Objectives: We hypothesized that the number and length of hospital admissions in people with Parkinson’s disease (PD) would increase immediately prior to admission to a care home relative to those ...who were able to continue living at home or who died. Method: PD patients at Hoehn and Yahr Stages III to V were followed-up over two and a half years with deaths and care home placements recorded. Hospital admissions data were collected over this period. Results: Of 286 patients included in the study, 7.3% entered a care home and 28.3% died. In the final 120 days prior to the study exit point (care home placement, death, or continued living at home), longer hospital stay was significantly associated with care home placement, after adjusting for the competing risk of death. Conclusion: Our data provide evidence that, for many people with PD, a period of crisis is reached immediately prior to care home placement.
Key points
Heavy‐intensity exercise causes a progressive increase in energy demand that contributes to exercise limitation.
This inefficiency arises within the locomotor muscles and is thought to be ...due to an increase in the ATP cost of power production; however, the responsible mechanism is unresolved.
We measured whole‐body O2 uptake and skeletal muscle ATP turnover by combined pulmonary gas exchange and magnetic resonance spectroscopy during moderate and heavy exercise in humans.
Muscle ATP synthesis rate increased throughout constant‐power heavy exercise, but this increase was unrelated to the progression of whole‐body inefficiency.
Our data indicate that the increased ATP requirement is not the sole cause of inefficiency during heavy exercise, and other mechanisms, such as increased O2 cost of ATP resynthesis, may contribute.
During constant‐power high‐intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2 sc ), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with 31P magnetic resonance spectroscopy (MRS) and whole‐body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee‐extension exercise in healthy participants (n = 14). Unlocalized 31P spectra were collected from the quadriceps throughout using a dual‐tuned (1H and 31P) surface coil with a simple pulse‐and‐acquire sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable V̇O2 sc (mean ± SD, 0.06 ± 0.12 l min−1) or change in PCr (30 ± 8 vs. 32 ± 7 mm) or ATPtot (24 ± 14 vs. 17 ± 14 mm min−1; each P = n.s.). During HVY, the V̇O2 sc was 0.37 ± 0.16 l min−1 (22 ± 8%), PCr decreased (19 ± 7 vs. 18 ± 7 mm, or 12 ± 15%; P < 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mm min−1, or 26 ± 30%; P < 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated with the V̇O2 sc during HVY (r2 = 0.06; P = n.s.). This lack of relationship between ΔATPtot and V̇O2 sc , together with a steepening of the PCr–V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O2 cost of ATP resynthesis; P/O).
Key points
Heavy‐intensity exercise causes a progressive increase in energy demand that contributes to exercise limitation.
This inefficiency arises within the locomotor muscles and is thought to be ...due to an increase in the ATP cost of power production; however, the responsible mechanism is unresolved.
We measured whole‐body O
2
uptake and skeletal muscle ATP turnover by combined pulmonary gas exchange and magnetic resonance spectroscopy during moderate and heavy exercise in humans.
Muscle ATP synthesis rate increased throughout constant‐power heavy exercise, but this increase was unrelated to the progression of whole‐body inefficiency.
Our data indicate that the increased ATP requirement is not the sole cause of inefficiency during heavy exercise, and other mechanisms, such as increased O
2
cost of ATP resynthesis, may contribute.
Abstract
During constant‐power high‐intensity exercise, the expected increase in oxygen uptake (
) is supplemented by a
slow component (
), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with
31
P magnetic resonance spectroscopy (MRS) and whole‐body
during moderate (MOD) and heavy (HVY) bilateral knee‐extension exercise in healthy participants (
n
= 14). Unlocalized
31
P spectra were collected from the quadriceps throughout using a dual‐tuned (
1
H and
31
P) surface coil with a simple pulse‐and‐acquire sequence. Total ATP turnover rate (ATP
tot
) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable
(mean ± SD, 0.06 ± 0.12 l min
−1
) or change in PCr (30 ± 8
vs
. 32 ± 7 m
m
) or ATP
tot
(24 ± 14
vs
. 17 ± 14 m
m
min
−1
; each
P =
n.s.). During HVY, the
was 0.37 ± 0.16 l min
−1
(22 ± 8%), PCr decreased (19 ± 7
vs
. 18 ± 7 m
m
, or 12 ± 15%;
P <
0.05) and ATP
tot
increased (38 ± 16
vs
. 44 ± 14 m
m
min
−1
, or 26 ± 30%;
P <
0.05) between 3 and 8 min. However, the increase in ATP
tot
(ΔATP
tot
) was not correlated with the
during HVY (
r
2
= 0.06;
P =
n.s.). This lack of relationship between ΔATP
tot
and
, together with a steepening of the PCr–
relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O
2
cost of ATP resynthesis; P/O).
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