Reports indicate that postexercise heat loss is modulated by baroreceptor input; however, the mechanisms remain unknown. We examined the time-dependent involvement of adenosine receptors, noradrenergic transmitters, and nitric oxide (NO) in modulating baroreceptor-mediated changes in postexercise heat loss. Eight males performed two 15-min cycling bouts (85% VO2max) each followed by a 45-min recovery in the heat (35°C). Lower body positive (LBPP), negative (LBNP), or no (Control) pressure was applied in three separate sessions during the final 30-min of each recovery. Four microdialysis fibres in the forearm skin were perfused with: 1) lactated Ringer’s (Ringer’s); 2) 4mM Theophylline (inhibits adenosine receptors); 3) 10mM Bretylium (inhibits noradrenergic transmitter release); or 4) 10mM L-NAME (inhibits NO synthase). We measured cutaneous vascular conductance (CVC; percentage of maximum) calculated as perfusion units divided by mean arterial pressure, and local sweat rate. Compared to Control, LBPP did not influence CVC at L-NAME, Theophylline or Bretylium during either recovery (P>0.07); however, CVC at Ringer’s was increased by ~5-8% throughout 30 min of LBPP during Recovery 1 (all P<0.02). In fact, CVC at Ringer’s was similar to Theophylline and Bretylium during LBPP. Conversely, LBNP reduced CVC at all microdialysis sites by ~7-10% in the last 15 min of Recovery 2 (all P<0.05). Local sweat rate was similar at all treatment sites as a function of pressure condition (P>0.10). We show that baroreceptor input modulates postexercise CVC to some extent via adenosine receptors, noradrenergic vasoconstriction, and NO whereas no influence was observed for postexercise sweating.

The effects of exercise intensity and duration on excess post-exercise oxygen consumption (EPOC) were examined. Eight males exercised in a thermoneutral environment at 60% of maximal aerobic power (V0₂ₘₐₓ) for 30 min and performed the same total work at 80% and 40% V0₂ₘₐₓ by varying exercise durations. In addition, 2 work bouts were performed at 60% VO₂ₘₐₓ for 90 and 60 min. A standardized meal was consumed 2 h post-exercise. Oxygen consumption (V0₂), respiratory exchange ratio (RER), rectal temperature (Tc) and heart rate (HR) were monitored on a control day and before, during and for 3 h following exercise. VO₂ was equivalent to control day values within 30 min post-exercise on each of the 5 d and no consistent relation between exercise condition and duration of EPOC was observed. When total post-exercise VO₂ was expressed relative to control values, differences were greatest during the first 30 min post-exercise. Total net caloric expenditure was small (32. 5-57.9 kcal) in all cases. RER tended to remain equivalent to control levels post-exercise, with intermittent elevations. Significant elevations in Tc were obtained until 60 to 150 min post-exercise. No significant exercise-related effects were noted for dietary induced thermogenesis or the cumulative effect of the 5 exercise bouts on resting metabolic rate. Although exercise over a wide range of intensities and durations resulted in a significant EPOC, in all cases it was of short duration and the total 3 h energy expenditure was small. Neither duration nor magnitude of EPOC was associated with post-exercise RER or Tc. / Thesis / Master of Science (MSc)

The mechanisms which cause post exercise hypotension (a phenomenon of prolonged, decreased resting blood pressure following physical exertion) are unknown. Atrial natriuretic peptide (ANP) is known to exert potent natriuretic and vasodilatory properties which play an integral role in fluid regulation and blood pressure control. Elevations in plasma ANP concentration have been shown to occur during dynamic endurance exercise, and to a lesser extent during heavy resistance exercise. The purposes of this investigation were to 1) examine the effects of resistance and endurance exercise on the release of ANP, 2) examine the effects of resistance and endurance exercise on post exercise blood pressure and 3) evaluate the potential correlations of ANP release with any observed changes. Thirteen males (24.3±2.4yrs.) performed 15 min of unilateral leg press (65% 1 RM) and, one week later ~15 min (based on summed cardiac cycles of the resistance trial) of cycle ergometry (65% V0₂ ₚₑₐₖ). Blood pressure was measured using an intra-arterial catheter during exercise and for 1 h post exercise. Arterial blood was drawn at rest, 5, 10 and 15 min of exercise and 1 1/2, 3, 5, 10, 15, 30, 45 and 60 min post exercise for subsequent analysis of hematocrit and αANP. No differences occurred in blood pressure responses between trials, but significant decrements in blood pressure occurred post exercise compared to pre exercise. Systolic pressure was ~20mmHg lower from 10 min post exercise until measurements terminated at 60 min post exercise. Mean pressure was also significantly attenuated by ~7 mmHg from 30 min post exercise onwards. Only slight (non significant) elevations in αANP concentration were detected immediately following exercise with no elevation present by 5 min post exercise. It was concluded that post exercise hypotension occurs with acute bouts of either resistance or endurance exercise and that αANP does not appear to be directly related to this hypotensive effect. This study was supported by the Natural Sciences and Engineering Research Council of Canada / Thesis / Master of Science (MSc)

Blood flow to the previously active skeletal muscle remains elevated for several hours following an acute bout of aerobic exercise and is dependent on activation of H1 and H2 histamine receptors. Many questions remain unanswered in humans regarding the mechanisms mediating this sustained post-exercise vasodilation and what benefits come of this physiological phenomenon. The studies detailed in this dissertation were designed to examine the upstream mechanisms and explore a potential benefit associated with sustained post-exercise vasodilation. In chapter IV, we examined if oxidative stress is the upstream exercise-related factor mediating sustained post-exercise vasodilation. Intravenously infusing the antioxidant ascorbate blunted sustained post-exercise vasodilation, and this reduction was similar in magnitude to that observed with H1/H2 blockade. However, ascorbate may directly degrade histamine and may also inhibit its formation. Therefore, we conducted a follow-up study to verify the findings in study 1. In this study, we intravenously infused n-acetylcysteine, a potent antioxidant with no known histaminergic interactions. We found that n-acetylcysteine had no effect on sustained post-exercise vasodilation, indicating that exercise-induced oxidative stress is not the exercise related factor mediating sustained post-exercise vasodilation. In chapter V, we attempted to measure interstitial histamine in an effort to demonstrate that exercise induces the local formation of histamine in previously active skeletal muscle. We found that histamine is increased in the interstitial fluid within skeletal muscle during and after exercise. Additionally, we determined that de novo synthesis via histidine decarboxylase contributes to the rise in histamine during and following exercise. We also demonstrated a possible role of mast cells as an additional mechanism augmenting histamine in skeletal muscle. Collectively, these studies demonstrate that histamine is the ligand activating histamine receptors and activation is due to the induction of histidine decarboxylase and mast cell activation. In chapter VI, we attempted to determine if histamine receptor activation contributes to the expression of pro- and anti-angiogenic growth factors during the recovery from exercise. Our preliminary findings indicate that activation of histamine receptors may play a role in the expression of pro-angiogenic growth factors during the recovery from acute aerobic exercise.

Purpose: To investigate the differential effects of solutions providing varying concentrations of carbohydrate and/or protein ingested between 200-meter sprints on sprint time. Subjects: Recruitment was from the Georgia State University track and field team. Methods: The study protocol was approved by the Georgia State University IRB. Ten subjects, 18 to 21 years of age, consented to be included in the study. Nine subjects (7 females; 2 males) completed trial 1, six subjects (5 females; 1 male) completed trial 2, and three subjects (2 females; 1 male) completed the final trial. Each trial consisted of a 200-meter sprint followed by the immediate ingestion of a post-exercise recovery beverage within the first fifteen minutes of a one-hour recovery period. Following the one-hour of recovery, subjects sprinted a second 200-meter sprint. Beverage solutions were formulated to contain 1.2 g of protein (PRO), 1.2 g carbohydrate (CHO), or 1.2 g carbohydrate with protein (CHO/PRO) per kg of subject body weight. Using a single blind, non-randomized design, subjects received the same recovery beverage in each trial. Each trial consisted of either PRO (trial 1), CHO (trial 2), or CHO/PRO (trial 3), with one week separating trials. Sprint times were recorded in seconds and ten hundredths of a second using a manual, digital stopwatch. Results: During PRO, two subjects sprinted faster (x= -.25 sec), three subjects saw no change in sprint time, and four subjects sprinted slower (x= +.98 sec). During CHO, two female subjects sprinted faster between sprints (x= -.85 sec); and all other subjects (n=4) sprinted slower (x= +.73 sec). During CHO/PRO, no subjects sprinted faster from sprint 1 to sprint 2 (x= +.33 sec) Conclusions: Post-exercise nutritional supplementation effects varied among subjects, with some subjects performing better following PRO, while others experiencing improvements with CHO. In general, subjects performed better following consumption of the CHO beverage. Of those who ran faster between sprints, the CHO beverage resulted in an average improvement of -.85 sec, while the PRO beverage resulted in an average improvement of -.25 sec. On average, CHO resulted in faster 2nd sprints (x= +.20 sec) than the PRO beverage (x= +.47 sec) or the CHO/PRO beverage (x= +.33 sec). Continued research in this population is necessary for elucidation of study results. This investigation may serve as the foundation for future, related studies.

<p> Resistance exercise training results in skeletal muscle hypertrophy due to accumulated periods ofprotein accretion, the magnitude ofwhich may be influenced by post-exercise feeding. One study suggests that hypertrophy is maximized by immediate provision ofprotein (26); how the type ofprotein ingested in this period affects protein accretion is not known. PURPOSE: To investigate the effect of consuming different post-exercise beverages -milk (MLK), an isonitrogenous and isoenergetic soy drink (PEC), or an isoenergetic control (CON)-on body mass, fat-bone free mass (FBFM), muscle fibre area, and strength during a 12-week progressive whole body resistance training program, in untrained men. METHODS: 34 men were randomized to postexercise consumption ofMLK (n=12; fat free), PEC (n=11; soy) or CON (n=11; maltodextrin) using single-blinded allocation, with characteristics-22.5 ± 0.6 yr, 25.6 ± 0.7 kg/m2• Participants trained 5 d/wk using a whole body split resistance training program and consumed 500 ml oftheir assigned drink immediately and 1h post-exercise following every training bout. RESULTS: Total body mass increased following training (P<0.01) but there were no differences between groups (MLK = 3.2 ± 0.8 kg, PEC = 2.9± 1.4 kg, CON= 2.0 ± 0.8 kg). Similarly, FBFM also increased post-training (P<0.01), but was not different between groups (MLK = 3.3 ± 0.6 kg, PEC = 2.7 ± 0.6kg, CON= 2.2 ± 0.6 kg). Muscle type II fibre area increased post-training (P<0.05) but was not different between groups (MLK = 1004 ± 249 pm2, PEC = 650 ± 192 pm2, CON= 565 ± 120 pm2). Training resulted in increases in 1RM strength for 13 different exercises (P<0.01) with no difference between groups (range= 29-101%). CONCLUSION: Immediate post-exercise provision ofeither milk (MLK), or an isonitrogenous I isoenergetic soy drink (PEC), as well as an isoenergetic carbohydrate beverage (CON), resulted in similar increases in body mass, FBFM, type II muscle fibre area, and strength. This study demonstrates that intact dietary proteins from milk and soy are effective for promoting skeletal muscle hypertrophy. Moreover, when given equivalent energy immediately postexercise, proteins consumed as part of a normal diet, outside ofthe immediate postexercise period are sufficient for hypertrophic and strength gains. Finally, post-exercise consumption ofprotein is no more effective than carbohydrate for promoting skeletal muscle hypertrophy when adequate protein is consumed within a regular diet. </p> / Thesis / Master of Science (MSc)

Current knowledge indicates that nonthermal muscle metaboreflex activity plays a critical role in the modulation of skin vasodilation and sweating. However, the mechanisms of control have primarily been studied during isometric handgrip exercise in which muscle metaboreceptor activation is induced by a brief post-exercise ischemia of the upper limb. While the reflex increase in mean arterial pressure associated with this period of ischemia is consistent with the activation of muscle metaboreceptors, the change in baroreflex activity may in itself modulate the response. Thus, we sought to understand how these nonthermal stimuli interact in modulating the control of skin perfusion and sweating under conditions of elevated hyperthermia. Furthermore, we examined the mechanisms responsible for the maintenance of arterial blood pressure under varying levels of heat stress during isometric handgrip exercise. Our study findings indicate that the parallel activation of muscle metaboreceptors and baroreceptors during post-exercise ischemia causes divergent influences on the control of skin blood flow and sweating; and these nonthermal stimuli are dependent on the level of hyperthermia. Moreover, we report that heat stress reduces the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is attributed to a blunted increase in peripheral resistance, since cardiac output increased to similar levels for all heat stress conditions. These results provide important insight and understanding into the role of muscle metabo- and baroreflex activity on the control of skin blood flow and sweating; along with further knowledge into the cardiovascular mechanisms responsible for the regulation of arterial blood pressure during hyperthermia.

Pre-hypertension (pre-HT) (Blood Pressure (BP) ≥120/80mmHg to ≤ 140/90mmHg) increases the risk of developing hypertension (HT). BP reductions following acute exercise are known as post exercise hypotension (PEH). BP and perhaps PEH shows a daily circadian rhythm. Purpose: To compare the magnitude of PEH after morning and evening aerobic exercise in adults with pre-HT. Hypothesis: The magnitude of PEH will be larger after evening versus morning exercise. Participants: Pre-HT men and women 50-65 years old. Study Design: Participants engaged in cycling exercise (60% VO2max) on two occasions: 1.5 and 11 hours following waking. Cardiovascular function was assessed for 30 minutes pre and one hour post exercise. Results: 1) Systolic PEH responses affected by TOD differed by gender. 2) Baseline Heart Rate Variability and its response to exercise differed gender but not TOD. The inconsistent significant gender and TOD differences of PEH and its mechanisms suggest that this group.

Aerobic exercise is recommended as a lifestyle intervention to reduce blood pressure (BP) in individuals with elevated BP (SBP/DBP >120/80 mmHg). However, the BP response is highly variable after both acute (SBP/DBP: –27 to 9/-8 to 7mmHg) and chronic aerobic exercise (-20 to 9/ -11 to 11.3mmHg). We attempt to identify those who are resistant or responsive to training based on their responses to acute (one-bout) exercise. 17 prehypertensive (120 to 139/80 to 89mmHg) males and females (45-60yrs) underwent acute exercise assessments before and after an 8-week walking/jogging program. The magnitude of change in BP after acute exercise significantly correlated (r=.89, p < .01) with the magnitude of change in resting BP after the training. The antihypertensive mechanisms (total peripheral resistance, baroreflex sensitivity) for acute exercise were not correlated to those for chronic exercise. Central cardiovascular controls may link BP reductions after both acute and chronic exercise.

Aerobic exercise such as cycling is known to elicit a post-exercise hypotensive (PEH) response. However, it is not known if swim exercise produces a similar effect in normotensive individuals. We tested the hypothesis that an acute bout of swimming would elicit a PEH response that is less compared to an equivalent bout of cycling. 10 trained and 11 untrained normotensive (SBP/DBP < 120/80 mmHg) individuals (23±1 years) underwent 30 min intensity-matched cycling and swimming sessions to assess changes in BP and cardiovascular responses. While PEH was similar between modalities within groups, the magnitude and temporality of change in BP following swimming was significantly different (p < 0.01) between groups, with untrained participants showing a significant PEH response. Attenuation of PEH in trained individuals was reflective of a significant increase in sympathetic outflow and slower vagal reactivation, suggesting training in an aquatic environment leads to alterations in post-exercise BP regulatory mechanisms.