marked increase in HR mediated by sympathetic activation. None-
theless, LF power decreased. Further studies also showed that
experimentally induced heart failure is associated with decreased
LF power (Watson, Hood, Ramchandra, McAllen, & May, 2007).
Passive orthostatic tilt is a common procedure to increase
cardiac sympathetic activity. Montano et al. (1994) reported that
tilt incline was accompanied by an increase in LF and a decrease in
HF oscillations (although no means or statistical results were pro-
vided), and they claimed that various studies documented rises in
normalized LF power and the LF/HF ratio during this procedure.
Mukai and Hayano (1995) found that LF power increased progres-
sively with tilt angle, but peaked at 30°. However, during high-level
tilt (30–90°) both the interbeat interval (IBI) and HF power
decreased progressively with tilt angle. Furlan et al. (2000) found
that tilt incline was accompanied by a decrease in absolute and
normalized HF HRV, whereas LF HRV increased only when
expressed in normalized units. Critical reviews of the orthostatic
tilt literature (Eckberg, 1997; Goldstein et al., 2011) led to the
conclusion that this maneuver is not associated clearly with
increased LF power, at least when expressed in absolute units (cf.
also Hopf et al., 1995; Peles et al., 1995; Piccirillo, Fimognari,
Viola,
&
Marigliano,
1995;
Vicek,
Radikova,
Penesova,
Kvetnansky, & Imrich, 2008; Wallin et al., 1992).
Psychophysiological studies commonly use psychological chal-
lenges such as mental arithmetic, attention and memory tasks,
shock avoidance, or video games to induce sympathetic activation.
In the Malliani et al. (1991) review, a study is reported in which
stress induced by mental arithmetic increased the LF and reduced
the HF bands. However, like the aforementioned manipulations,
most available studies on the effects of mental stress showed reduc-
tions of both HF and LF oscillations (e.g., Bernardi et al., 2000;
Duschek, Muckenthaler, Werner, & Reyes del Paso, 2009; Mulder,
1985, 1988; Sloan et al., 1996; van Roon, 1998). Given the con-
sistency of this effect, some authors proposed that the reduction in
HR oscillations around 0.1 Hz can be taken as an index of mental
effort/load (Mulder, 1988; van Roon, Mulder, Althaus, & Mulder,
situations associated with sympathetic stimulation decrease LF
HRV instead of increasing it and that this effect is widely inde-
pendent of the type of manipulation applied.
Effects of Pharmacological Manipulations of
Cardiovascular Regulation
From the hypothesis that LF HRV is a marker of cardiac sympa-
thetic activity, it can be deduced that pharmacological manipula-
tions inducing reflex increase in sympathetic outflow enhance the
LF component and that manipulations reducing sympathetic
drive diminish LF power. Pagani et al. (1997) found that during
nitroprusside-induced hypotension the LF component increased,
Parameters of Physically Active (A) and Sedentary (S) Participants
in the Martín-Vázquez and Reyes del Paso (2010) Study during
Baseline and a Mental Arithmetic Task
Baseline
Task
F(1,39)
p
h2
IBI
A
820 (93)
753 (76)
5.86
.020
.283
S
733 (126)
690 (100)
VLF
A
279 (218)
172 (114)
3.75
.060
.183
S
191 (133)
93 (58)
LF
A
1035 (774)
632 (406)
8.50
.006
.238
S
580 (388)
330 (214)
HF
A
1016 (1295)
598 (740)
4.61
.039
.128
S
295 (218)
193 (149)
Note. HRV was analyzed by means of adaptive autoregressive models
following algorithms by Bianchi, Mainardi, Melonni, Chierchiu, and
Cerutti (1997). IBI = interbeat interval, VLF = very low frequency,
LF = low frequency, HF = high frequency; F, p, and h2 values of the
ANOVA for group comparisons.
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