Fibre-specific responses to endurance and low volume high intensity interval training: striking similarities in acute and chronic adaptation

Abstract

The current study involved the completion of two distinct experiments. Experiment 1 compared fibre specific and whole muscle responses to acute bouts of either low-volume high-intensity interval training (LV-HIT) or moderate-intensity continuous endurance exercise (END) in a randomized crossover design. Experiment 2 examined the impact of a six-week training intervention (END or LV-HIT; 4 days/week), on whole body and skeletal muscle fibre specific markers of aerobic and anaerobic capacity. Six recreationally active men (Age: 20.7 ± 3.8 yrs; VO2peak: 51.9 ± 5.1 mL/kg/min) reported to the lab on two separate occasions for experiment 1. Following a muscle biopsy taken in a fasted state, participants completed an acute bout of each exercise protocol (LV-HIT: 8, 20-second intervals at ∼ 170% of VO2peak separated by 10 seconds of rest; END: 30 minutes at ∼ 65% of VO2peak), immediately followed by a muscle biopsy. Glycogen content of type I and IIA fibres was significantly (p<0.05) reduced, while p-ACC was significantly increased (p<0.05) following both protocols. Nineteen recreationally active males (n = 16) and females (n = 3) were VO2peak-matched and assigned to either the LV-HIT (n = 10; 21 ± 2 yrs) or END (n = 9; 20.7 ± 3.8 yrs) group for experiment 2. After 6 weeks, both training protocols induced comparable increases in aerobic capacity (END: Pre: 48.3 ± 6.0, Mid: 51.8 ± 6.0, Post: 55.0 ± 6.3 mL/kg/min LV-HIT: Pre: 47.9 ± 8.1, Mid: 50.4 ± 7.4, Post: 54.7 ± 7.6 mL/kg/min), fibre-type specific oxidative and glycolytic capacity, glycogen and IMTG stores, and whole-muscle capillary density. Interestingly, only LV-HIT induced greater improvements in anaerobic performance and estimated whole-muscle glycolytic capacity. These results suggest that 30 minutes of END exercise at ∼ 65% VO2peak or 4 minutes of LV-HIT at ∼ 170% VO2peak induce comparable changes in the intra-myocellular environment (glycogen content and signaling activation); correspondingly, training-induced adaptations resulting for these protocols, and other HIT and END protocols are strikingly similar.

Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1. Effects of acute exercise on fibre-type specific glycogen depletion and phosphorylation of AMPKα.

A: Representative slides of immunofluorescent fibre-type analysis (blue fibres are type I, green are type IIA, red/green are type IIAX/IIX) with serial sections of glycogen (periodic acid-Schiff staining) and p-AMPKα Thr172 content before (Rest) and immediately after (Ex) an acute bout of END or LV-HIT. B–C: Fold change in glycogen content from Rest and Ex in type I and IIA fibres. D–E: Fold change in p-AMPKα content from Rest and Ex in type I and IIA fibres. Bars represent 100 µm. AU, arbitrary units; µm, micrometre. *Significant (p<0.05) main effect of exercise.

Figure 2. Effects of an acute bout of endurance (END) and low-volume high-intensity interval training (LV-HIT) on whole-muscle signaling.

A–D: Fold change in p-AMPKα Thr172 (A), p-ACC Ser79 (B) and p38 MAPK Thr180/Tyr182 (C) content from Rest and Ex. D: Representative western blots, including loading control are also shown. AU, arbitrary units. *Significant (p<0.05) main effect of exercise.

Figure 3. Effects of training (LV-HIT) on aerobic exercise performance, fibre-type distribution and fibre specific oxidative capacity.

Relative VO2peak (A) and time to 500 kcal (B) at Pre, Mid, and Post for both END and LV-HIT groups are shown. C: Representative slides of immunofluorescent fibre-type analysis (blue fibres are type I, green are type IIA, red/green are type IIAX/IIX) with serial sections of succinate dehydrogenase (SDH) activity Pre and Post END or LV-HIT. D: Percentage of total fibre distribution of type I, IIA and IIAX/IIX fibres Pre and Post END or LV-HIT. E: Fibre-type specific fold change in SDH activity post-training compared to pre-training in type I, IIA and IIAX/IIX fibres. F: Absolute change in estimated oxidative capacity. Bars represent 100 µm. AU, arbitrary units; µm, micrometre. *Significant (p<0.05) main effect of exercise.

Figure 4. Effects of 6 weeks of endurance (END) and low-volume high-intensity interval training (LV-HIT) on cardiovascular capacity and capillary density.

A: Representative slides of capillarisation Pre and Post training. B: Absolute change in capillary density (capillaries/mm2). C: Change in O2 pulse (mL O2/beat). Bars represent 100 µm. mL, milliliter; mm, millimeter; O2, oxygen; µm, micrometre. *Significant (p<0.05) main effect of exercise.

Figure 5. Effects of endurance (END) and low-volume high-intensity interval training (LV-HIT) on anaerobic exercise performance and glycolytic capacity.

A: Representative slides of α-glycerophosphate dehydrogenase (GPD) activity Pre and Post training (see Fig. 3C for corresponding fibre-type slides). B: Total work performed during all 4 Wingate bouts. C: Fibre-type specific fold change in GPD activity post-training compared to pre-training in type I, IIA and IIAX/IIX fibres. D: Absolute change in estimated glycolytic capacity. Bars represent 100 µm. AU, arbitrary units; µm, micrometre. †Significant (pSignificant (p<0.05) within group difference (derived from paired t-test).

Figure 6. Effects of endurance (END) and low-volume high-intensity interval training (LV-HIT) on intramuscular glycogen and triglyceride storage.

A: Representative slides of glycogen (periodic acid-Schiff reaction) and intramuscular triglyceride (IMTG) content (Oil red O staining) Pre and Post training (see Fig. 3C for corresponding fibre-type slides for IMTG stain only). B. Fibre-type specific fold changes in glycogen content in type I, IIA and IIAX/IIX fibres. C. Fibre-type specific fold changes in IMTG content in type I, IIA and IIAX/IIX fibres. Bars represent 100 µm. AU, arbitrary units; µm, micrometre. *Significant (p