIT training better? Not necessarily, according to this new study. With test subjects performing HIIT training on a stationary bike, the researchers “used a training model with a progressively increasing exercise load during an intervention of four weeks.” The researchers said, “We closely follow changes in glucose tolerance, mitochondrial function and dynamics, physical exercise capacity and whole-body metabolism. Following the week with the highest exercise load, we found a striking reduction in intrinsic mitochondrial function that coincided with the disturbance in glucose tolerance and insulin secretion. We also assessed continuous blood glucose profiles in world-class endurance athletes and found that they had impaired glucose control compared with the match control group.” During the study, the researchers performed muscle biopsies of the exercise subjects to measure mitochondrial function as well as glucose measurements to monitor insulin levels. The insulin resistance was similar to someone with diabetes. Also, mitochondrial respiration fell by an average of 40%. But oxygen consumption and power output levels improved. The shortcoming of this study is that it was small and only involved 11 adults that exercised regularly, but not competitive athletes. A larger study is needed over a longer period of time to see if the same results occur. The bottom line is the health benefits of exercise are clear. High-Intensity interval training (HIIT) is safe and very effective workout for improving health and performance. It is not necessary to do HIIT training every day. Do HIIT training two to three times weekly, and on other days of the week do moderate-intensity exercise of longer duration to achieve optimum metabolic health, fat loss and aerobic fitness. To enhance muscle performance and recovery after high-intensity exercise, take mitochondrial regulator and protector nutrients such as leucine (5 grams), creatine monohydrate (5 grams) and betaine (2.5 grams) as present in Advanced Molecular Labs (AML) Post Workout. Research has shown that these mitochondrial activators can help enhance and preserve skeletal muscle mitochondrial biogenesis and function.
- Study finds intense training sessions temporarily impair mitochondrial function. MedicalXpress. June 24, 2021. American Physiological Society. https://medicalxpress.com/news/2021-06-intense-sessions-temporarily-impair-mitochondrial.html
- Short term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes. Daniele A Cardinale, Kasper D Gejl, Kristine Grøsfjeld Petersen, Joachim Nielsen, Niels Ørtenblad, and Filip J Larsen. June 10, 2021. Journal of Applied Physiology https://doi.org/10.1152/japplphysiol.00829.2020
- Flockhart M, Nilsson LC, Tais S, Ekblom B, Apró W, Larsen FJ. Excessive exercise training causes mitochondrial functional impairment and decreases glucose tolerance in healthy volunteers. Cell Metab 2021; Mar 13:S1550-4131(21)00102-9. doi: 10.1016/j.cmet.2021.02.017. Epub ahead of print. PMID: 33740420.
- Cell Press. How exercise - interval training in particular - helps your mitochondria stave off old age. ScienceDaily, 7 March 2017. www.sciencedaily.com/releases/2017/03/170307155214.htm
- Matthew M Robinson, Surendra Dasari, Adam R. Konopka, Matthew L Johnson, S Manjunatha, Raul Ruiz Esponda, Rickey E Carter, Ian R Lanza, K Sreekumaran Nair. Enhanced Protein Translation Underlies Improved Metabolic and Physical Adaptations to Different Exercise Training Modes in Young and Old Humans. Cell Metabolism 2017; 25 (3): 581 DOI: 10.1016/j.cmet.2017.02.009
- Modulation of Energy Sensing by Leucine Synergy With Natural Sirtuin Activators: Effects on Healthspan. Journal of Medicinal Foods, November 6, 2020. Michael Zemel.
- Betaine increases mitochondrial content and improves hepatic lipid metabolism. Food Function, December 4, 2018.
- Betaine enhances the cellular survival via mitochondrial fusion DRP1. Animal Cells and Systems, published online August 30, 2018.
- Leucine regulates slow-twitch muscle fiber expression and mitochondrial function by SIRT1/AMPK signaling in porcine skeletal muscle satellite cells. Animal Science Journal, February 2019, Xiaoling Chen et al.
- Leucine modulation of mitochondrial mass and oxygen consumption in skeletal muscle cells and adipocytes. Nutrition & Metabolism, published online June 5, 2009. Xiaocun Sun and Michael B Zemel.
- Betaine is a positive regulator of mitochondrial respiration. Biochemical and Biophysical Research Communications, published online December 8, 2014. Icksoo Lee.
- Enhanced mitochondrial biogenesis is associated with ameliorative action of creatine supplementation in rat soleus and cardiac muscles. Exp Ther Med, January 2020.
- Creatine supplementation reduces skeletal muscle degeneration and enhances mitochondrial function in mdx mice. Neuromuscular Disorders, February 2002. Anne-Catherine Passaquin et al.
- Effects of creatine supplementation on muscular strength and body composition. Medicine Science Sports & Exercise, March 2000. MD Becque et al.
- Leucine Modulates Mitochondrial Biogenesis and SIRT1-AMPK Signaling in C2C12 Myotubes. Chunzi Liang, Benjamin J Curry, Patricia L Brown, and Michael B Zemel. October 7, 2014. Journal of Nutrition & Metabolism. Hindawi. https://www.hindawi.com/journals/jnme/2014/239750/
- Sun X, Zemel MB. Leucine modulation of mitochondrial mass and oxygen consumption in skeletal muscle cells and adipocytes. Nutr Metab (Lond). 2009;6:26. Published 2009 Jun 5. doi:10.1186/1743-7075-6-26
- Li H, Xu M, Lee J, He C, Xie Z. Leucine supplementation increases SIRT1 expression and prevents mitochondrial dysfunction and metabolic disorders in high-fat diet-induced obese mice. Am J Physiol Endocrinol Metab. 2012 Nov 15;303(10):E1234-44. doi: 10.1152/ajpendo.00198.2012. Epub 2012 Sep 11. PMID: 22967499; PMCID: PMC3517633.
- Leucine increases muscle mitochondrial respiration and attenuates glucose intolerance in diet-induced obesity in Swiss mice. Henver Simionato, Brunettaaek Gabriela, Cristinade Paulab, Matheus Fritzene, Manuela Sozo Cecchinid, Gustavo Jorge dos Santosae, Evelise Maria, Nazarid Alex, Rafachoae Andreza, Fabrode Bembc, Everson Araújo Nunesa. Journal of Functional Foods. ScienceDirect. November 2019. https://www.sciencedirect.com/science/article/abs/pii/S1756464619304682
- Leucine augments specific skeletal muscle mitochondrial respiratory pathways during recovery following 7 days of physical inactivity in older adults. Emily J Arentson-Lantz, Jasmine Mikovic, Nisha Bhattarai, Christopher S Fry, Séverine Lamon, Craig Porter, and Douglas Paddon-Jones. Journal of Applied Physiology 2021 130:5, 1522-1533. May 11, 2021. https://doi.org/10.1152/japplphysiol.00810.2020
- Walsh B, Tonkonogi M, Söderlund K, Hultman E, Saks V, Sahlin K. The role of phosphorylcreatine and creatine in the regulation of mitochondrial respiration in human skeletal muscle. J Physiol. 2001;537(Pt 3):971-978. doi:10.1111/j.1469-7793.2001.00971.x
- Creatine supplementation reduces skeletal muscle degeneration and enhances mitochondrial function in mdx mice. Anne-Catherine Passaquin, Mathilde Renard, Laurence Kay, Corinne Challet, Armand Mokhtarian, Theo Wallimann, Urs T. Ruegg, Neuromuscular Disorders. February 2002 https://doi.org/10.1016/S0960-8966(01)00273-5
- Jung Kim M. Betaine enhances the cellular survival via mitochondrial fusion and fission factors, MFN2 and DRP1. Anim Cells Syst (Seoul). 2018;22(5):289-298. Published 2018 Aug 30. doi:10.1080/19768354.2018.1512523.
- Leucine Supplementation: A Novel Strategy for Modulating Lipid Metabolism and
Energy Homeostasis. Lingyu Zhang, Fengna Li , Qiuping Guo, Yehui Duan, Wenlong Wang,
Yinzhao Zhong, Yuhuan Yang and Yulong Yin. Nutreints May 2, 2020