Molecular characteristics of aged muscle reflect an altered ability to respond to exercise.

Studies have been performed in humans to identify changes in gene expression that may account for the relatively weak and variable response of aged muscle to resistance exercise. The gene expression profile of skeletal muscle from elderly (62-75 years old) compared to younger (20-30 years old) men demonstrated elevated expression of genes typical of a stress or damage response. The expression of the majority of these genes was unaffected by a single bout of high-intensity resistance exercise in elderly subjects but was altered acutely by exercise in younger subjects so as to approach the pre-exercise levels observed in older subjects. The inability of muscle from elderly subjects to respond to resistance exercise was also apparent in the expression of inflammatory response genes, which increased within 24 hours of the exercise bout only in younger subjects. Othergenes with potentially important roles in the adaptation of muscle to exercise, showed a similar or even more robust response in older compared to younger subjects. Taken together, these results may help to explain the variable hypertrophic response of muscle from older individuals to resistance training.

Aged human muscle demonstrates an altered gene expression profile consistent with an impaired response to exercise.

The gene expression profile of skeletal muscle from healthy older (62-75 years old) compared with younger (20-34 years old) men demonstrated elevated expression of genes typical of a stress or damage response, and decreased expression of a gene encoding a DNA repair/cell cycle checkpoint protein. Although the expression of these genes was relatively unaffected by a single bout of resistance exercise in older men, acute exercise altered gene expression in younger men such that post-exercise gene expression in younger men was similar to baseline gene expression in older men. The lack of response of muscle from older subjects to resistance exercise was also apparent in the expression of the inflammatory response gene IL-1beta, which did not differ between the age groups at baseline, but increased within 24 h of the exercise bout only in younger subjects. Other genes with potentially important roles in the adaptation of muscle to exercise, specifically in the processes of angiogenesis and cell proliferation, showed a similar response to exercise in older compared with younger subjects. Only one gene encoding the multifunctional, early growth response transcription factor EGR-1, showed an opposite pattern of expression in response to exercise, acutely decreasing in younger and increasing in older subjects. These results may provide a molecular basis for the inherent variability in the response of muscle from older as compared with younger individuals to resistance training.

Changes in power with resistance training in older and younger men and women.

BACKGROUND: Muscle power diminishes with increasing age and inactivity. The capacity for older adults to increase muscle power with resistance exercise has not been examined; therefore, we examined the influence of progressive resistance training (PRT) on muscle power output in 17 men and women aged 56-66 years, and compared their responses to 15 men and women aged 21-30 years. METHODS: All subjects performed 12 weeks of PRT at a workload equivalent to 80% of the one repetition maximum (1RM). All training and assessments of 1RM and power were made on Keiser pneumatic resistance machines. Subjects performed five exercises, three sets per exercise, twice weekly. Muscle power was measured (isotonically) at resistances equivalent to 40, 60, and 80% of the 1RM, on the knee extension and arm pull machines. RESULTS: All subjects increased arm pull power similarly at 40 and 60% of 1RM, independent of age or sex. There was not a significant increase in arm pull power at 80% of 1RM. Older and younger subjects also had similar absolute increases in leg extensor power at 40 and 60% of 1RM, but men responded with greater absolute gains than women at these percentages (p < .05). The increase in leg extensor power at 80% of 1RM was similar in all groups. Older and younger subjects increased strength similarly in all exercises except the left knee extension. Independent of age, men increased strength more than women in all exercises except the double leg press. CONCLUSIONS: These data demonstrate that individuals in their sixth decade can still improve muscle power (and strength); however, men may realize greater absolute gains than women.

Regulation of blood volume during training in post-menopausal women.

UNLABELLED: In younger people the increase in aerobic capacity following training is related, in part, to blood volume (BV) expansion and the consequent improvements in maximal cardiac output. This training-induced hypervolemia is associated with a decrease in cardiopulmonary baroreflex (CPBR) control of peripheral vascular tone. PURPOSE: To test the hypothesis that improvement in peak oxygen consumption (VO2peak) during training in older women is associated with specific central adaptations, such as BV expansion and a reduction in CPBR control of vascular tone. METHODS: Seventeen healthy older women were randomized into training (N = 9, 71 +/- 2 yr) and control (N = 8, 73 +/- 3 yr) groups. The training group exercised three to four times per wk for 30 min at 60% peak heart rate for 12 wk and then 40-50 min at 75% peak heart rate for 12 wk. The control group participated in yoga exercises over the same time period. We measured resting BV (Evans blue dye), VO2peak, and the forearm vascular resistance response to unloading low pressure mechanoreceptors during low levels of lower body negative pressure (through -20 mm Hg) before and after aerobic training. The slope of the increase in forearm vascular resistance (response) per unit decrease in central venous pressure (stimulus) was used to assess CPBR responsiveness. RESULTS: Aerobic training increased VO2peak 14.2% from 24.2 mL x kg(-1) x min(-1) to 27.7 mL x kg(-1) x min(-1) (P < 0.05), a smaller improvement than typically seen in younger subjects. Blood volume (59.9 +/- 1.9 and 60.9 +/- 1.9 mL x kg[-1]) and CPBR function (-3.98 +/- 0.92 and -3.46 +/- 0.94 units x mm(-1) Hg) were similar before and after training. CONCLUSIONS: These data indicate that the inability to induce adaptations in CPBR function may limit BV expansion during training in older women. In addition, the absence of these specific adaptations may contribute to the relatively poor improvements in VO2peak in older women during short (10-12 wk) periods of training.

Energy expenditure of swimmers during high volume training.

The purpose of this study was to examine the total energy expenditure (TEE) of swimmers during high volume training (17.5 +/- 1.0 km.d-1) using the doubly labeled water method. Five female swimmers (age, 19 +/- 1 yr; height, 178.3 +/- 2.2 cm; weight 65.4 +/- 1.6 kg) were administered a dose of 2H2(18)O and monitored for 5 days. Training consisted of two sessions per day, lasting a total of 5-6 h. Energy intake (EI) was calculated from dietary records. Resting energy expenditure (REE) was measured on a non-training day and averaged 7.7 +/- 0.5 MJ.d-1 (1840 +/- 130 kcal.d-1). There were no changes in body weight (day 1, 65.4 +/- 1.6; day 5, 65.2 +/ 1.5 kg) over the measurement period. TEE of the swimmers during the training period averaged 23.4 +/- 2.1 MJ.d-1 (5593 +/- 495 kcal.d-1). EI averaged 13.1 +/- 1.0 MJ.d-1 (3136 +/- 227 kcal.d-1), implying a negative energy balance of 43 +/- 2%. TEE expressed as a multiple of REE was 3.0 +/- 0.2. The results of this investigation describe the total energy demands of high volume swimming training, which may be used to address the dietary concerns of the competitive swimming athlete.

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.

The influence of starch structure on glycogen resynthesis and subsequent cycling performance.

The present study was designed to evaluate the influence of starch structure on muscle glycogen resynthesis and cycling performance. Eight male cyclists (22 +/- 1 yr) completed an exercise protocol (DP) to decrease vastus lateralis glycogen concentration. This exercise consisted of 60 min cycling at 75% VO2max, followed by six 1-min sprints at approximately 125% VO2max with 1 min rest intervals. In the 12 hr after the exercise each subject consumed approximately 3000 kcal (65:20:15% carbohydrate, fat and protein). All of the carbohydrate (CHO) consumed was derived from one of four solutions; 1) glucose, 2) maltodextrin (glucose polymer), 3) waxy starch (100% amylopectin), or 4) resistant starch (100% amylose). Muscle biopsies were taken from the vastus lateralis muscle after DP and 24 hr later to determine glycogen concentrations. A 30 min cycling time trial (TT) was performed following the 24 hr post-DP muscle biopsy to examine the influence of the feeding regimen on total work output. The post-DP glycogen concentrations were similar among the four trials, ranging from 220.3 +/- 29.2 to 264 +/- 48.3 mmol.kg-1 dry weight (d.w.) muscle. Twenty-four hours after DP, muscle glycogen concentration had increased less (p < 0.05) in the resistant starch trial (+90.8 +/- 12.8 mmol.kg-1 d.w.) than in the glucose (+197.7 +/- 31.6 mmol.kg-1 d.w.), maltodextrin (+136.7 +/- 24.5 mmol.kg-1 d.w.) and waxy starch (+171.8 +/- 37.1 mmol.kg-1 d.w.) trials. There were no differences in total work output during the TT, or blood lactate concentration immediately following the TT in any of the CHO trials. In summary, glycogen resynthesis was attenuated following ingestion of starch with a high amylose content, relative to amylopectin or glucose; however, short duration time trial performance was unaffected.

The effects of pre-exercise starch ingestion on endurance performance.

This study compared the physiological responses and performance following the ingestion of a waxy starch (WS), resistant starch (RS), glucose (GL) and an artificially-sweetened placebo (PL) ingested prior to exercise. Ten college-age, male competitive cyclists completed four experimental protocols consisting of a 30 min isokinetic, self-paced performance ride preceded by 90 min of constant load cycling at 66% VO2max. Thirty min prior to exercise, they ingested 1 g.kg-1 body weight of GL, WS, RS, or PL At rest, GL elicited greater (p < 0.05) serum glucose and insulin responses than all other trials. During exercise, however, serum glucose, insulin, blood C-peptide and glucagon responses were similar among trials. The mean total carbohydrate oxidation rates (CHOox) were higher (p < 0.05) during the GL, WS, and RS trials (2.59 +/- 0.13, 2.49 +/- 0.10, and 2.71 +/- 0.15 g.min-1, respectively) compared to PL (2.35 +/- 0.12 g.min-1). Subjects were able to complete more work (p < 0.05) during the performance ride when they ingested GL (434 +/- 25.2 kj) or WS (428 +/- 22.5 kj) compared to PL (403 +/- 35.1 kj). They also tended to produce more work with RS ingestion (418 +/- 31.4 kj), although this did not reach statistical significance (p < 0.09). These results indicate that preexercise CHO ingestion in the form of starch or glucose maintained higher rates of total carbohydrate oxidation during exercise and provided an ergogenic benefit during self-paced cycling.

Thermal responses to swimming in three water temperatures: influence of a wet suit.

The primary objective of this investigation was to determine the thermal and metabolic effects of wearing a rubberized wet suit (WS) while swimming for 30 min in 20.1, 22.7, and 25.6 degrees C water. Metabolic and body temperature measurements were recorded in each water temperature with subjects wearing either a WS or a competitive swimming suit (SS). Immediately after each swim the subjects cycled for 15 min on a stationary cycle ergometer. Energy expenditure (VO2), heart rate, post-swim blood lactate, work completed on the cycle ergometer, and rating of perceived exertion (RPE) were similar in all trials. Mean (+/- SE) core temperature (Tc) during swimming in the SS trials increased 0.56 (+/- 0.33), 0.48 (+/- 0.20), and 1.22 (+/- 0.24) degrees C, whereas in the WS trial Tc rose 0.62 (+/- 0.22), 1.02 (+/- 0.15), and 0.89 (+/- 0.13) degrees C in the 20.1, 22.7, and 25.6 degrees C treatments, respectively. Following swimming many of the subjects experienced a decrease in Tc, but it was significantly elevated above preimmersion by the end of cycling in all trials except the SS 20.1 degrees C trial. Mean trunk temperatures (Ttr) during swimming in the WS trials were 4.32 +/- 0.16 (20.1 degrees C), 3.90 +/- 0.25 (22.7 degrees C), and 3.21 +/- 0.20 (25.6 degrees C) degrees C warmer than in the SS. Ttr rose after the subjects exited the water, but remained significantly below baseline throughout cycling in all trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of swimming suit design on the energy demands of swimming.

Eight competitive male swimmers completed a standardized 365.8 m (400 yd) freestyle swimming trial at a fixed pace (approximately 90% of maximal effort) while wearing a torso swim suit (TOR) or a standard racing suit (STD). Oxygen uptake (VO2), blood lactate, heart rate (HR), and distance per stroke (DPS) measurements were obtained. In addition, a video-computer system was used to collect velocity data during a prone underwater glide following a maximal leg push-off from the side of the pool while wearing the TOR and STD suits. These data were used to calculate the total distance covered during the glides. VO2 (3.76 +/- 0.16 vs 3.92 +/- 0.18 l.min-1) and lactate (8.08 +/- 0.53 vs, 9.66 +/- 0.66 mM) were significantly (P < 0.05) lower during the TOR trial than the STD trial. HR was not different (P > 0.05) between the TOR (170.1 +/- 5.1 b.min-1) and STD (173.5 +/- 5.7 b.min-1) trials. DPS was significantly greater during the TOR (2.70 +/- 0.066 m.stroke-1) versus STD (2.58 +/- 0.054 m.stroke-1) trial. A significantly greater total distance was covered during the prone glide while wearing the TOR (2.05 +/- 0.067 m) compared to the STD (2.00 +/- 0.080 m) suit. These findings demonstrate that a specially designed torso suit reduces the energy demand of swimming compared to a standard racing suit which may be due to a reduction in body drag.

Osmoregulatory modulation of thermal sweating in humans: reflex effects of drinking.

To gain better insight into the interaction between thermoregulation and osmoregulation, we examined the thermal sweating response to drinking in cell-dehydrated humans. Cell dehydration (CDH) was induced by infusion of a 3% NaCl solution, at 1.2 ml/kg, for 2 h; infusion of a 0.9% NaCl solution in a separate experiment served as a control (euhydrated condition, EH). After infusion, subjects were heated by immersion of the lower legs in 42 degrees C water at an ambient temperature of 28 degrees C for 90 min. Subjects drank 4.3 ml/kg of H2O (approximately 38 degrees C) at 60 min of heating. The 3% NaCl infusion increased plasma osmolality by 13.6 +/- 0.8 mosmol/kgH2O and plasma arginine vasopressin concentration ([AVP]) by 3.3 +/- 0.7 pg/ml. Neither variable was altered with 0.9% NaCl infusion. Before drinking, esophageal temperature (Tes) had increased by 0.91 +/- 0.08 degrees C in CDH and by 0.40 +/- 0.11 degrees C in EH. Local chest sweating rate (SRch) had increased by 0.67 +/- 0.08 and 0.63 +/- 0.07 mg.min-1.cm-2 in CDH and EH, respectively. Thus the change in SRch per unit rise in Tes was much lower in CDH than in EH. Drinking immediately increased SRch and reduced Tes in CDH, with a reduction in plasma [AVP] and thirst rating. Drinking did not change thermoregulatory and osmoregulatory responses in EH. These results suggest that the act of drinking itself eliminates, at least partially, an osmotic inhibitory input to the thermoregulatory center, as well as osmotic AVP secretion and thirst.