Examples of Moderate and Vigorous Physical Activity

Exercise experts measure activity in metabolic equivalents, or METs.

One MET is defined as the energy it takes to sit quietly. For the
average adult, this is about one calorie per every 2.2 pounds of body
weight per hour; someone who weighs 160 pounds would burn
approximately 70 calories an hour while sitting or sleeping.

Moderate-intensity activities are those that get you moving fast

enough or strenuously enough to burn off three to six times as much
energy per minute as you do when you are sitting quietly, or exercises
that clock in at 3 to 6 METs. Vigorous-intensity activities burn more
than 6 METs.

One limitation to this way of measuring exercise intensity is that it

does not consider the fact that some people have a higher level of
fitness than others. Thus, walking at 3 to 4 miles-per-hour is
considered to require 4 METs and to be a moderate-intensity activity,
regardless of who is doing the activitya young marathon runner or a
90-year-old grandmother. As you might imagine, a brisk walk would
likely be an easy activity for the marathon runner, but a very hard
activity for the grandmother.
Physiological basis
Cardiac chronotropy can be represented in two ways. Representation of cardiac
chronotropy by heart rate (HR) as beats per minute (bpm) has a long history
because it is readily and easily accessible by simple palpation of an artery.
However, HR provides an estimate that is normalized to time (i.e., 60 s). With
the development of the electrocardiogram (ECG), physiologists were able to
minutely assess the time interval between beats in milliseconds. In fact, this
linear measure of cardiac chronotropy better reflects its autonomic regulators.
The interval between R waves in the ECG (RRi) is most commonly used and
reflects a linear relationship to both parasympathetic (vagal) and sympathetic
stimulation [1, 2]. Given that HR is the inverse of RRi, fluctuations in the two
do not always conform to one another (Fig. 1). Hence, heart rate variability
should not be used as anything more than a misnomer and instead RRi
variability should be used. In this review, out of convenience and convention,
we will use the widely adopted term heart rate variability (HRV) to discuss the
physiology and measurement of RRi variability.

Measurement of heart rate variability

Changes in RRi defined as HRV indicate a normal response of the heart to
multiple physiological and environmental stimuli such as breathing, physical
exercise, mental stress, hemodynamic alterations, and metabolic changes [46,
47]. One way of understanding HRV is considering the variance with respect to
the mean, i.e., a measure of the spread of the distribution. The fluctuations
occur either in a random pattern (noise) or exhibit deterministic variations. As
described above, changes in RRi reflect autonomic modulation and provide a
sensitive and early indicator of health impairments. While high HRV is
associated with efficient autonomic mechanisms in healthy individuals, low
HRV is an indicator of abnormal and inadequate adaptations of the ANS and,
in some cases, increased mortality and morbidity. Thus, HRV has been
identified as a promising marker to study autonomic function and to diagnose
pathological states, both in research and clinical setups. A range of indexes
have been derived from fluctuations not just in heart period but also in blood
pressure, sympathetic nerve activity, blood flow, “spontaneous” bareoreflex
sensitivity, and cerebral "autoregulation". However, the significance and
meaning of HRV is more complex than generally appreciated and careful
examinations should be considered in measuring and interpreting it.
Quantitative approaches in assessing HRV include linear methods, time
domain, frequency domain, and nonlinear methods.
Rating of perceived exertion and heart rate as indicators
of exercise intensity in different environmental
temperatures.
Department of Health, Physical Education and Recreation, University of
Kansas, Lawrence 66045.
Abstract
This study examined the validity of rating of perceived exertion (RPE) and
heart rate (HR) obtained during incremental exercise (INC) as indicators of
intensity during constant load exercise (CL). Nine cyclists (VO2max = 53.3 +/-
8.9 ml.kg-1.min-1) performed INC to determine intensity at the onset of blood
lactate accumulation (OBLA). Three CL work bouts at OBLA were performed
in an environmental chamber with temperatures (30 degrees C, 22 degrees C,
14 degrees C) randomly assigned. RPE and HR were determined every 5 min.
Data during CL from initial 5 min (5 MIN), second 5 min (10 MIN), midpoint
(MID), and exhaustion (END) were used in treatment by time ANOVA to
examine differences between temperature conditions, with repeated measures
ANOVA testing for differences between INC and CL. Tukey HSD post-hoc
tests identified mean differences, with significance set at P < or = 0.01. No
significant differences across temperature conditions for RPE or HR were
found. RPE obtained at OBLA during INC (13.7 +/- 0.9) was significantly
different from 5 MIN, 10 MIN, MID, and END during CL in all temperatures.
HR obtained at OBLA during INC (165.4 +/- 12.3 bpm) was significantly
higher than 5 MIN for all temperatures (30 degrees C = 153.0 +/- 9.9; 22
degrees C = 151.0 +/- 11.8; 14 degrees C = 150.2 +/- 13.8), but was not
significantly different from INC for 10 MIN, MID, or END measures. The data
indicate HR is a more valid marker of exercise intensity than RPE.
Physiological Pacing: Present Status and Future
Developments
Abstract

With the increasing tendency to implant pacemakers not only for

life‐threatening bradycardias but also for improving cardiodynamics in patients
with bradycardia, it soon became apparenf that classical VVI pacing is not truly
able to optimize circulatory performance. Experience has shown fbat with
ventricular pacing augmentation of cardiac output takes place only initially but
is not maintained on a long‐term basis,1, 2 exercise capacity remains markedly
reduced,3, 5 (here is only an unsatisfactory influence on the degree and course
of heart failure2, 4, 6–9 and, in an occasional patient, cardiac function may
even deteriorate as compared to the situation prior to pacing.10–13 Because the
disappointing hemodynamic effect of fixed rate ventricular stimulation was at
least partly due to the “unphysiological” mode of pacing provided by those
systems which fail to restore AV synchrony and to increase heart rate with
changing metabolic requirements, so called physiological pacemakers were
developed. These pacing systems either maintain AV‐synchrony and/or
reestablish some way to adapt the pacing rate (Table I). This study delineates
the hemodynamics of the paced heart with special reference to the role of AV
relationship and rate control; it describes the clinical experience with
physiological pacing and provides some ideas leading to present and future
developments for rate adaptive pacing systems.