Article ID: 0512050014
The purpose of this study was two-fold: (i) to investigate if sprint-interval training (SIT) alters myosin heavy chain (MyHC) isoform composition and bioenergetic properties within the rat diaphragm; and (ii) to determine if mild normobaric hypoxia would enhance the effects of SIT-induced diaphragmatic adaptation. Male Wistar rats (8 weeks old) were randomly assigned to one of four groups (n = 7/group): (i) normoxic control (NC); (ii) normoxic training (NT); (iii) hypoxic control (HC); or (iv) hypoxic training (HT). NT and HT groups were engaged in SIT (1 min sprint and 2–5 min rest, 6–10 sets/day, 5–6 days/week) on a treadmill for 9 weeks. Animals in the HC and HT groups were exposed to normobaric hypoxia (14.5% O2) during SIT program from the 4th week of the training period. After completion of the training program, MyHC composition, citrate synthase (CS) activity, and lactate dehydrogenase (LDH) activity in the diaphragm and plantaris muscle were analyzed. Analysis of diaphragmatic MyHC composition demonstrated increased type IIa and decreased type IId/x for the both training groups (P < 0.05), with HT group producing greater such changes than NT (P < 0.05). The plantaris muscle, on the other hand, showed increased Type IIa and IId/x, and decreased Type IIb for both NT and HT groups (P < 0.05). CS activity increased only for the training groups (P < 0.05), and this change was greater for HT group in the diaphragm, but for NT in the plantaris muscle (P < 0.05). Further, diaphragmatic LDH activity in HT was significantly lower (P < 0.05) than HC and NT. These findings demonstrated that SIT could induce alterations in MyHC composition from fast to slow within type II isoforms, and also improve the oxidative capacity in the diaphragm and plantaris muscles. Importantly, our data revealed that SIT-induced diaphragmatic adaptations were enhanced when SIT was performed in normobaric hypoxia.
