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Twelve healthy active subjects (6 male, 6 female) performed 60 min of exercise (60% VO_2max) on 3 occasions after supplementing with L-Carnitine L-tartrate (LCLT) or placebo. Each subject received a chronic dose, an acute dose, and placebo in a randomized, double-blind crossover design. Dietary intake and exercise were replicated for 2 d prior to each trial. In males there was a significant difference in rate of carbohydrate (CHO) oxidation between placebo and chronic trials (P = 0.02) but not placebo and acute trials (P = 0.70), and total CHO oxidation was greater following chronic supplementation vs. placebo (mean ± standard deviation) of 93.8 (17.3) g/hr and 78.2 (23.3) g/h, respectively). In females, no difference in rate of, or total, CHO oxidation was observed between trials. No effects on fat oxidation or hematological responses were noted in either gender group. Under these experimental conditions, chronic LCLT supplementation increased CHO oxidation in males during exercise but this was not observed in females

Dual energy x-ray absorptiometry (DXA) is a popular tool to determine body composition (BC) in athletes, and is used for analysis of fat-free soft tissue mass (FFST) or fat mass (FM) gain/loss in response to exercise or nutritional interventions. The aim of the current study was to assess the effect of exercise-heat stress induced hypohydration (HYP, >2% of body mass (BM) loss) vs. maintenance of euhydration (EUH) on DXA estimates of BC, sum of skinfolds (SF), and impedance (IMP) measurements in athletes. Competitive athletes (23 males and 15 females) recorded morning nude BM for 7 days before the first main trial. Measurements on the first trial day were conducted in a EUH condition, and again after exercise-heat stress induced HYP. On the second trial day, fluid and electrolyte losses were replaced during exercise using a sports drink. A reduction in total BM (1.6 ± 0.4 kg; 2.3 ± 0.4% HYP) and total FFST (1.3 ± 0.4 kg), mainly from trunk (1.1 ± 0.5 kg), was observed using DXA when participants were HYP, reflecting the sweat loss. Estimated fat percent increased (0.3 ± 0.3%), however, total FM did not change (0.1 ± 0.2 kg). SF and IMP declined with HYP (losses of 1.5 ± 2.9% and 1.6 ± 3% respectively) suggesting FM loss. When EUH was maintained there were no significant changes in BM, DXA estimates, or SF values pre to post exercise, but IMP still declined. We conclude that use of DXA for FFST assessment in athletes must ensure a EUH state, particularly when considering changes associated with nutritional or exercise interventions.

Twenty-two tennis players were individually studied on 2 occasions. They performed a prematch skill test, a 2-hr tennis match against an equally ranked opponent, and a postmatch skill test. A carbohydrate-electrolyte (CHO-E; Lucozade Sport) or flavor-matched placebo-electrolyte (PL) beverage was administered in a double-blind fashion. During the trials, heart-rate and movement intensity were monitored, and the match was recorded for performance analysis. There were no differences in skill-test scores pre- to postmatch or between trials (154 ± 38 pre- and 160 ± 35 postmatch on PL, 155 ± 36 pre- and 165 ± 33 postmatch on CHO-E). CHO-E ingestion elevated blood glucose concentration throughout the match, and participants reported feeling more energetic (general activation) and more tense (high activation) 1 hr into the match than at baseline (p < .05). Participants in the CHO-E trial spent more time in moderate-intensity activity and less time in low-intensity activity than on PL. Performance analysis revealed that CHO-E ingestion increased overall serve success (M ± SD, 68% ± 7% for CHO-E vs. 66% ± 7% for PL; p < .05) and success of first serves (65% ± 9% for CHO-E, 61% ± 7% for PL; p < .01) and serves to the advantage side (70% ± 9% for CHO-E, 66% ± 7% for PL; p < .05). Return success was greater during the second set of the match (p < .05) in the CHO-E trial. Differences in serve and return success were not associated with blood glucose response to CHO or player ability.

The present study examined the impact of hormonal differences between late follicular (LF) and midluteal (ML) phases on restoration of fluid balance following dehydration. Ten eumenorrheic female participants were dehydrated by 2% of their body mass through overnight fluid restriction followed by exercise-heat stress. Trials were undertaken during the LF (between Days 10 and 13 of the menstrual cycle) and ML phases (between Days 18 and 23 of the menstrual cycle) with one phase repeated to assess reliability of observations. Following dehydration, participants ingested a volume equivalent to 100% of mass loss of a commercially available sports drink in four equal volumes over 30 min. Mean serum values for steroid hormones during the ML (estradiol [E2]: 92 ± 11 pg/ml, progesterone: 19 ± 4 ng/ml) and LF (estradiol [E2]: 232 ± 64 pg/ml, progesterone: 3 ± 2 ng/ml) were significantly different between phases. Urine tests confirmed no luteinizing hormone surge evident during LF trials. There was no effect of menstrual cycle phase on cumulative urine volume during the 3-hr rehydration period (ML: 630 [197–935] ml, LF: 649 [180–845] ml) with percentage of fluid retained being 47% (33–85)% on ML and 46% (37–89)% on LF (p = .29). There was no association between the progesterone:estradiol ratio and fluid retained in either phase. Net fluid balance, urine osmolality, and thirst intensity were not different between phases. No differences in sodium (ML: −61 [−36 to −131] mmol, LF: −73 [−5 to −118] mmol; p = .45) or potassium (ML: −36 [−11 to −80] mmol, LF: −30 [−19 to −89] mmol; p = .96) balance were observed. Fluid replacement after dehydration does not appear to be affected by normal hormonal fluctuations during the menstrual cycle in eumenorrheic young women.

In a randomized, placebo-controlled, double-blind crossover design, 15 trained males undertook exercise trials during two 4 wk supplementation periods, with either 3 g L-Carnitine L-tartrate (LCLT) or 3 g placebo (P) daily. Total carbohydrate and fat oxidation during 90 min steady state cycling were not different between 0 or 4 wk within LCLT or P trials (mean ± standard deviation: carbohydrate oxidation P₀ 99 ± 36, P_4W 111 ± 27, LCLT₀ 107 ± 33, LCLT_4W 112 ± 32 g, respectively; fat oxidation P₀ 99 ± 28, P_4W 92 ± 21, LCLT₀ 94 ± 18, LCLT_4W 90 ± 22 g, respectively). Subsequent 20 km time trial duration was shorter after P (P₀ 31:29 ± 3:50, P_4W 29:55 ± 2:58 min:s, P < 0.01), with no significant change over LCLT (LCLT₀ 31:46 ± 4:06, LCLT_4W 31.19 ± 4.08 min:s). Four weeks LCLT supplementation had no effect on substrate utilization or endurance performance.

Twenty nonvegetarian active males were pair-matched and randomly assigned to receive 2 g of L-carnitine L-tartrate (LC) or placebo per day for 2 wk. Participants exercised for 90 min at 70% VO2max after 2 days of a prescribed diet (M ±SD: 13.6 ± 1.6 MJ, 57% carbohydrate, 15% protein, 26% fat, 2% alcohol) before and after supplementation. Results indicated no change in carbohydrate oxidation, nitrogen excretion, branched-chain amino acid oxidation, or plasma urea during exercise between the beginning and end of supplementation in either group. After 2 wk of LC supplementation the plasma ammonia response to exercise tended to be suppressed (0 vs. 2 wk at 60 min exercise, 97 ± 26 vs. 80 ± 9, and 90 min exercise, 116 ± 47 vs. 87 ± 25 μmol/L), with no change in the placebo group. The data indicate that 2 wk of LC supplementation does not affect fat, carbohydrate, and protein contribution to metabolism during prolonged moderate-intensity cycling exercise. The tendency toward suppressed ammonia accumulation, however, indicates that oral LC supplementation might have the potential to reduce the metabolic stress of exercise or alter ammonia production or removal, which warrants further investigation.

The effects of 15 d of supplementation with L-carnitine L-tartrate (LC) on metabolic responses to gradedintensity exercise under conditions of altered substrate availability were examined. Fifteen endurance-trained male athletes undertook exercise trials after a 2-d high-carbohydrate diet (60% CHO, 25% fat) at baseline (D0), on Day 14 (D14), and after a single day of high fat intake (15% CHO, 70% fat) on Day 15 (D15) in a double-blind, placebo-controlled, pair-matched design. Treatment consisted of 3 g LC (2 g L-carnitine/d; n = 8) or placebo (P, n = 7) for 15 d. Exercise trials consisted of 80 min of continuous cycling comprising 20-min periods at each of 20%, 40%, 60%, and 80% VO_2peak. There was no significant difference between whole-body rates of CHO and fat oxidation at any workload between D0 and D14 trials for either the P or LC group. Both groups displayed increased fat and reduced carbohydrate oxidation between the D14 and D15 trials (p < .05). During the D15 trial, heart rate (p < .05 for 20%, 40%, and 60% workloads) and blood glucose concentration (p < .05 for 40% and 60% workloads) were lower during exercise in the LC group than in P. These responses suggest that LC may induce subtle changes in substrate handling in metabolically active tissues when fattyacid availability is increased, but it does not affect whole-body substrate utilization during short-duration exercise at the intensities studied.

This study assessed fluid balance, sodium losses, and effort intensity during indoor tennis match play (17 ± 2 °C, 42% ± 9% relative humidity) over a mean match duration of 68.1 ± 12.8 min in 16 male tennis players. Ad libitum fluid intake was recorded throughout the match. Sweat loss from change in nude body mass; sweat electrolyte content from patches applied to the forearm, calf, and thigh, and back of each player; and electrolyte balance derived from sweat, urine, and daily food-intake analysis were measured. Effort intensity was assessed from on-court heart rate compared with data obtained during a maximal treadmill test. Sweat rate (M ± SD) was 1.1 ± 0.4 L/hr, and fluid-ingestion rate was 1.0 ± 0.6 L/hr (replacing 93% ± 47% of fluid lost), resulting in only a small mean loss in body mass of 0.15% ± 0.74%. Large interindividual variabilities in sweat rate (range 0.3–2.0 L/hr) and fluid intake (range 0.31–2.52 L/hr) were noted. Whole-body sweat sodium concentration was 38 ± 12 mmol/L, and total sodium losses during match play were 1.1 ± 0.4 g (range 0.5–1.8 g). Daily sodium intake was 2.8 ± 1.1 g. Indoor match play largely consisted of low-intensity exercise below ventilatory threshold (mean match heart rate was 138 ± 24 beats/min). This study shows that in moderate indoor temperature conditions players ingest sufficient fluid to replace sweat losses. However, the wide range in data obtained highlights the need for individualized fluid-replacement guidance.

The monitoring of body composition is common in sports given the association with performance. Surface anthropometry is often preferred when monitoring changes for its convenience, practicality, and portability. However, anthropometry does not provide valid estimates of absolute lean tissue in elite athletes. The aim of this investigation was to develop anthropometric models for estimating fat-free mass (FFM) and skeletal muscle mass (SMM) using an accepted reference physique assessment technique. Sixty-four athletes across 18 sports underwent surface anthropometry and dual-energy X-ray absorptiometry (DXA) assessment. Anthropometric models for estimating FFM and SMM were developed using forward selection multiple linear regression analysis and contrasted against previously developed equations. Most anthropometric models under review performed poorly compared with DXA. However, models derived from athletic populations such as the Withers equation demonstrated a stronger correlation with DXA estimates of FFM (r = .98). Equations that incorporated skinfolds with limb girths were more effective at explaining the variance in DXA estimates of lean tissue (Sesbreno FFM [R ² = .94] and Lee SMM [R ² = .94] models). The Sesbreno equation could be useful for estimating absolute indices of lean tissue across a range of physiques if an accepted option like DXA is inaccessible. Future work should explore the validity of the Sesbreno model across a broader range of physiques common to athletic populations.