The aim of this study was to determine if gender differences in muscle mass explain the gender differences in running and cycling sprint performance. Body composition (dual-energy X-ray absorptiometry), and running (30 and 300 m test) and cycling (Wingate test) sprint performance were assessed in 123 men and 32 women. Peak power (PP) output in the Wingate test expressed per kg of lower extremities lean mass (LM) was similar in males and females (50.4 +/- 5.6 and 50.5 +/- 6.2 W kg(-1), P = 0.88). No gender differences were observed in the slope of the linear relation between LM and PP or mean power output (MP). However, when MP was expressed per kg of LM, the males attained a 22% higher value (26.6 +/- 3.4 and 21.9 +/- 3.2 W kg(-1), P < 0.001). The 30 and 300-m running time divided by the relative lean mass of the lower extremities (RLM = LM x 100/body mass) was significantly lower in males than in females. Although, the slope of the linear relationship between RLM and 300-m running time was not significantly different between genders, the males achieved better performance in the 300-m test than the females. The main factor accounting for gender differences in peak and mean power output during cycling is the muscle mass of the lower extremities. Although, the peak power generating capability of the muscle is similar in males and females, muscle mass only partially explains the gender difference in running sprints, even when expressed as a percentage of the whole body mass.

The effects of professional tennis participation on dominant and non-dominant upper extremity muscle volumes, and on fiber types of triceps brachii (lateral head) and vastus lateralis muscles were assessed in 15 professional tennis players. Magnetic resonance imaging (MRI, n=8) examination and dual-energy x-ray absorptiometry (DXA, n=7) were used to assess muscle volumes and lean body mass. Muscle fiber-type distribution assessed by biopsy sampling was similar in both triceps brachii (2/3 were type 2 and 1/3 type 1 fibers). The VL was composed of 1/3 of type 2 and 2/3 of type 1 fibers. The dominant had 12-15% higher lean mass (DXA/MRI) than the non-dominant (P<0.05). Type 1, 2a and 2x muscle fibers of the dominant were hypertrophied compared with the non-dominant by 20%, 22% and 34% (all P<0.01), respectively. The deltoid, triceps brachii, arm flexors and forearm superficial flexor muscles of the dominant were hypertrophied (MRI) compared with the non-dominant by 11-15%. These muscles represented a similar fraction of the whole muscle volume in both upper extremities. Dominant muscle volume was correlated with 1RM on the one-arm cable triceps pushdown exercise (r=0.84, P<0.05). Peak power during vertical jump correlated with VL muscle fibers's cross-sectional area (r=0.82-0.95, P<0.05).

This study was designed to examine potential in vivo mechanisms of AMP-activated protein kinase (AMPK) phosphorylation inhibition and its downstream signaling consequences during the recovery period after a single bout of sprint exercise. Sprint exercise induces Thr(172)-AMPK phosphorylation and increased PGC-1alpha mRNA, by an unknown mechanism. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before exercising to inhibit AMPKalpha phosphorylation. Exercise elicited different patterns of Ser(221)-ACCbeta, Ser(473)-Akt and Thr(642)-AS160 phosphorylation, during the recovery period after glucose ingestion. Thirty minutes after the control sprint, Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation was reduced by 33% coinciding with increased Thr(172)-AMPKalpha phosphorylation (both, P < 0.05). Glucose abolished the 30-min Thr(172)-AMPKalpha phosphorylation. Ser(221)-ACCbeta phosphorylation was elevated immediately following and 30 min after exercise in C and G, implying a dissociation between Thr(172)-AMPKalpha and Ser(221)-ACCbeta phosphorylation. Two hours after the sprint, PGC-1alpha protein expression remained unchanged while SIRT1 (its upstream deacetylase) was increased. Glucose ingestion abolished the SIRT1 response without any significant effect on PGC-1alpha protein expression. In conclusion, glucose ingestion prior to a sprint exercise profoundly affects Thr(172)-AMPKalpha phosphorylation and its downstream signaling during the recovery period.

No abstract