Thomas J. Wetter

Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans

1 We tested the hypothesis that reflexes arising from working respiratory muscle can elicit increases in sympathetic vasoconstrictor outflow to limb skeletal muscle, in seven healthy human subjects at rest. 2 We measured muscle sympathetic nerve activity (MSNA) with intraneural electrodes in the peroneal nerve while the subject inspired (primarily with the diaphragm) against resistance, with mouth pressure (PM) equal to 60 % of maximal, a prolonged duty cycle (TI/TTot) of 0.70, breathing frequency (fb) of 15 breaths min−1 and tidal volume (VT) equivalent to twice eupnoea. This protocol was known to reduce diaphragm blood flow and cause fatigue. 3 MSNA was unchanged during the first 1–2 min but then increased over time, to 77 ± 51 % (s.d.) greater than control at exhaustion (mean time, 7 ± 3 min). Mean arterial blood pressure (+12 mmHg) and heart rate (+27 beats min−1) also increased. 4 When the VT, fb and TI/TTot of these trials were mimicked with no added resistance, neither MSNA nor arterial blood pressure increased. 5 MSNA and arterial blood pressure also did not change in response to two types of increased central respiratory motor output that did not produce fatigue: (a) high inspiratory flow rate and fb without added resistance; or (b) high inspiratory effort against resistance with PM of 95 % maximal, TI/TTot of 0.35 and fb of 12 breaths min−1. The heart rate increased by 5–16 beats min−1 during these trials. 6 Thus, in the absence of any effect of increased central respiratory motor output per se on limb MSNA, we attributed the time‐dependent increase in MSNA during high resistance, prolonged duty cycle breathing to a reflex arising from a diaphragm that was accumulating metabolic end products in the face of high force output plus compromised blood flow.

Effects of respiratory muscle training versus placebo on endurance exercise performance

We evaluated the effects of a 5 week (25 sessions); (30-35 min/day, 5 days/week), respiratory muscle training (RMT) program in nine competitive male cyclists. The experimental design included inspiratory resistance strength training (3-5 min/session) and hyperpnea endurance training (30 min/session), a placebo group which used a sham hypoxic trainer (n=8), and three exercise performance tests, including a highly reproducible 8 km time trial test. RMT intensity, measured once a week in terms of accumulated inspiratory pressure and the level of sustainable hyperpnea increased significantly after 5 weeks (+64% and +19%, respectively). The RMT group showed a significant 8% increase in maximal inspiratory pressure (P<0.05) while the placebo group showed only a 3.7% increase (P>0.10). RMT and placebo groups both showed significant increases in the fixed work-rate endurance test performance time (+26% and +16%, respectively) and in the peak work-rate achieved during the incremental maximal oxygen consumption (V(O2)max) test (+9 and +6%). The 8 km time trial performance increased 1.8+/-1.2% (or 15+/-10 sec; P<0.01) in the RMT group with 8 of 9 subjects increasing; the placebo group showed a variable non-significant change in 5 of 8 subjects (-0.3+/-2.7%, P=0.07). The changes observed in these three performance tests were not, however, significantly different between the RMT and placebo groups. Heart rate, ventilation, or venous blood lactate, at equal work-rates during the incremental exercise test or at equal times during the fixed work-rate endurance test were not changed significantly across these exercise trials in either group. We propose that the effect of RMT on exercise performance in highly trained cyclists does not exceed that in a placebo group. Significant placebo and test familiarization effects must be accounted for in experimental designs utilizing performance tests which are critically dependent on volitional effort.

Effect of calorie restriction on in vivo glucose metabolism by individual tissues in rats

We evaluated the effects of 8 mo of calorie restriction [CR: 60% of ad libitum (AL) food intake] on glucose uptake by 14 tissues in unanesthetized, adult (12 mo) F344×BN rats. Glucose metabolism was assessed by the 2-[3H]deoxyglucose tracer technique at 1500 or 2100. Despite an ∼60% decline in insulinemia with CR, plasma 2-[3H]deoxyglucose clearance for CR was greater than for AL at both times. A small, CR-related decrease in glucose metabolic index ([Formula: see text]) occurred only at 1500 in the spleen and heart, and this decrease was reversed at 2100. In some tissues (cerebellum, lung, kidney, soleus, and diaphragm),[Formula: see text] was unaffected by diet, regardless of time. In the other tissues (brown fat, 3 white fat pads, epitrochlearis, plantaris, and gastrocnemius),[Formula: see text] was higher or tended to be higher for CR vs. AL at one or both times. These findings indicate that 8 mo of CR did not cause a continuous reduction in in vivo glucose uptake by any tissue studied, and, in several insulin-sensitive tissues, glucose uptake was at times greater for CR vs. AL rats.

Low doses of caffeine reduce heart rate during submaximal cycle ergometry

BackgroundThe purpose of this study was to examine the cardiovascular effects of two low-levels of caffeine ingestion in non habitual caffeine users at various submaximal and maximal exercise intensities.MethodsNine male subjects (19–25 yr; 83.3 ± 3.1 kg; 184 ± 2 cm), underwent three testing sessions administered in a randomized and double-blind fashion. During each session, subjects were provided 4 oz of water and a gelatin capsule containing a placebo, 1.5 mg/kg caffeine, or 3.0 mg/kg caffeine. After thirty minutes of rest, a warm-up (30 Watts for 2 min) the pedal rate of 60 rpm was maintained at a steady-state output of 60 watts for five minutes; increased to 120 watts for five minutes and to 180 watts for five minutes. After a 2 min rest the workload was 180 watts for one minute and increased by 30 watts every minute until exhaustion. Heart rate (HR) was measured during the last 15-seconds of each minute of submaximal exercise. Systolic blood pressure (BP) was measured at rest and during each of the three sub-maximal steady state power outputs. Minute ventilation (VE), Tidal volume (VT), Breathing frequency (Bf), Rating of perceived exertion (RPE), Respiratory exchange ratio (RER), and Oxygen consumption (VO2) were measured at rest and during each minute of exercise.ResultsCaffeine at 1.5 and 3.0 mg/kg body weight significantly lowered (p < 0.05) HR during all three submaximal exercise intensities compared to placebo (range – 4 to 7 bpm lower) but not at rest or maximal exercise. BP was significantly higher (p < 0.05) at rest and after the 3 mg/kg caffeine vs placebo (116 ± 13 vs 123 ± 10 mm Hg). Neither dose of caffeine had any effect on BP during submaximal exercise. Caffeine had no effect on VE, VT, VO2, RPE, maximal power output or time to exhaustion.ConclusionIn non habitual caffeine users it appears that consuming a caffeine pill (1.5 & 3.0 mg/kg) at a dose comparable to 1–3 cups of coffee lowers heart rate during submaximal exercise but not at near maximal and maximal exercise. In addition, this caffeine dose also only appears to affect systolic blood pressure at rest but not during cycling exercise.

Comparison of the effects of 20 days and 15 months of calorie restriction on male Fischer 344 rats.

The aim of this study was to compare, in 19-month-old male Fischer 344 rats, the influence of brief (20 days) and prolonged (∼15 months) calorie restriction (CR; consuming ∼60% of ad libitum, AL, intake) on circulating levels of glucose, insulin, C-peptide, and free fatty acids (FFA); age-matched AL rats were also studied. In the prolonged CR group, there was an ∼85% decline in fat pad masses (epididymal and retroperitoneal) compared to AL and brief CR rats (these latter groups did not differ significantly). Compared to AL levels, glucose was 15% lower with prolonged CR (p <0.05) while the brief CR values tended to be lower (10%) than AL; the CR groups did not differ significantly. Plasma FFA levels were significantly (p <0.05) greater (85–106%) in the brief CR group compared to each of the other groups. Plasma insulin concentrations for the CR groups were lower (p<0.05; ∼50–60%) than AL levels. Plasma concentrations of C-peptide (an indicator of insulin secretion) were also lower for each CR group vs AL levels, and a high correlation was found between plasma insulin and C-peptide concentrations (r2 =0.90; p<0.001). The C-peptide/ insulin ratios for the CR groups were similar, and the value of each CR group exceeded that for the AL rats. These results demonstrate that: the CR-induced reduction in plasma insulin is attributable in large part to reduced insulin secretion; these decreases in insulin secretion and concentration are essentially undiminished when brief CR is initiated rather late in life, and the reductions are independent of substantial reductions in body fat.

Das atemsystem schränkt die leistung eines gesunden athleten ein: Einige antworten, noch mehr fragen!

Jahrgang 63, Nr. 6 (2012) DEUTSCHE ZEITSCHRIFT FÜR SPORTMEDIZIN 157 Das respiratorische System begrenzt den arteriellen Sauerstoffgehalt und/oder den Blutfluss während hochintensiven Belastungen auf drei unterschiedliche Weisen: 1.) belastungsinduzierte arterielle Hypoxämie (EIAH), die bei hochtrainierten männlichen und weiblichen Läufern verbreitet ist; 2.) Effekte von intrathorakalen Druckänderungen auf das Schlagvolumen; und 3.) metabolischreflektorisch bedingte Effekte von Atemmuskulatur-ermüdenden Kontraktionen welche konsekutiv zu einer vegetativ bedingten Vasokonstriktion führt und die Gefäßleitfähigkeit und den Blutfluss in der Bewegunsgmuskulatur reduziert. Die Folgen dieser atemabhängigen Limitationen auf die Ermüdung der Extremitäten wurden durch eine supramaximale Magnetstimulation des Femoralnervs vor und nach Ausdauerbelastung untersucht. Um den Einfluss dieser Limitationen auf Erschöpfung und Leistung zu bestimmen, wurde das Auftreten durch Steigerung des O2-Anteils (um die arterielle Hypoxämie zu reduzieren) und eine mechanische Atemunterstützung verhindert (um den intra-thorakalen Druck zu reduzieren). Der Effekt jeder einzelnen respiratorischen Limitation am Sauerstofftransport wirkte sich negativ auf die VO2max aus und führte zu einer Anhäufung von Muskelmetaboliten sowie zu einer Ermüdung der Bewegungsmuskulatur. Dies führte über eine Rückkopplung zu einer Blockade der zentral motorischen Steuerung und beeinflusste dadurch die Ausdauerleistungsfähigkeit. Weiterhin werden die Gründe für die Ursachen sowie die Folgen von den atemabhängigen Limitationen zusammen gefasst, zudem werden die ungelösten Probleme und Widersprüche herausgestellt.

LOW DOSES OF CAFFEINE REDUCE HEART RATE DURING SUBMAXIMAL CYCLE ERGOMETRY

BACKGROUND The purpose of this study was to examine the cardiovascular effects of two low-levels of caffeine ingestion in non habitual caffeine users at various submaximal and maximal exercise intensities. METHODS Nine male subjects (19-25 yr; 83.3 +/- 3.1 kg; 184 +/- 2 cm), underwent three testing sessions administered in a randomized and double-blind fashion. During each session, subjects were provided 4 oz of water and a gelatin capsule containing a placebo, 1.5 mg/kg caffeine, or 3.0 mg/kg caffeine. After thirty minutes of rest, a warm-up (30 Watts for 2 min) the pedal rate of 60 rpm was maintained at a steady-state output of 60 watts for five minutes; increased to 120 watts for five minutes and to 180 watts for five minutes. After a 2 min rest the workload was 180 watts for one minute and increased by 30 watts every minute until exhaustion. Heart rate (HR) was measured during the last 15-seconds of each minute of submaximal exercise. Systolic blood pressure (BP) was measured at rest and during each of the three sub-maximal steady state power outputs. Minute ventilation (VE), Tidal volume (VT), Breathing frequency (Bf), Rating of perceived exertion (RPE), Respiratory exchange ratio (RER), and Oxygen consumption (VO2) were measured at rest and during each minute of exercise. RESULTS Caffeine at 1.5 and 3.0 mg/kg body weight significantly lowered (p < 0.05) HR during all three submaximal exercise intensities compared to placebo (range - 4 to 7 bpm lower) but not at rest or maximal exercise. BP was significantly higher (p < 0.05) at rest and after the 3 mg/kg caffeine vs placebo (116 +/- 13 vs 123 +/- 10 mm Hg). Neither dose of caffeine had any effect on BP during submaximal exercise. Caffeine had no effect on VE, VT, VO2, RPE, maximal power output or time to exhaustion. CONCLUSION In non habitual caffeine users it appears that consuming a caffeine pill (1.5 & 3.0 mg/kg) at a dose comparable to 1-3 cups of coffee lowers heart rate during submaximal exercise but not at near maximal and maximal exercise. In addition, this caffeine dose also only appears to affect systolic blood pressure at rest but not during cycling exercise.

INFLUENCE OF RESPIRATORY MUSCLE WORK ON VO2 AND LEG BLOOD FLOW DURING SUBMAX EXERCISE

The work of breathing (W(b)) normally incurred during maximal exercise not only requires substantial cardiac output and O(2) consumption (VO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q(leg)). We wondered whether the W(b) normally incurred during submaximal exercise would also reduce Q(leg). Therefore, we investigated the effects of changing the W(b) on Q(leg) via thermodilution in 10 healthy trained male cyclists [maximal VO(2) (VO(2 max)) = 59 +/- 9 ml. kg(-1). min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of VO(2 max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W(b) during submaximal exercise caused VO(2) to increase; decreasing the W(b) was associated with lower VO(2) (DeltaVO(2) = 0.12 and 0.21 l/min at 50 and 75% of VO(2 max), respectively, for approximately 100% change in W(b)). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or Q(leg) when W(b) was reduced or increased. Why are LVR, norepinephrine spillover, and Q(leg) influenced by the W(b) at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W(b) required makes insufficient demands for VO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W(b) during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or Q(leg).