OBJECTIVETo assess differences between the effects of aerobic and resistance training on HbA1c (primary outcome) and several metabolic risk factors in subjects with type 2 diabetes, and to identify predictors of exercise-induced metabolic improvement.RESEARCH DESIGN AND METHODSType 2 diabetic patients (n = 40) were randomly assigned to aerobic training or resistance training. Before and after 4 months of intervention, metabolic phenotypes (including HbA1c, glucose clamp–measured insulin sensitivity, and oral glucose tolerance test–assessed β-cell function), body composition by dual-energy X-ray absorptiometry, visceral (VAT) and subcutaneous (SAT) adipose tissue by magnetic resonance imaging, cardiorespiratory fitness, and muscular strength were measured.RESULTSAfter training, increase in peak oxygen consumption (VO2peak) was greater in the aerobic group (time-by-group interaction P = 0.045), whereas increase in strength was greater in the resistance group (time-by-group interaction P < 0.0001). HbA1c was similarly reduced in both groups (−0.40% [95% CI −0.61 to −0.18] vs. −0.35% [−0.59 to −0.10], respectively). Total and truncal fat, VAT, and SAT were also similarly reduced in both groups, whereas insulin sensitivity and lean limb mass were similarly increased. β-Cell function showed no significant changes. In multivariate analyses, improvement in HbA1c after training was independently predicted by baseline HbA1c and by changes in VO2peak and truncal fat.CONCLUSIONSResistance training, similarly to aerobic training, improves metabolic features and insulin sensitivity and reduces abdominal fat in type 2 diabetic patients. Changes after training in VO2peak and truncal fat may be primary determinants of exercise-induced metabolic improvement.

Spontaneous oscillations of heart period and arterial pressure can be analysed by mathematical tools to extract the main frequency-related information. This is generally contained within three principal bands: a high-frequency (HF) band, related to the respiratory rate, a low-frequency (LF) band, centred around 0.1 Hz and a very-low-frequency (VLF) band, spanning the leftmost part of the spectrum.Pressure oscillations at the respiratory frequency are linked to rhythmic changes of intrathoracic pressure due to respiratory mechanics, while low-frequency fluctuations, often identified as Mayer's waves, are the result of efferent sympathetic activity (Polosa, 1984;Cevese et al. 1995). The interpretation of heart period fluctuations is more problematic, because it has to account for the interplay of sympathetic and vagal Baroreflex and oscillation of heart period at 0.1 Hz studied by a-blockade and cross-spectral analysis in healthy humansAntonio Cevese, Giosuè Gulli, Enrico Polati *, Leonardo Gottin * and Renato Grasso † 1. Parameters derived from frequency-domain analysis of heart period and blood pressure variability are gaining increasing importance in clinical practice. However, the underlying physiological mechanisms in human subjects are not fully understood. Here we address the question as to whether the low frequency variability (›0.1 Hz) of the heart period may depend on a baroreflex-mediated response to blood pressure oscillations, induced by the a-sympathetic drive on the peripheral resistance.2. Heart period (ECG), finger arterial pressure (Finapres) and respiratory airflow were recorded in eight healthy volunteers in the supine position with metronome respiration at 0.25 Hz. We inhibited the vascular response to the sympathetic vasomotor activity with a peripheral a-blocker (urapidil) and maintained mean blood pressure at control levels with angiotensin II.3. We performed spectral and cross-spectral analysis of heart period (RR) and systolic pressure to quantify the power of low-and high-frequency oscillations, phase shift, coherence and transfer function gain.4. In control conditions, spectral analysis yielded typical results. In the low-frequency range, cross-spectral analysis showed high coherence (> 0.5) and a negative phase shift (_65.1 ± 18 deg) between RR and systolic pressure, which indicates a 1-2 s lag in heart period changes in relation to pressure. In the high-frequency region, the phase shift was close to zero, indicating simultaneous fluctuations of RR and systolic pressure. During urapidil + angiotensin II infusion the low-frequency oscillations of both blood pressure and heart period were abolished in five cases. In the remaining three cases they were substantially reduced and lost their typical cross-spectral characteristics.5. We conclude that in supine rest conditions, the oscillation of RR at low frequency is almost entirely accounted for by a baroreflex mechanism, since it is not produced in the absence of a 0.1 Hz pressure oscillation.6. The results provide physiological support fo...

The recovery of the baseline autonomic control of cardiovascular activity after exercise has not been extensively studied. In 12 healthy subjects, we assessed the time-course of recovery by autoregressive spectrum and cross-spectrum analysis of heart period and systolic blood pressure during the 3 h after the end of 20 min of steady-state exercise at 50% (light workload, LW) and 80% (moderate workload, MW) of the individual's anaerobic threshold. The electrocardiogram and non-invasive blood pressure were simultaneously recorded during 10 min periods in the sitting position, at rest before exercise, and at 15, 60 and 180 min of recovery after exercise. At 15 min we observed a persistent tachycardia and relative hypotension; after MW, at 60 min heart rate was still slightly higher. Spectrum and cross-spectrum analysis showed, at 15 min, an increase in the low frequency component of systolic blood pressure, a reduction in the high frequency component of heart rate (larger in MW), and a decrease in baroreceptor sensitivity. After 60 and 180 min none of these parameters was significantly different from those at rest, although, in MW, some subjects still displayed signs of sympathetic activation after 1 h. We concluded that, after 15 min of recovery, the cardiovascular reflexes were blunted, that sympathetic nerve activity was still enhanced, and that the tone in the vagus had not fully recovered. Only the persistent vagal restraint seemed to be exercise intensity-dependent. For complete restoration of autonomic control after LW 1 h of rest was sufficient, and just enough after MW.

The effect in healthy elderly subjects of cycle ergometer or arm ergometer training on peak oxygen consumption (VO(2peak)) and ventilatory threshold (VT) was studied. The aim was to determine the benefit of each training modality on specific and cross exercise capacity. The cross-effect was also evaluated as an index of the central nature of the adaptive response to training. Twelve non-smoking healthy males (age: 67 +/- 5 year; body mass: 75 +/- 9 kg) were randomly divided in two age-matched groups of six, performing an arm cranking (ARM) or a cycloergometer (CYC) training (12-week, 30 min, 3 times/week), while a third group of 6 subjects (age: 73 +/- 4 year; body mass: 80 +/- 8 kg) performed no training (control, C). At baseline and following the intervention, subjects carried out an incremental test to exhaustion both on the ergometer on which they trained (specific test) and on the other ergometer (cross test). Respiratory variables were measured breath by breath and heart rate (HR) was recorded. Peak oxygen consumption (VO(2peak)), ventilation (VE(peak)), oxygen pulse (O2P(peak)) and heart rate (HR(peak)) were averaged over the last 10 s of exercise. Following training, while HR(peak) remained unchanged, significantly higher W(peak), VO(2peak), VE(peak) and O2P(peak) were obtained in both training groups, on both ergometers. The amplitude of the increase in W(peak), VO(2peak) and O2P(peak) was significantly higher for specific than for cross tests ( approximately 19% vs. approximately 8 % in CYC; approximately 22% vs. approximately 9% in ARM, P < 0.01) while the increase in same test condition was similar. No change was observed in the C group. The results indicate that aerobic training brought about with different muscle masses, produce similar improvements in maximal and submaximal exercise capacity. Roughly half of such improvements are specific to exercise mode, which suggests peripheral adaptations to training. The other half is non-specific since it influences also the alternative exercise modality, and is probably due to central adaptations.

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The spontaneous variability of heart rate and arterial blood pressure was investigated in chloralose-anesthetized dogs with the left iliac vascular bed mechanically uncoupled from the central circulation. Electrocardiogram, mean arterial pressure (ABP), iliac perfusion and venous pressures, and flow (FLOW) were recorded for 5 min in steady state. Autoregressive spectral and cross-spectral analyses and digital filtering were performed. The variation coefficient (VC%), calculated from the overall variance of each signal, was 5-7%, with the exception of perfusion pressure (VC% = 1%). The frequency-related percentage of total variance was distributed among three frequency bands: two were < 0.20 Hz [lower (F1) and higher (F2; low-frequency range = F1 + F2)], and one was > 0.20 Hz (respiratory, F3). F3 was not always present in RR, which, however, oscillated also in F1 and F2, although with limited amplitude; ABP showed large respiratory and low-frequency oscillations; the FLOW oscillations were in the low-frequency range. Cross-spectral analysis showed high squared coherence in the relevant frequency bands between variables in the three couples: RR-ABP, RR-FLOW, and ABP-FLOW. Changes in RR preceded changes in ABP and in FLOW by > or = 3 s, whereas FLOW was approximately in phase opposition to ABP. It was concluded that, in the chloralose-anesthetized dog, 1) arterial pressure and heart rate oscillate with frequencies corresponding to those described in conscious humans, 2) low-frequency arterial pressure oscillations are due to changes in peripheral vascular resistance, and 3) peripheral vascular resistance does not display respiratory oscillations. Furthermore it was suggested that oscillations of vasomotor tone are generated by a rhythm of central origin and that F1 and F2 oscillations may recognize a common mechanism.

We tested the validity of an new methodological approach to the calculation of oxygen uptake efficiency slope (OUES) [i.e. the use of exercise end-points based on fractions of heart rate reserve (HR(res))], as an alternative to the traditional time-based calculation. Twenty-nine healthy sedentaries >60 years of age (18 males, 11 females) performed an incremental cycling exercise to exhaustion. Respiratory variables and HR were measured breath by breath. Resting and peak variables were calculated and ventilatory threshold (VT) was identified by standard technique. OUES was calculated on 75, 90 and 100% of the incremental exercise data (OUES75, OUES90, OUES100) and on data corresponding to 60 and 80% of the HR(res) (OUES60%HR(res), OUES80%HR(res)). No significant difference (repeated measures ANOVA) was detected between time-based (OUES100, OUES90, OUES75) as well as HR(res)-based measures of OUES (OUES80%HR(res), OUES60%HR(res)). The Bland-Altman analysis revealed a bias not significantly different from 0 (22.0 and 53.3 for OUES80%HR(res)-OUES100 and OUES60%HR(res)-OUES100, respectively), a precision of 171.2 and 289.0 and 95% limits of agreement from -313 to +358 and from -513 to +620 for OUES80%HR(res)-OUES100 and for OUES60%HR(res)-OUES100, respectively. High correlations were detected between (VO(2peak)) and OUES60%(res) and OUES80%HR(res) (r (2) = 0.70 and 0.81, respectively) and between VT and OUES60%(res) and OUES80%HR(res) (r (2) = 0.58 and 0.66, respectively). The main finding of this study is that OUES can be reliably calculated based on HR(res) end-points during incremental cycling exercise, in healthy elderly subjects. Furthermore, our study confirms the validity of OUES as an indicator of aerobic exercise capability in this population.

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