Beschreibung:
<jats:p>Increasing skeletal muscle carnitine availability increases pyruvate dehydrogenase (PDC) flux during continuous exercise at 80% maximal aerobic capacity (VO<jats:sub>2</jats:sub>max<jats:sub>−</jats:sub>), as evidenced by greater free carnitine acetylation [1]. Whether free carnitine availability is limiting to PDC flux and mitochondrial ATP production during consecutive bouts of more intense exercise is unclear. If it is, then increasing carnitine availability during high‐intensity interval training (HIT) could serve to enhance the gains to this type of exercise.</jats:p><jats:p>In seven healthy male volunteers (age 23 ± 4 years; BMI 23.6 ± 2.0 kg/m<jats:sup>2</jats:sup>; VO<jats:sub>2</jats:sub>max 48 ± 6 ml/kg/min) we determined skeletal muscle carnitine, PDC activation status, glycogenolysis and non‐mitochondrial ATP production (NMAP; from changes in phosphocreatine [PCr], lactate and ATP concentrations) during two 3 minute bouts of cycling exercise at 100% VO<jats:sub>2</jats:sub>max separated by 5 minutes recovery (Study A). In a further 14 volunteers (23.2 ± 1.1 years; 24.4 ± 0.9 kg/m<jats:sup>2</jats:sup>; 41.6 ± 2.1 ml/kg/min) we subsequently investigated the effects of twice daily L‐carnitine (1.5 g) and carbohydrate (80 g) supplementation (CARN) during 24 weeks of HIT (3×3 min at 100% VO<jats:sub>2</jats:sub>max thrice weekly), versus HIT with carbohydrate alone (CON; Study B). In addition to the same outcome measures in study A, study B included VO<jats:sub>2</jats:sub>max, work output, and mechanical efficiency. Both studies were approved by local ethics committee</jats:p><jats:p>In study A, muscle free carnitine declined similarly by 33% and 41%, whilst PDC activation increased 3 and 5‐fold, during bout one and bout two, respectively. Glycogenolysis tended to increase 2‐fold (54 ± 14 [bout one] vs. 99 ± 18 [bout two] mmol/kg dw; P=0.1) and although NMAP was not significantly different between bouts (158 ± 14 [bout one] vs. 110 ± 40 [bout two] mmol/kg dw; P=0.29), PCr degradation was 2‐fold greater during bout two (29 ± 9 [bout one] vs. 61 ± 8 [bout two] mmol/kg dw; P<0.05).</jats:p><jats:p>In study B, the change in muscle total carnitine following HIT was greater in CARN than CON (1.5 ± 0.7 [CARN] vs. −0.9 ± 0.6 [CON] mmol/kg dw; P<0.05), resulting in elevated free carnitine concentrations in CARN throughout bout one and prior to the start of bout two compared to CON (P<0.05). During bout one, NMAP was significantly lower following training in CARN (P<0.05) but not CON, whilst glycogenolysis was unchanged in both groups. During bout two, the HIT‐induced reduction in NMAP (~60%; P<0.01) and glycogenolysis (~60%; P<0.05) was similar between CON and CARN. Likewise, the overall improvements in VO<jats:sub>2</jats:sub>max (11% [CON] vs. 8% [CARN]) and work output (28% [CON] vs. 18% [CARN]) following HIT were similar between groups. However, mechanical efficiency increased in CARN only, such that the change from baseline was greater than in CON (1.9 ± 0.8 [CARN] and −0.2 ± 0.7% [CON]; P<0.05).</jats:p><jats:p>This novel data demonstrate that mitochondrial ATP production declines during a second bout of intense fixed workload cycling. However, increasing muscle carnitine availability during a 24 week period of HIT does not prevent this decline, despite improving efficiency during a first bout. As such, increasing muscle carnitine did not enhance the gains in exercise performance and capacity beyond the robust adaptations observed here with HIT training alone.</jats:p><jats:p><jats:bold>Support or Funding Information</jats:bold></jats:p><jats:p>BBSRC DTA Studentship</jats:p>