Biomedical subjects

S C Dennis

Publications and source records attributed to S C Dennis.

At least 19 recordsLinked to original sources

PubMed2001

Sodium replacement and fluid shifts during prolonged exercise in humans.

In the study presented here, we examined the affects of a close to complete replacement of sweat water and Na+ losses on fluid shifts during exercise. Six cyclists performed three 4-h rides at 55% of their peak oxygen uptake in a 20 degrees C environment while consuming 3.85 l of an 8% carbohydrate solution containing 5, 50 or 100 mEq.l-1 of Na+. Increases in Na+ intake reduced renal free water clearance from around 40 ml.h-1 to -8 and -121 ml.h-1 and led to a decrease in urine volume from approximately equal to 1.0 to 0.5 l (P < 0.05). In contrast, the 3.5-3.9 l fluid and 150-190 mEq Na+ losses in sweat were similar in each trial, as were the approximately equal to 80 mEq K+ losses in sweat and urine and the 282-288 mosmol.kg-1 plasma osmolalities. During the low-Na+ trial, plasma osmolality was maintained by a approximately equal to 1.3 l contraction of extracellular fluid (ECF) with the loss of approximately equal to 200 mEq Na+. However, in the other trials, approximately equal to 1.3 l of water was lost from the intracellular fluid. During the medium-Na+ trial, a loss of only approximately equal to 40 mEq Na+ maintained ECF volume, and during the high-Na+ trial, a gain of approximately equal to 160 mEq Na+ expanded the ECF by approximately equal to 0.8 l. However, corresponding changes in plasma volumes from -0.20 to 0.15 l had no effect on cardiovascular drift or thermoregulation. These data suggest that during prolonged exercise of moderate intensity under mild environmental conditions when sweat rates are approximately equal to 0.9 l.h-1, complete Na+ replacement maintains plasma volume and reduces dehydration, but when fluid intake matches sweat rate, has little effect on plasma osmolality.

Administration, Oral↗

PubMed2001

Influence of ambient temperature on plasma ammonia and lactate accumulation during prolonged submaximal and self-paced running.

This study examined the effects of heat stress on the accumulation of plasma ammonia, lactate, and urate during prolonged running. Nine highly trained endurance runners completed two running trials in a counterbalanced fashion in cool (15 degrees C) and in hot (35 degrees C) humid (60% relative humidity) conditions. Subjects ran on a motorised treadmill at 70% of peak treadmill running speed for 30 min (submaximal) followed by a self-paced 8-km performance run. Blood was drawn at pre-exercise, end-submaximal and end-performance run and analysed for plasma ammonia, lactate, and urate. Four subjects failed to complete the performance run in the heat and the performance times for the rest of the subjects was increased from 27.3 (0.6) min in cool conditions to 31.3 (1.2) min in hot conditions (P < 0.05). The end-performance rectal temperature was 38.6 (0.1) and 39.2 (0.1) degrees C (P<0.05) in cool and hot conditions, respectively. Differences in plasma lactate at the end of submaximal running were not significant. However, at the end of performance runs lactate was 6.0 (0.9) m mol x l(-1) in cool and 3.1 (0.5) mmol x l(-1) in hot conditions, values that were significantly different (P<0.05). Plasma ammonia increased from pre-exercise to approximately equal to 59 micromol x l(-1) at the end-submaximal runs for both coditions and further at the end of performance runs to 108.5 (11) micromol x l(-1) (P<0.05) in hot but not in cool conditions. Plasma urate increased from pre-exercise to 311.2 (25.9) micromol x l(-1) at end-submaximal runs and to approximately equal to 320.4 micromol x l(-1) at end-performance runs in hot and cool environments. The findings that plasma urate accumulation was similar at the completion of running in both conditions, while ammonia was significantly augmented in hot conditions compared with cool, suggest that ammonia accumulation during heat stress exercise might be derived from sources other than purine catabolism.

Adult↗

PubMed2001

High-fat diet versus habitual diet prior to carbohydrate loading: effects of exercise metabolism and cycling performance.

We examined the effects of a high-fat diet (HFD-CHO) versus a habitual diet, prior to carbohydrate (CHO)-loading on fuel metabolism and cycling time-trial (TT) performance. Five endurance-trained cyclists participated in two 14-day randomized cross-over trials during which subjects consumed either a HFD (> 65% MJ from fat) or their habitual diet (CTL) (30 +/- 5% MJ from fat) for 10 day, before ingesting a high-CHO diet (CHO-loading, CHO > 70% MJ) for 3 days. Trials consisted of a 150-min cycle at 70% of peak oxygen uptake (VáO2peak), followed immediately by a 20-km TT. One hour before each trial, cyclists ingested 400 ml of a 3.44% medium-chain triacylglycerol (MCT) solution, and during the trial, ingested 600 ml/hour of a 10% 14C-glucose + 3.44% MCT solution. The dietary treatments did not alter the subjects' weight, body fat, or lipid profile. There were also no changes in circulating glucose, lactate, free fatty acid (FFA), and b-hydroxybutyrate concentrations during exercise. However, mean serum glycerol concentrations were significantly higher (p < .01) in the HFD-CHO trial. The HFD-CHO diet increased total fat oxidation and reduced total CHO oxidation but did not alter plasma glucose oxidation during exercise. By contrast, the estimated rates of muscle glycogen and lactate oxidation were lower after the HFD-CHO diet. The HFD-CHO treatment was also associated with improved TT times (29.5 +/- 2.9 min vs. 30.9 +/- 3.4 min for HFD-CHO and CTL-CHO, p <.05). High-fat feeding for 10 days prior to CHO-loading was associated with an increased reliance on fat, a decreased reliance on muscle glycogen, and improved time trial performance after prolonged exercise.

Adult↗

PubMed2001

Peak rates of diuresis in healthy humans during oral fluid overload.

OBJECTIVE: To determine whether rates of intestinal fluid absorption and renal diuresis can match high rates of fluid ingestion in healthy humans exposed to oral fluid overload, thereby preventing the development of hyponatraemia either by reverse sodium movement across the intestine (the Priestley-Haldane effect) or by expansion of the extracellular fluid volume. METHODS: Changes in renal function and in plasma chemical measurements in response to an oral fluid overload (0.9-1.8 l/h x 3 h) were investigated in 6 healthy control subjects at rest, and in a subject with a history of exercise-induced symptomatic hyponatraemia, during both prolonged (160-minute) exercise and at rest. FINDINGS: All control subjects gained weight (2.7 +/- 0.2 kg, mean +/- standard error of mean (SEM)) because the rate of oral fluid intake exceeded the peak rate of urine production (778 +/- 39 ml/h). Blood volume rose by 7.1 (+/- 0.5)% and plasma sodium concentrations fell progressively from 144 +/- 2.6 to 136 +/- 1.1 mmol/l (P < 0.05) in the control subjects. Plasma potassium and angiotensin II concentrations were unchanged and creatinine clearance was normal (approximately 125 ml/min). Free water clearance reached a maximum of 11.2 +/- 0.9 ml/min after 2 hours. The increase in body mass could be accounted for by calculated or measured changes in extra- and intracellular fluid volumes. Similar changes were measured in the subject with a previous history of symptomatic hyponatraemia. CONCLUSION: The rate of intestinal fluid absorption appeared to match the rate of oral fluid ingestion and there was no evidence of fluid accumulation in the intestine with reverse sodium movement from the extracellular space into intestinal fluid. The results of this study are therefore at variance with the Priestley-Haldane hypothesis and suggest that reverse sodium movement did not contribute to the hyponatraemia induced by oral fluid overload in these subjects. Rather it appears that humans may have a limited capacity to excrete fluid at rates in excess of approximately 900 ml/h in response to higher rates of oral fluid intake. When the rate of intestinal fluid absorption matches the rate of fluid ingestion and exceeds the kidneys' maximum capacity for fluid excretion, the excess fluid accumulates in the extra- and intracellular fluid compartments, inducing the dilutional hyponatraemia of water intoxication. These findings may have relevance to other clinical conditions in which hyponatraemia develops in response to high rates of oral or intravenous fluid provision.

Adult↗

PubMed2000

Advantages of smaller body mass during distance running in warm, humid environments.

The purpose of this study was to examine the extent to which lighter runners might be more advantaged than larger, heavier runners during prolonged running in warm humid conditions. Sixteen highly trained runners with a range of body masses (55-90 kg) ran on a motorised treadmill on three separate occasions at 15, 25 or 35 degrees C, 60% relative humidity and 15 km x h(-1) wind speed. The protocol consisted of a 30-min run at 70% peak treadmill running speed (sub-max) followed by a self-paced 8-km performance run. At the end of the submax and 8-km run, rectal temperature was higher at 35 degrees C (39.5+/-0.4 degrees C, P<0.05) compared with 15 degrees C (38.6+/-0.4 degrees C) and 25 degrees C (39.1+/-0.4 degrees C) conditions. Time to complete the 8-km run at 35 degrees C was 30.4+/-2.9 min (P<0.05) compared with 27.0+/-1.5 min at 15 degrees C and 27.4+/-1.5 min at 25 degrees C. Heat storage determined from rectal and mean skin temperatures was positively correlated with body mass (r=0.74, P<0.0008) at 35 degrees C but only moderately correlated at 25 degrees C (r=0.50, P<0.04), whereas no correlation was evident at 15 degrees C. Potential evaporation estimated from sweat rates was positively associated with body mass (r=0.71, P<0.002) at 35 degrees C. In addition, the decreased rate of heat production and mean running speed during the 8-km performance run were significantly correlated with body mass (r=-0.61, P<0.02 and r=-0.77, P<0.0004, respectively). It is concluded that, compared to heavier runners, those with a lower body mass have a distinct thermal advantage when running in conditions in which heat-dissipation mechanisms are at their limit. Lighter runners produce and store less heat at the same running speed; hence they can run faster or further before reaching a limiting rectal temperature.

Blood Volume↗

PubMed2000

Effect of fluid intake volume on 2-h running performances in a 25 degrees C environment.

PURPOSE: In this study, we examined the effects of greater than ad libitum rates of fluid intake on 2-h running performances. METHODS: Eight male distance runners performed three runs on a treadmill at 65% of peak oxygen uptake (VO2peak) for 90 min and then ran "as far as possible" in 30 min in an air temperature of 25 degrees C, a relative humidity of 55% and a wind speed of 13-15 km x h(-1). During the runs, the subjects drank a 6.9% carbohydrate (CHO)-electrolyte solution either ad libitum or in set volumes of 150 or 350 mL x 70 kg(-1) body mass (approximately 130 or 300 mL) every 15-20 min. RESULTS: Higher (approximately 0.9 vs 0.4 L x h(-1)) rates of fluid intake in the 350 mL x 70 kg(-1) trial than in the other trials had minimal effects on the subjects' urine production (approximately 0.1 L x h(-1)), sweat rates (approximately 1.2 L x h(-1)), declines in plasma volume (approximately 8%), and rises in serum osmolality (approximately 5 mosmol x L(-1)) and Na+ concentrations (approximately 7 mEq x L(-1)). A greater (approximately 1.0 vs 0.5 g x min(-1)) rate of CHO ingestion in the 350 mL x 70 kg(-1) trial than in the other trials also did not affect plasma concentrations of glucose (> or = 5 mmol x L(-1)) and lactate (approximately 3 mmol x L(-1)) during the performance runs. In all three performance runs, increases in running speeds from approximately 14 to 15-16 km x h(-1) and rises in exercise intensities from approximately 65% to 75% of VO2peak elevated plasma lactate concentrations from approximately 1.5 to 3 mmol x L(-1) and accelerated CHO oxidation from approximately 13 to 15 mmol x min(-1). The only effect of the additional intake of approximately 1.0 L of fluid in the 350 mL x 70 kg(-1) trial was to produce such severe gastrointestinal discomfort that two of the eight subjects failed to complete their performance runs. CONCLUSION: Greater rates of fluid ingestion had no measurable effects on plasma volume and osmolality and did not improve 2-h running performances in a 25 degrees C environment.

Abdominal Pain↗

PubMed2000

Low back pain.

The communication between radiologists and their surgical colleagues is particularly important in the setting of back pain. This common disorder often does not have a definable cause, even when the imaging findings are abnormal. A shared understanding of the various causes of back pain, the appropriate terminology, and the needs of the surgeon is vital to proper patient treatment. Unfortunately, little standardization in the terminology for and management of back pain syndromes exists. This article elucidates the approaches to problems of back pain used in one clinical setting.

Humans↗

PubMed1999

Advantages of a smaller bodymass in humans when distance-running in warm, humid conditions.

Using a 65-kg athlete running a 2 h 10 min marathon as an example, we estimated that imbalances between approximately 1400 W of heat production and dissipation would occur in ambient temperatures of 17 degrees C at 90% relative humidity (rh) to 37 degrees C at 50% rh. Because heat production during running depends on body mass and heat loss depends on surface area, intercepts between predicted heat production and maximal heat loss with increasing speeds depend on an athlete's body mass. At 35 degrees C and 60% rh, a 45-kg athlete could maintain thermal balance by running a 2 h 13 min marathon at 19.1 km x h(-1) but a 75-kg athlete would only be able run a 3 h 28 min marathon at 12.2 km x h(-1). In both cases, the production of 970-1020 W of heat would necessitate the evaporation of at least 1.5-1.6 l of sweat per hour. A lower metabolic heat production in lighter runners at any given speed may be one reason why smallness of stature is an asset in distance running.

Adult↗

PubMed1999

Water and electrolyte shifts with partial fluid replacement during exercise.

In this study, we examined whether athletes, who typically replace only approximately 50% of their fluid losses during moderate-duration endurance exercise, should attempt to replace their Na+ losses to maintain extracellular fluid volume. Six male cyclists performed three 90-min rides at 65% of peak O2 uptake in a 32 degrees C environment and ingested either no fluid (NF), 1.21 of water (W), or saline (S) containing 100 mmol of NaCl x l(-1) to replace their electrolyte losses. Both W and S conditions decreased final heart rates by approximately 10 betas min(-1) (P<0.005) and reduced falls in plasma volume (PV) by approximately 4% (P<0.05). Maintenance of PV after 10 min in the W trial prevented further rises in plasma concentrations of Na+ [Na+], Cl- and protein but in the S and NF trials, plasma [Na+] continued to increase by approximately 4 mEq x l(-1). Differences in plasma [Na+] had little effect on the approximately 2.4 l fluid, approximately 120 mEq Na+ and approximately 50 mEq K+ losses in sweat and urine in the three trials. The main effects of W and S were on body fluid shifts. During the NF trial, PV and interstitial fluid (ISF) and intracellular fluid (ICF) volumes decreased by approximately 0.1, 1.2 and 1.0 l, respectively. In the W trial, the approximately 1.2 l fluid and approximately 120 mEq Na+ losses contracted the ISF volume, and in the S trial, ISF volume was maintained by the movement of water from the ICF. Since the W and S trials were equally effective in maintaining PV, Na+ ingestion may not be of much advantage to athletes who typically replace only approximately 50% of their fluid losses during competitive endurance exercise.

Adult↗

PubMed1999

Metabolic adaptations to a high-fat diet in endurance cyclists.

We examined the time course of metabolic adaptations to 15 days of a high-fat diet (HFD). Sixteen endurance-trained cyclists were assigned randomly to a control (CON) group, who consumed their habitual diet (30% +/- 8% mJ fat), or a HFD group, who consumed a high-fat isocaloric diet (69% +/- 1% mJ fat). At 5-day intervals, the subjects underwent an oral glucose tolerance test (OGTT); on the next day, they performed a 2.5-hour constant-load ride at 70% peak oxygen consumption (VO2peak), followed by a simulated 40-km cycling time-trial while ingesting a 10% 14C-glucose + 3.44% medium-chain triglyceride (MCT) emulsion at a rate of 600 mL/h. In the OGTT, plasma glucose concentrations at 30 minutes increased significantly after 5 days of the HFD and remained elevated at days 10 and 15 versus the levels measured prior to the HFD (P < .05). The activity of carnitine acyltransferase (CAT) in biopsies of the vastus lateralis muscle also increased from 0.45 to 0.54 micromol/g/min over days 0 to 10 of the HFD (P < .01) without any change in citrate synthase (CS) or 3-hydroxyacyl-coenzyme A dehydrogenase (3-HAD) activities. Changes in glucose tolerance and CAT activity were associated with a shift from carbohydrate (CHO) to fat oxidation during exercise (P < .001), which occurred within 5 to 10 days of the HFD. During the constant-load ride, the calculated oxidation of muscle glycogen was reduced from 1.5 to 1.0 g/min (P < .001) after 15 days of the HFD. Ingestion of a HFD for as little as 5 to 10 days significantly altered substrate utilization during submaximal exercise but did not attenuate the 40-km time-trial performance.

Adaptation, Physiological↗

PubMed1999

Effects of ingesting a sports bar versus glucose polymer on substrate utilisation and ultra-endurance performance.

The purpose of this study was to determine whether the ingestion of a sports bar (BAR) containing a mixture of fat (7 g), protein (14 ) and carbohydrate (CHO; 19 ) improved ulta-endurance cycling performance compared to when an equicaloric amount of CHO was consumed. On two occasions separated by a minimum of 7 days, six highly trained (peak power output [PPO] 414 +/- 8 W) endurance cyclists rode for 330 min at approximately 50% of PPO (203 +/- 8 W) while ingesting either the BAR or just CHO, before performing a 400 k] time trial as fast as possible. Rates of fat oxidation were significantly greater at the end of the submaximal ride when subjects ingested the BAR compared to CHO (1.09 +/- 0.08 vs 0.73 +/- 0.08g x min(-1); P<0.05), and accordingly total fat oxidation was significantly higher (280 +/- 24 vs 203 +/- 25 g, P < 0.05). However, two subjects failed to complete the time trial after they consumed the BAR during the prolonged, submaximal ride, whereas all subjects managed to finish the time trial when ingesting CHO. In conclusion, ingestion of the sports bar enhanced fat metabolism during prolonged, submaximal exercise, but impaired subsequent high-intensity time-trial performance.

Adult↗

PubMed1999

Effects of different interval-training programs on cycling time-trial performance.

PURPOSE: We have investigated the effect of varying the intensity of interval training on 40-km time-trial performance in 20 male endurance cyclists (peak oxygen uptake 4.8+/-0.6 L x min(-1), mean +/- SD). METHODS: Cyclists performed a 25-kJ sprint test, an incremental test to determine peak aerobic power (PP) and a simulated 40-km time-trial on a Kingcycle ergometer. They were then randomly assigned to one of five types of interval-training session: 12x30 s at 175% PP, 12x60 s at 100% PP, 12x2 min at 90% PP, 8x4 min at 85% PP, or 4x8 min at 80% PP. Cyclists completed 6 sessions over 3 wk, in addition to their usual aerobic base training. All laboratory tests were then repeated. RESULTS: Performances in the time trial were highly reliable when controlled for training effects (coefficient of variation = 1.1%). The percent improvement in the time trial was modeled as a polynomial function of the rank order of the intensity of the training intervals, a procedure validated by simulation. The cubic trend was strong and statistically significant (overall correlation = 0.70, P = 0.005) and predicted greatest enhancement for the intervals performed at 85% PP (2.8%, 95% CI = 4.3-1.3%) and at 175% PP (2.4%, 95% CI = 4.0-0.7%). Intervals performed at 100% PP and 80% PP did not produce statistically significant enhancements of performance. Quadratic and linear trends were weak or insubstantial. CONCLUSIONS: Interval training with work bouts close to race-pace enhance 1-h endurance performance; work bouts at much higher intensity also appear to improve performance, possibly by a different mechanism.

Adult↗

PubMed1999

Effects of medium-chain triaclyglycerol ingested with carbohydrate on metabolism and exercise performance.

The effects of ingesting different amounts of medium-chain triacylglycerol (MCT) and carbohydrate (CHO) on gastric symptoms, fuel metabolism, and exercise performance were measured in 9 endurance-trained cyclists. Participants, 2 hr after a standardized lunch, cycled for 2 hr at 63% of peak oxygen consumption and then performed a simulated 40-km time trial (Ttrial). During the rides, participants ingested either 10% 14C-glucose (GLU), 10% 14C-GLU + 1.72% MCT (LO-MCT), or 10% 14C-GLU +3.44% MCT (HI-MCT) solutions: 400 ml at the start of exercise and then 100 ml every 10 min. MCT ingestion did not affect gastrointestinal symptoms. It only raised serum free fatty acid (FFA) and beta-hydroxybutyrate concentrations. Higher FFA and beta-hydroxybutyrate concentrations with MCT ingestion did not affect fuel oxidation or T-trial performance. The high CHO content of the pretrial lunch increased starting plasma insulin levels, which may have promoted CHO oxidation despite elevated circulating FFA concentrations with MCT ingestion.

3-Hydroxybutyric Acid↗

PubMed1998

Fuel metabolism during ultra-endurance exercise.

Cyclists either ingested 300 ml 100 g/l U-[14C] glucose solution every 30 min during 6 h rides at 55% of VO2max (n=6) or they consumed unlabelled glucose and were infused with U-[14C] lactate (n=5). Maintenance of euglycaemia limited rises in circulating free fatty acids, noradrenaline and adrenaline concentrations to 0.9+/-0. 1 mM, 27+/-4 nM and 2.0+/-0.5 nM, respectively, and sustained the oxidation of glucose and lactate. As muscle glycogen oxidation declined from 100+/-13 to 71+/-9 micromol/min/kg in the last 3 h of exercise, glucose and lactate oxidation and interconversion rates remained at approximately 60 and 50 and at about 4 and 5 micromol/min/kg, respectively. Continued high rates of carbohydrate oxidation led to a total oxidation of around 270 g glucose, 130 g plasma lactate and 530 g muscle glycogen. Oxidation of some 530 g of muscle glycogen far exceeded the predicted (about 250 g) initial glycogen content of the active muscles and suggested that there must have been a considerable diffusion of unlabelled lactate from glycogen breakdown in inactive muscle fibres to adjacent active muscle fibres via the interstitial fluid that did not equilibrate with 14C lactate in the circulation.

Beverages↗

PubMed1998

Influence of muscle glycogen content on metabolic regulation.

Euglycemia was maintained in 13 subjects with low muscle glycogen [low glycogen, euglycemic (LGE), n = 8; low glycogen, euglycemic, hyperinsulinemic (LGEI), n = 5] and 6 subjects with normal muscle glycogen (NGE), whereas hyperglycemia was maintained in 8 low muscle glycogen subjects (LGH). All subjects cycled for 145 min at 70% of maximal oxygen uptake during the infusions. Insulin was infused in LGEI at 0.2 mU.kg-1.min-1. During exercise, respiratory exchange ratio (RER) was lower and norepinephrine higher in LGE than in NGE. In LGEI and LGH, RER at the start of exercise was the same as in LGE but did not decrease as in LGE. Free fatty acids (FFA) were higher and plasma insulin concentrations lower in LGE than NGE, LGEI, or LGH over the first 45 min of exercise. Rate of glucose infusion (Ri) and rate of glucose oxidation (Rox) were higher in LGH and LGEI than in NGE or LGE, and Ri matched Rox in all groups except LGH, in which Ri was greater than Rox. Muscle glycogen disappearance was greater in NGE than LGE, LGEI, or LGH, but the latter three groups did not differ. In conclusion, this study showed that low muscle glycogen content results in a decrease in RER, an increase in FFA, fat oxidation, and norepinephrine both at rest and during exercise, and does not affect Rox when euglycemia is maintained by infusion of glucose alone. Rox was increased only during insulin and hyperglycemia.

Adult↗

PubMed1998

Preexercise muscle glycogen content affects metabolism during exercise despite maintenance of hyperglycemia.

Trained cyclists with low muscle glycogen (LGH; n = 8) or normal glycogen (NGH; n = 5) exercised for 145 min at 70% of maximal oxygen uptake during a hyperglycemic clamp. Respiratory exchange ratio was higher in NGH than LGH, and free fatty acid concentrations were lower in NGH than LGH. Areas under the curve for insulin and lactate were lower in LGH than NGH. Total glucose infusion and total glucose oxidation were not different between NGH and LGH, and total glucose oxidation amounted to 65 and 66% of total glucose infusion in NGH and LGH, respectively. Rates of glucose oxidation rose during exercise, reaching peaks of 9.2 +/- 1.7 and 8.3 +/- 1.1 mmol/min in NGH and LGH, respectively. Muscle glycogen disappearance was greater in NGH than LGH. Thus 1) low muscle glycogen content does not cause increased glucose oxidation, even during hyperglycemia; instead there is an increase in fat oxidation, 2) there is an upper limit to the rate of glucose oxidation during exercise with hyperglycemia irrespective of muscle glycogen status, and 3) net muscle glycogen utilization is determined by muscle glycogen content at the start of exercise, even during hyperglycemia.

Adult↗

PubMed1997

Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists.

Skeletal muscle buffering capacity (beta m), enzyme activities and exercise performance were measured before and after 4 weeks of high-intensity, submaximal interval training (HIT) undertaken by six well-trained competitive cyclists [mean maximal oxygen consumption (VO2max) = 66.2 ml.kg-1.min-1]. HIT replaced a portion of habitual endurance training and consisted of six sessions, each of six to eight repetitions of 5 min duration at 80% of peak sustained power output (PPO) separated by 1 min of recovery. beta m increased from 206.6 (17.9) to 240.4 (34.1) mumol H+.g muscle dw-1.pH-1 after HIT (P = 0.05). PPO, time to fatigue at 150% PPO (TF150) and 40-km cycle time trial performance (TT40) all significantly improved after HIT (P < 0.05). In contrast, there was no change in the activity of either phosphofructokinase or citrate synthase. In addition, beta m correlated significantly with TT40 performance before HIT (r = -0.82, P < 0.05) and the relationship between change in beta m and change in TT40 was close to significance (r = -0.74). beta m did not correlate with TF150. These results indicate that beta m may be an important determinant of relatively short-duration (< 60 min) endurance cycling activity and responds positively to just six sessions of high-intensity, submaximal interval training.

Adult↗

PubMed1997

Metabolic and performance adaptations to interval training in endurance-trained cyclists.

This study examined the effects of sustained high-intensity interval training (HIT) on the athletic performances and fuel utilisation of eight male endurance-trained cyclists. Before HIT, each subject undertook three baseline peak power output Wpeak tests and two simulated 40-km time-trial cycling performance (TT40) tests, of which the variabilities were 1.5 (1.3)% and 1.0 (0.5)%, respectively [mean (SD)]. Over 6 weeks, the cyclists then replaced 15 (2)% of their 300 (66) km.week-1 endurance training with 12 HIT sessions, each consisting of six to nine 5-min rides at 80% of Wpeak, separated by a l-min recovery. HIT increased Wpeak from 404 (40) to 424 (53) W (P < 0.01) and improved TT40 speeds from 42.0 (3.6) to 43.0 (4.2) km.h-1 (P < 0.05). Faster TT40 performances were due to increases in both the absolute work rates from 291 (43) to 327 (51) W (P < 0.05) and the relative work rates from 72.6 (5.3)% of pre-HIT Wpeak to 78.1 (2.8)% of post-HIT Wpeak (P < 0.05). HIT decreased carbohydrate (CHO) oxidation, plasma lactate concentration and ventilation when the cyclists rode at the same absolute work rates of 60, 70 and 80% of pre-HIT Wpeak (P < 0.05), but not when they exercised at the same relative (% post-HIT Wpeak) work rates. Thus, the ability of the cyclists to sustain higher percentages of Wpeak in TT40 performances after HIT was not due to lower rates of CHO oxidation. Higher relative work rates in the TT40 rides following HIT increased the estimated rates of CHO oxidation from approximately 4.3 to approximately 5.1 g.min-1.

Adaptation, Physiological↗