R. D. Starling

Exercise-induced muscle damage: effect on circulating leukocyte and lymphocyte subsets.

The purpose of this study was to determine the effect of downhill and level running on circulating leukocyte and lymphocyte subsets and T lymphocyte activation. Using a random cross-over design, 10 runners completed two trials of 60 min of level running (0% grade; LR) and downhill running (-10% grade; DHR) at 70% of level VO2max. Blood samples were obtained preexercise and immediately postexercise (POST) and at 1.5, 12, 24, and 48 h of recovery. Creatine kinase activity peaked at 12 h of recovery from DHR and was not significantly altered following LR. The number of total T, CD16+, CD3+CD56+ cells were significantly higher POST DHR compared with LR. Leukocyte and neutrophil counts were significantly higher at 1.5 and 12 h of recovery from DHR compared with LR. The number of activated CD8+ cells (CD25+ CD8+) was significantly higher at 12 h of DHR compared to LR. Total T cells were significantly reduced at various time points during the 48 h of recovery from LR and DHR. In summary, DHR relative to LR resulted in a greater mobilization of lymphocytes (post), neutrophils (1.5-12 h of recovery) and activation of CD8+ cells at 12 h of recovery. In addition, reductions in circulating T lymphocyte subsets occurred following both conditions.

Effect of inosine supplementation on aerobic and anaerobic cycling performance

Ten competitive male cyclists completed a Wingate Bike Test (WIN), a 30-min self-paced cycling performance bout (END), and a constant load, supramaximal cycling spring (SPN) to fatigue following 5 d of oral supplementation (5,000 mg.day-1) with inosine and placebo. Blood samples were obtained prior to and following both supplementation periods, and following each cycling test. Uric acid concentration was higher (P < 0.05) following supplementation with inosine versus placebo, but 2,3-DPG concentration was not changed. The data from WIN demonstrate that there were no significant differences in peak power (8.5 +/- 0.3 vs 8.4 +/- 0.3 W.kg body mass-1), end power (7.0 +/- 0.3 vs 6.9 +/- 0.2 W.kg body mass-1), fatigue index (18 +/- 2 vs 18 +/- 2%), total work completed (0.45 +/- 0.02 vs 0.45 +/- 0.02 kJ.kg body mass-1.30-s-1), and post-test lactate (12.2 +/- 0.5 vs 12.9 +/- 0.6 mmol.l-1) between the inosine and placebo trials, respectively. No difference was present in the total amount of work completed (6.1 +/- 0.3 vs 6.0 +/- 0.3 kJ.kg body mass-1) or post-test lactate (8.4 +/- 1.0 vs 9.9 +/- 1.3 mmol.l-1) during END between the inosine and placebo trials, respectively. Time to fatigue was longer (P < 0.05) during SPN for the placebo (109.7 +/- 5.6 s) versus the inosine (99.7 +/- 6.9 s) trial, but post-test lactate (14.8 +/- 0.7 vs 14.6 +/- 0.8 mmol.l-1) was not different between the treatments, respectively. These findings demonstrate that prolonged inosine supplementation does not appear to improve aerobic performance and short-term power production during cycling and may actually have an ergolytic effect under some test conditions.

Relationships between muscle carnitine, age and oxidative status

Muscle carnitine levels were examined in 31 younger [mean (SD), 27 (5) years] and 27 older [49 (8) years] men. Needle biopsies were obtained from the lateral gastrocnemius or vastus lateralis muscles and assayed for free and total carnitine concentrations via a 5,5′-Dithiobis-(2-nitrobenzoic acid) DTNB-linked spectrophotometric procedure. A subgroup of subjects (n = 28) were assessed for citrate synthase (CS) and succinate dehydrogenase (SDH) activity, and type 1 muscle fiber composition (% type I fibers). An additional sub-group of nine subjects was assessed for free and total serum carnitine levels. No mean (SEM) differences in free [21.6 (0.7) vs 20.3 (0.9) μmol·g dry weight-1]] and total [26.4 (0.6) vs 26.1 (0.9) μmol·g dry weight−1) muscle carnitine levels were found between the younger and older subjects, respectively. Correlational data revealed no significant relationships between total muscle carnitine and CS (r = − 0.36), SDH (r = − 0.26), or % type I fibers (r = − 0.16). In addition, there was a low non-significant relationship between serum and muscle total carnitine concentrations (r = − 0.44). These findings suggest that muscle carnitine levels are similar between younger and older males, and there does not appear to be any relationship between muscle carnitine and markers of muscle oxidative potential (i.e., oxidative enzymes, % type I fiber). Since serum carnitine is often used as an indicator of body carnitine status, it is noteworthy that we found a low negative relationship between blood and muscle carnitine concentrations.

MAXIMAL ACCUMULATED OXYGEN DEFICIT OF RESISTANCE TRAINED MEN 404

The primary purpose of the study was to compare maximal accumulated oxygen deficit (MAOD) in resistance-trained (RT), endurance-trained (ET), and untrained men (UT). A secondary purpose was to determine the influence of leg muscle mass (MM) on MAOD by examining the relationship between MM and MAOD and by comparing MAOD expressed relative to MM between the groups. MAOD was determined during 2-4 min of constant-load fatiguing cycling. MM, estimated via anthropometric measurements, was higher (p < .05) for RT (mean +/- SE; 25.5 +/- 3.4 kg) compared to ET (20.3 +/- 3.5) and UT (21.6 +/- 3.4). MAOD in liters O2eq was larger in RT (4.75 +/- 0.3) compared to UT (3.07 +/- 0.3) and ET (3.75 +/- 0.3). A significant positive correlation was observed between MAOD (LO2eq) and MM (kg) for RT only (RT, r = .85; ET, r = .55; UT, r = .20). Based on the correlational and mean MM data, the higher MAOD (LO2eq) in RT relative to ET and UT is predominantly the result of their larger leg muscle mass.