Maja Schlittler1,2, Daria Neyroud3,4, Christian Tanga3, Nadège Zanou3, Sigitas Kamandulis2, Albertas Skurvydas2, Bengt Kayser3, Håkan Westerblad1,2, Nicolas Place5, Daniel C Andersson1,6. 1. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. 2. Sports Science and Innovation Institute, Lithuanian Sports University, Kaunas, Lithuania. 3. Institute of Sport Sciences, Quartier UNIL-Centre, Faculty of Biology-Medicine, University of Lausanne, Bâtiment Synathlon, 1015, Lausanne, Switzerland. 4. Department of Physical Therapy, University of Florida Health Science Center, Gainesville, FL, USA. 5. Institute of Sport Sciences, Quartier UNIL-Centre, Faculty of Biology-Medicine, University of Lausanne, Bâtiment Synathlon, 1015, Lausanne, Switzerland. nicolas.place@unil.ch. 6. Heart and Vascular Theme, Arrhythmia, Heart Failure and GUCH Unit, Karolinska University Hospital, Stockholm, Sweden.
Abstract
PURPOSE: Mechanisms underlying the efficacy of sprint interval training (SIT) remain to be understood. We previously reported that an acute bout of SIT disrupts the integrity of the sarcoplasmic reticulum (SR) Ca2+ release channel, the ryanodine receptor 1 (RyR1), in recreationally active human subjects. We here hypothesize that in addition to improving the exercise performance of recreationally active humans, a period of repeated SIT sessions would make the RyR1 protein less vulnerable and accelerate recovery of contractile function after a SIT session. METHODS: Eight recreationally active males participated in a 3-week SIT program consisting of nine sessions of four-six 30-s all-out cycling bouts with 4 min of rest between bouts. RESULTS: Total work performed during a SIT session and maximal power (Wmax) reached during an incremental cycling test were both increased by ~ 7.5% at the end of the training period (P < 0.05). Western blots performed on vastus lateralis muscle biopsies taken before, 1 h, 24 h and 72 h after SIT sessions in the untrained and trained state showed some protection against SIT-induced reduction of full-length RyR1 protein expression in the trained state. SIT-induced knee extensor force deficits were similar in the untrained and trained states, with a major reduction in voluntary and electrically evoked forces immediately and 1 h after SIT (P < 0.05), and recovery after 24 h. CONCLUSIONS: Three weeks of SIT improves exercise performance and provides some protection against RyR1 modification, whereas it does not accelerate recovery of contractile function.
PURPOSE: Mechanisms underlying the efficacy of sprint interval training (SIT) remain to be understood. We previously reported that an acute bout of SIT disrupts the integrity of the sarcoplasmic reticulum (SR) Ca2+ release channel, the ryanodine receptor 1 (RyR1), in recreationally active human subjects. We here hypothesize that in addition to improving the exercise performance of recreationally active humans, a period of repeated SIT sessions would make the RyR1 protein less vulnerable and accelerate recovery of contractile function after a SIT session. METHODS: Eight recreationally active males participated in a 3-week SIT program consisting of nine sessions of four-six 30-s all-out cycling bouts with 4 min of rest between bouts. RESULTS: Total work performed during a SIT session and maximal power (Wmax) reached during an incremental cycling test were both increased by ~ 7.5% at the end of the training period (P < 0.05). Western blots performed on vastus lateralis muscle biopsies taken before, 1 h, 24 h and 72 h after SIT sessions in the untrained and trained state showed some protection against SIT-induced reduction of full-length RyR1 protein expression in the trained state. SIT-induced knee extensor force deficits were similar in the untrained and trained states, with a major reduction in voluntary and electrically evoked forces immediately and 1 h after SIT (P < 0.05), and recovery after 24 h. CONCLUSIONS: Three weeks of SIT improves exercise performance and provides some protection against RyR1 modification, whereas it does not accelerate recovery of contractile function.
Authors: Nadège Zanou; Haikel Dridi; Steven Reiken; Tanes Imamura de Lima; Chris Donnelly; Umberto De Marchi; Manuele Ferrini; Jeremy Vidal; Leah Sittenfeld; Jerome N Feige; Pablo M Garcia-Roves; Isabel C Lopez-Mejia; Andrew R Marks; Johan Auwerx; Bengt Kayser; Nicolas Place Journal: Nat Commun Date: 2021-12-10 Impact factor: 14.919
Authors: Riley E G Cleverdon; Jessica L Braun; Mia S Geromella; Kennedy C Whitley; Daniel M Marko; Sophie I Hamstra; Brian D Roy; Rebecca E K MacPherson; Val A Fajardo Journal: iScience Date: 2022-08-18