Previous studies have suggested that if exercise intensity is established by perceived effort, the metabolic demand varies among exercise machines and the treadmill optimizes energy expenditure (EE). However, these studies have been completed utilizing young people with normal body fat percentages. Therefore, the purpose of this study was to assess whether there was a difference in acute energy expenditure when obese people used different exercise modes at a self-selected intensity (RPE 11-12) commonly recommended for overweight individuals. Twelve obese subjects (7 male; 5 female; BMI >29 kg/m2), aged 37-71 years completed two familiarization trials on four machines: treadmill (TM), stationary cycle (C), Body Trec elliptical arm/leg (BT), and Airdyne (AD). On separate days, subjects then completed a 15 minute trial on each machine at a self-selected intensity corresponding to a target RPE of I 1-12 on the Borg 15 point scale. Machine order was randomly assigned, and subjects were blinded to the workload throughout each trial. Workload was self-adjusted during the first 5 minutes and then remained stable for the rest of the trial. Physiological data were obtained during the last five minutes of each trial via HR telemetry and the Aerosport TEEM 100. The group means were compared across modes using a one-way repeated measures ANOVA. Significant differences (p <0.05) were observed across exercise modes for energy expenditure. The BT produced the highest rate of energy expenditure among exercise machines and C the lowest (8.0±2.0, 6.6±2.1, 6.3±2.0, 5.3±2.1 Kcal/min, for BT, TM, AD, and C, respectively). These results suggest that perceptually-based exercise prescriptions are not reliable across modes typically found in a fitness center environment, and that weight-bearing arm/leg exercise optimizes EE during self-selected exercise of moderate intensity in obese subjects. / School of Physical Education

The purpose of this investigation was to examine the effects of exercise and diet on muscle triglyceride. Seven endurance-trained men completed a 120min cycling bout at 65% of V O2max in an attempt to lower muscle glycogen and triglyceride. Each subject then ingested an isocaloric, high-carbohydrate (HI-CHO; 83% of kcal) or high-fat (HI-FAT; 68% of kcal) diet for the ensuing 24 h. A 1600 kJ cycling time trial was completed following this 24-h dietary period. Muscle glycogen concentration before (571±38 vs. 599±41 mmol•kg dw-1) and after (241±36 vs. 285±41 mmol•kg dw-1) the 120-min cycling bout was not different (P>0.05) between the HI-CHO and HI-FAT trials, respectively. Muscle triglyceride concentration before (33.0±2.3 vs. 37.0±2.1 mmol•kg dw-1) and after (30.9±2.4 vs. 32.8±1.6 mmol•kg dw-1) the 120-min cycling bout was also not different between the HI-CHO and HI-FAT trials, respectively. In addition, muscle triglyceride did not decrease significantly during the cycling bout for the HI-CHO (2.1±2.1 mmol•kg dw-1) or HI-FAT (4.2±1.8 mmol•kg dw-1) trial. Over the 24-h dietary period, a significantly greater amount of glycogen was resynthesized during the HI-CHO (308±41 mmol•kg dw-1) versus the HI-FAT trial (42±23 mmol•kg dw-1). Muscle triglyceride concentration increased 11.9±1.6 mmol•kg dw-1 (P<0.05) and decreased 3.4±1.8 mmol•kg dw-1 (P>0.05) during the 24-h dietary period for the HI-FAT and HI-CHO trials, respectively. Cycling performance time was significantly greater during the HI-FAT (139.3±7.1 min) compared to the HICHO (117.1±3.2) trial. The average V02 (3.40±0.12 vs. 2.96±0.17 L•min-1) and RER (0.89±0.01 vs. 0.82±0.01) during the time trial were higher for the HI-CHO than the HI-FAT trial, respectively. These data demonstrate that a small, insignificant amount of muscle triglyceride is utilized during prolonged, moderate-intensity cycling. Furthermore, 24 h of a high-fat diet increased muscle triglyceride concentration and reduced endurance performance. / Human Performance Laboratory

Two experiments were done to study the effects of L-carnitine supplementation (CNsup) during exercise. EXP 1, examined the effect of CNsup on lipid oxidation and muscle glycogen utilization during submaximal EX. Triglycerides were elevated by a fat feeding (90g fat), 3 h later subjects cycled for 60 min at 70% VO2max (CON). Muscle biopsies were obtained preEX, after 30 and 60 min of EX. Blood samples were taken preEX and every 15 min of EX. Subjects randomly completed two additional trials following 7 and 14 days of CNsup (6 g/day). During one of the trials, subjects received 2000 units of heparin 15 min prior to EX to elevate FFA (CNhep). There were no differences in V02, RER, HR, g of CHO and fat oxidized among the three trials. Serum total acid soluble (TASC) and free carnitine (FC) increased with CNsup (CON, 71.3 ± 2.9; CN, 92.8 ± 5.4; CNhep, 109.8 ± 3.5 mol·g'). Muscle carnitine concentration at rest was unaffected by CNsup. During EX, TASC did not change, FC decreased (p<0.05) and SCAC increased (p<0.05). With CNsup the decrease in FC was less (~50%) (p<0.05) and the increase in SCAC was greater (~200-300%) (p<0.05) compared to CON (free 65%; SCAC 150%). Pre and postEX muscle glycogens were not different. EXP 2, examined the effects of CNsup on blood lactate accumulation during maximal EX. Subjects cycled for 4 min at ~100% VO2max (CON). Exercise was repeated following 6 and 13 days of CNsup (6 g/day). Serum TASC and FC were elevated due to CNsup. Blood Lactate was measured prior to and 0, 3, 5, and 7 min postEX. CNsup resulted in less (p<0.05) lactate accumulation compared to CON. There were no differences between DAY-6 and DAY-13. / Human Performance Laboratory

This study was designed to determine if highly caffeine sensitive (HS) and less caffeine sensitive (LS) individuals differ in metabolic substrate use and endurance performance following caffeine ingestion. Twenty subjects were placed into HS and LS groups based on a series of 6 isokinetic cycle ergometer rides in which perceived exertion was held constant and work output was measured. Subjects who performed significantly more work following caffeine ingestion were classified as HS while those who did not were classified as LS. Seven subjects were selected from each of these groups to perform the experimental trials. These trials were conducted 60 min after ingestion of 6 mg-kg-1 caffeine or a placebo and consisted of a 30 min ride at70% VO2max followed by a 60 min isokinetic performance ride. The HS group achieved a higher accumulated workload over the last 30 min of the ride following caffeine ingestion compared to the placebo condition. No increase in work output was observed in the LS group following caffeine ingestion. There were no significant differences between treatments in either the HS or LS group in amount of muscle glycogen utilized during the first 30 min of the ride. During the caffeine trials serum glucose was elevated at 20, 30, and 50 min, free fatty acid concentration was elevated at the zero time point, and glycerol concentration was elevated at 60 and 90 min compared to the placebo trials. However, there were no differences between the HS and LS groups in these parameters. These data suggest that the ergogenic effects of caffeine in some individuals are not due to an alteration in substrate utilization, but may be related to an alteration in neural perception of effort. / School of Physical Education

This study compared the exercise responses 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. A familiarization trial was first conducted to eliminate a potential order effect. An order effect was evidenced by lower (p<0.05) work rates during the performance ride of the first trial (390 ± 26.1 kJ) than the other four trials. No order effect was observed for the remainder of the experimental treatments which were performed in a single-blind, randomized fashion. At rest, GL elicited greater (P<0.05) serum glucose and insulin responses than all other trials. During exercise, however, serum glucose and insulin responses were similar among trials. Blood C-peptide and glucagon responses were also 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 pre-exercise 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. / Human Performance Laboratory

Uncoupling protein, UCP, present in the inner mitochondrial membrane of brown adipose tissue (BAT) contributes to adaptive thermogenesis. UCP functions as a proton pore and can dissipate the proton electrochemical gradient established by the respiratory chain during fuel oxidation, and thus generates heat without producing ATP. However, the brown adipose tissue thermogenesis is not likely to be a major mechanism in controlling energy expenditure for humans because adults have only residual amounts of the tissue. Two new members of the UCP family have been identified based on their high sequence homology to UCP in BAT and named UCP2 and UCP3. The original UCP was renamed UCP1. At the amino acid level, human UCP2 and UCP3 are 59% and 57% identical to UCP1, respectively. In contrast to UCP1, UCP2 is expressed in many tissues such as brown adipose tissue, white adipose tissue, muscle, spleen and macrophages. UCP3 is expressed preferentially in skeletal muscle in humans, and brown adipose tissue and skeletal muscle in rodents. Since their identification many functional studies, including transgenic animals and ectopic expression of UCP2 or UCP3 in yeast, showed uncoupling activity of UCP2 and UCP3. A number of studies have been done that show increased expression of UCP2 and UCP3 by fasting, high-fat diets and suckling of newborn mice. A common characteristic of these circumstances is an associated increase in plasma free fatty acid levels. This study aimed to investigate effects of fatty acids, peroxisome proliferator-activated receptors (PPARs) and other transcription factors on UCP2 and UCP3 gene expression and to explore the molecular mechanism of their regulation through analysis of the promoter of the UCP2 and UCP3 genes. The 3.1 kb and 3.2 kb 5�-flanking regions of the mouse UCP2 and UCP3 genes, respectively, were cloned and used to construct promoter reporter gene (firefly luciferase) plasmids. The cloned region of the UCP2 and UCP3 genes contained putative binding motifs for several transcription factors, including PPAR, myogenin, and MyoD. Luciferase assays of both constructs showed basal promoter activity with 20~190-fold induction for the UCP2 promoter and 1.3~23-fold induction for the UCP3 promoter in several transfected cell lines, including 3T3-L1, C2C12, L6, COS7 and HepG2. Oleic acid (0.3 mM) up-regulated endogenous UCP2 mRNA by 2.3-fold in 3T3-L1 preadipocytes but not in C2C12 myotubes, and UCP3 mRNA by 2.5-fold in C2C12 myotubes. Responsiveness of the cloned promoter to oleic acid reflected the tissue-specific responsiveness of their endogenous genes but with less fold induction, 1.4-fold for UCP2 promoter in 3T3-L1 preadipocytes and 1.5-fold for UCP3 promoter in C2C12 myotubes. Forced expression of PPAR isotypes (PPARα, PPAR[delta] and PPARγ) showed tissue and isotype-specific activation of the UCP2 promoter. UCP2 promoter activity was induced by 2-fold by PPARγ in 3T3-L1 and by 2.8-fold by PPAR[delta] in C2C12. Treatment of oleic acid (0.3 mM) brought about further induction of the UCP2 promoter activity only in 3T3-L1. In contrast, all three isotypes induced activation of the UCP3 promoter in 3T3-L1, C2C12 and HepG2 cells. Treatment with oleic acid (0.3 mM) or isotype-specific agonist (10 [mu]M) resulted in further increased activity of the UCP3 promoter in 3T3-L1 and HepG2 cells. In particular, rosiglitazone (10 [mu]M) induced a 41-fold increase in UCP3 promoter activity in PPARγ transfected HepG2 cells, and this induction returned to basal level by treatment with bisphenol A diglycidyl ether (BADGE) (50 [mu]M), an antagonist for PPARγ. In addition, UCP3 promoter activity increased up to 20-fold 4 days after induction of C2C12 myoblasts differentiation, whereas UCP2 promoter activity increased only up to 2-fold. Forced expression of myogenin and MyoD in C2C12 myoblasts to mimic differentiation, induced UCP3 promoter activity in an additive manner, consistent with UCP3 being regulated by muscle differentiation. In the present study, it has been shown that UCP2 and UCP3 genes are regulated differently by fatty acids. The tissue-type dependence in regulation of endogenous UCP2 and UCP3 paralleled the cell type-specific effect of oleic acid on the promoter-reporter constructs, suggesting that fatty acid effects are at the transcriptional level. UCP2 and UCP3 promoters showed differences in their response to PPARs. Mediation of the fatty acid effect through PPARs has been also demonstrated, but direct binding of PPARs and particular regulatory motifs on the cloned promoter region have not yet been investigated.

Little is known about the strain and consequences of very prolonged and sustained exercise lasting multiple days. This thesis comprises two multi-day exercise field studies and a 24-h, controlled-trial field/laboratory study. The field studies were undertaken using international adventure races (2003 and 2004 Southern Traverses: 86-120 h) to profile exercise intensity and associated physiological and psychophysical strain, and physical and cognitive performance. The 2003 study showed that exercise intensity (from heart rate range) averaged 64% during the first 12 h, dropped to 41% by 24 h, and remained so thereafter. Body core temperature (gastrointestinal pills), throughout racing (n=8) was relatively stable (min 36.0�C and only briefly >39�C), despite widely varying endogenous and exogenous thermal stress. Blood samples obtained before (n=34), during (n=11) and after (n=34) racing revealed a large plasma volume expansion (24%), with stable [sodium]plasma (n=6). Acute (15-30 h) and chronic (96-120 h) elevation of neutrophil, monocyte and lymphocyte numbers were observed across the race. Standardised exercise tests (rest, 25 and 50% peak power output (PPO)) before and after racing (n=9) revealed an extreme shift toward fat utilisation, consistent with lowered fat mass (11%; n=44) and high [free fatty acids]plasma (up 370%; n=9) at race-finish, although [HAD]muscle was unchanged. Muscle glycogen was only 50% lower post-race (290 nmol�kg⁻�d.w.). Complex cognitive performance (Stroop test) impairment was attenuated during 50% PPO post-race. Perceived exertion uncoupled from HR at standardised workloads. Explosive power (jump test; n=24) and anaerobic power (30-s Wingate; n=27) were modestly (<10%) impacted. Strength reduction of arms (11%) and legs (17%) was equivalent (p=0.17). The 2004 study (n=4) involved dissimilar terrain, vegetation, and sequence of exercise modes, yet the profile of exercise intensity was similar: first 12 h 65%, then 45% by 24 h and thereafter. Thus, athletes reliably attain sustainable, low-to-moderate exercise intensity by 24 h. Plasma volume, neutrophil and monocyte responses were reliable across races, whereas lymphocytes were not. Plasma [IL-6] and [S100β] were elevated, substantially in some individuals (IL-6: 223 pg�mL⁻�; S100β: 113 pg�mL⁻�), during racing. A 24-h adventure race simulation (n=9) was then undertaken to investigate physiological and psychophysical factors influencing exercise intensity, autonomic function and orthostatic tolerance. Tests were at 0, ~7, ~15 and 24 h. The 24-h HR profile matched that observed during racing: first 12 h 58% (including 3-h testing), remainder 41%. The shift toward fat utilisation was almost complete within 7 h, and similar to that following 2003 race. The perceived exertion-to-HR uncoupling was also similar; being complete within 15 h. Plasma [noradrenaline] for rest and 12-km�h⁻� run was elevated post-simulation. Plasma [IL-6] peaked by 7 h, although not as high as field observations. The timeframe of metabolic change and perceived exertion uncoupling coincided with that of pace reduction, and may be important regulatory components of very prolonged exercise intensity. Orthostatic intolerance was evident during the simulation (n=6/9), as was cerebral hypo-perfusion (15 h & 24 h). Autonomic function (baroreflex sensitivity, sympathetic activation, parasympathetic withdrawal) was altered only at 7 h, whereas postural-induced hypotension (via impaired venous response) and hypocapnia were always present.

Thesis (Ph.D.)--Indiana University, School of Health, Physical Education and Recreation, 2006. / Includes bibliographical references (leaves 196-206).

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.