Inclusion of sprints in moderate intensity continuous training leads to muscle oxidative adaptations in trained individuals

Abstract

This study examined adaptations in muscle oxidative capacity and exercise performance induced by two work- and duration-matched exercise protocols eliciting different muscle metabolic perturbations in trained individuals. Thirteen male subjects ( $\dot{V}$ O₂ -max 53.5 ± 7.0 mL·kg^-1 ·min^-1 ) (means ± SD) performed 8 weeks (three sessions/week) of training consisting of 60 min of moderate intensity continuous cycling (157 ± 20 W) either without (C) or with (C+S) inclusion of 30-s sprints (473 ± 79 W) every 10 min. Total work performed during training was matched between groups. Muscle biopsies and arm venous blood were collected before as well as immediately and 2 h after exercise during the first and last training session. Plasma epinephrine and lactate concentrations after the first and last training session were 2-3-fold higher in C+S than in C. After the first and last training session, muscle phosphocreatine and pH were lower (12-25 mmol·kg d.w.^-1 and 0.2-0.4 units, respectively) and muscle lactate higher (48-64 mmol·kg d.w.^-1 ) in C+S than in C, whereas exercise-induced changes in muscle PGC-1α mRNA levels were similar within- and between-groups. Muscle content of cytochrome c oxidase IV and citrate synthase (CS) increased more in C+S than in C, and content of CS in type II muscle fibers increased in C+S only (9-17%), with no difference between groups. Performance during a 45-min time-trial improved by 4 ± 3 and 9 ± 3% in C+S and C, respectively, whereas peak power output at exhaustion during an incremental test increased by 3 ± 3% in C+S only, with no difference between groups. In conclusion, addition of sprints in moderate intensity continuous exercise causes muscle oxidative adaptations in trained male individuals which appear to be independent of the exercise-induced PGC-1α mRNA response. Interestingly, time-trial performance improved similarly between groups, suggesting that changes in content of mitochondrial proteins are of less importance for endurance performance in trained males.

Keywords: High-intensity interval training (HIIT); PGC-1a mRNA; human performance; metabolic stress; skeletal muscle single fibers.

Figure 1

(A) 45‐min time‐trial performance (W), (B) maximum oxygen uptake, and (C) exhaustive peak power output (W) during incremental test before (pre) and after (post) an 8‐week intervention period consisting of 60 min of moderate intensity continuous cycling exercise without (C; white bars and black triangles; n = 7) or with (C+S; hatched bars and black circles; n = 6) inclusion of sprints. Mean and individual values are displayed. *Different (P < 0.05) from pre.

Figure 2

(A) blood lactate, (B) plasma FFA, (C) plasma epinephrine, and (D) plasma norepinephrine during the first (circles) and last (triangles) training session of an 8‐week intervention period consisting of 60 min of moderate intensity continuous cycling exercise without (C; white symbols; n = 7) or with (C+S; black symbols; n = 6) inclusion of sprints. Values are expressed as means±SD. *Different (P < 0.05) from first training session. ^#Different (P > 0.05) from same time point in C.

Figure 3

Peroxisome proliferator‐activated receptor‐ϒ coactivator‐1α (PGC‐1α) mRNA before (rest; white bars), immediately (gray bars) and 2 h (black bars) after 60 min of moderate intensity continuous cycling exercise without (C; white bars; n = 6) or with (C+S; black bars; n = 6) inclusion of sprints, before and after an 8‐week intervention period. Values are expressed as means±SD. *Different (P < 0.01) from before (rest) and immediately after (0 h) exercise.

Figure 4

Relative change in muscle protein expression after an 8‐week intervention period consisting of 60 min of moderate intensity continuous cycling exercise without (C; white bars; n = 6) or with (C+S; black bars; n = 6) inclusion of sprints. Values are expressed as means±SD. *Different (P < 0.05) from before the intervention period. $Group x time interaction effect (P < 0.05). Cytochrome C Oxidase complex IV (COX IV), β‐hydroxyacyl‐CoA dehydrogenase (HAD), citrate synthase (CS), and phosphofructokinase (PFK).

Figure 5

Relative change in muscle protein expression of (A) citrate synthase and (B) phosphofructokinase in type I (cross‐hatched bars) and type II (hatched bars) single muscle fibers after an 8‐week intervention period consisting of 60 min of moderate intensity continuous cycling exercise without (C; n = 6) or with (C+S; n = 6) inclusion of sprints. Values are expressed as means ± SD. *Different (P < 0.05) from before the intervention period.