Resistance training diminishes mitochondrial adaptations to subsequent endurance training in healthy untrained men

• Published in: The Journal of physiology Vol. 601; no. 17; pp. 3825 - 3846
• Main Authors: Mesquita, Paulo H. C., Godwin, Joshua S., Ruple, Bradley A., Sexton, Casey L., McIntosh, Mason C., Mueller, Breanna J., Osburn, Shelby C., Mobley, C. Brooks, Libardi, Cleiton A., Young, Kaelin C., Gladden, L. Bruce, Roberts, Michael D., Kavazis, Andreas N.
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.09.2023
• Subjects: Acclimatization; Adaptation; Adaptation, Physiological; aerobic training; Biopsy; Body composition; Body Composition - physiology; Body fat; Cell number; Cell size; Citrate synthase; Endurance Training; HIIT; Humans; Immunohistochemistry; Male; Mitochondria; mitochondrial remodelling; Muscle, Skeletal - physiology; Physical training; Resistance Training - methods; Satellite cells; skeletal muscle; Strength training; Western blotting; Young Adult; Young adults; mitochondrial remodelling; strength training; aerobic training; skeletal muscle; HIIT
• ISSN: 0022-3751; 1469-7793; 1469-7793
• DOI: 10.1113/JP284822

We investigated the effects of performing a period of resistance training (RT) on the performance and molecular adaptations to a subsequent period of endurance training (ET). Twenty‐five young adults were divided into an RT+ET group (n = 13), which underwent 7 weeks of RT followed by 7 weeks of ET, and an ET‐only group (n = 12), which performed 7 weeks of ET. Body composition, endurance performance and muscle biopsies were collected before RT (T1, baseline for RT+ET), before ET (T2, after RT for RT+ET and baseline for ET) and after ET (T3). Immunohistochemistry was performed to determine fibre cross‐sectional area (fCSA), myonuclear content, myonuclear domain size, satellite cell number and mitochondrial content. Western blots were used to quantify markers of mitochondrial remodelling. Citrate synthase activity and markers of ribosome content were also investigated. RT improved body composition and strength, increased vastus lateralis thickness, mixed and type II fCSA, myonuclear number, markers of ribosome content, and satellite cell content (P < 0.050). In response to ET, both groups similarly decreased body fat percentage (P < 0.0001) and improved endurance performance (e.g. V̇O2max${\dot V_{{{\mathrm{O}}_2}\max }}$, and speed at which the onset of blood lactate accumulation occurred, P < 0.0001). Levels of mitochondrial complexes I–IV in the ET‐only group increased 32–66%, while those in the RT+ET group increased 1–11% (time, P < 0.050). Additionally, mixed fibre relative mitochondrial content increased 15% in the ET‐only group but decreased 13% in the RT+ET group (interaction, P = 0.043). In conclusion, RT performed prior to ET had no additional benefits to ET adaptations. Moreover, prior RT seemed to impair mitochondrial adaptations to ET. Key points Resistance training is largely underappreciated as a method to improve endurance performance, despite reports showing it may improve mitochondrial function. Although several concurrent training studies are available, in this study we investigated the effects of performing a period of resistance training on the performance and molecular adaptations to subsequent endurance training. Prior resistance training did not improve endurance performance and impaired most mitochondrial adaptations to subsequent endurance training, but this effect may have been a result of detraining from resistance training. figure legend We investigated the effects of resistance training (RT) on performance and molecular adaptations to a subsequent block of endurance training (ET). We hypothesized that RT‐induced increases in myonuclei and ribosome content would increase skeletal muscle transcriptional and translational capacity, ultimately enhancing mitochondrial adaptations to subsequent ET. In the current study, RT elicited commonly reported adaptations, such as increases in strength, muscle size, myonuclei, ribosome and satellite cells. However, even though both groups increased endurance performance similarly, prior RT impaired most mitochondrial adaptations to subsequent ET.